This is framed as anti-Trump. He’s certainly not doing us much good during the times of Corona. This sounds like Governor’s are going to do an end around the FDA regulations! It looks like FAST Covid-19 tests may be on their way in a number of states. Bloomberg reports:
States Show Fury at Trump With Bipartisan Testing Plan
The seven-state effort to buy more than 3 million coronavirus antigen tests was born of need and disappointment. It was midwifed by the Rockefeller Foundation and Maryland Governor Larry Hogan and skirts President Donald Trump’s administration, even if many governors would prefer an approach coordinated by the federal government.
Looks like residents of Louisiana, Maryland, Massachusetts, Michigan, Ohio, North Carolina and Virginia may soon have access to fast turn around time antigen tests for Covid. Fast means 15-20 minutes.
The 500,000 tests for each of the listed states will likely not be enough to fill the need for fast tests. But this move by states will also be an important economic signal for manufacturers of fast response tests: There will be a market for these fast turn around antigen tests (which are having a difficult time getting FDA approval.)
The FDA does not take kindly to an end run. They will shut stuff down instantly if they can. It’s basically their entire reason for existence. They do need to go to a higher risk model than “peace time” for this coronavirus outbreak IMO.
The media would do themselves a favor by trying pretty hard to not frame things as pro/anti Trump due to people/organizations having a massive psychological problem with reversing a position once it has been publicly stated.
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I laughed this morning when the NYT ran an article about the CHOP zone in Seattle where all the business owners stated they thought in was Antifa causing all the problems, this after a parade of articles in the NYT denying this was the issue, all likely because Trump said it was Antifa.
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This is becoming the NYT’s MO lately, running a “balanced” counter narrative article weeks after it has stopped becoming news and burying it. Here they describe business owners in the CHOP having to profess loyalty to local groups and pay for “protection” from the newly established local mafia.
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Abolish the Police? Those Who Survived the Chaos in Seattle Aren’t So Sure
What is it like when a city abandons a neighborhood and the police vanish? Business owners describe a harrowing experience of calling for help and being left all alone.
https://www.nytimes.com/2020/08/07/us/defund-police-seattle-protests.html
Tom,
This is 7 states; I foresee lawsuits. 🙂
I’m sure those governors forsee it too. Presumably, their legal eagles have theories of of why they are allowed to do this. We’ll see how persuasive courts act. Given how courts work, some judges might stall with rulings that allow the testing to be in place until further decisions. That would allow the testing while forcing the FDA to make its case. So.. we’ll see!
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This is a BIG enough move, Enough people care about covid that it’s going to get press. It could get Congress off their collective ass to write something to deal with the need for regulation to require consideration of *epidemilogic need*. In principle, Trump is against unnecessary and counter productive regulation. Executive Orders have been known to direct federal agencies to change things.
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Congressional action certainly does.
I believe the FDA has some very clear legislative power, directives, and enforcement ability to protect people from rogue medical devices. They will likely win in court, you have to prove your device/drug effective to the FDA first, period, end of story, no exceptions. You can see this in action with Theranos, although they skated the regulations for a few years. The FDA will literally chain your doors shut.
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There are some gray areas for products that don’t make any medical claims in the food supplement/vitamin area. There is also some “off label” use gray area. Do not get caught as a company representative making any unapproved medical claims or the sh** will hit the fan.
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States lighting a fire under the FDA’s butt is a good thing though.
The FDA has rushed through all sorts of emergency approvals. Why is that not the case here? Maybe it is the case and this is just a few Democrat governors playing political games. OK, DeWine is a Republican, but it seems like he has been acting like a Democrat with regard to the Wuhan virus.
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By the way, what good are antibody tests? They are really valuable for research, but do they have a public health application?
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In case it is necessary: Real questions.
FL cases are down 40% in the last 3 weeks. Deaths are likely just past peak now. Hospitalizations are down, and there is about 20% ICU availability depending on region.
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Many states are showing strong declines with eerily similar timing.
https://www.washingtonpost.com/graphics/2020/national/coronavirus-us-cases-deaths/
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This is a bit too correlated and I’m not sure what to make of it. There was some behavior changes with mask rules but I’ll I’m seeing now is mass shut down fatigue. People only doing “mask theater” and lots of open defiance of social distancing. It’s really hard to connect cause and effect at the moment.
Tom,
I agree it would be wiser if the media didn’t frame this as anti-Trump. While I think Trump isn’t being effective wrt to tests, I don’t think he specifically is the problem. It’s “THE FDA” and principally, long time people who simply have come to see their philosophy of regulation as “THE RIGHT” philosophy. That regulation of diagnostic tests were developed for a different problem isn’t necessarily something they automatically think of.
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This is something of a human failing– theyve been enforcing and creating ‘the rules’ and the reason for them sort of fades into obscurity.
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Trumps failing here– and, ahem, he has them, is to not be speaking out on the need for *epidemilogical* tests and– assuming an executive order to tailor considerations could help– not issuing one. This is either because he also doesn’t understand the epidemiological need or because.. well… Trump’s kinda sort about Trump or something. At that, journal articles discussing exactcly why these tests are what we need are just coming out. So perhaps the amount of “blame” isn’t that severe all around. But Trump does have access to advisors, he’s not really developing the vision we need on this. He certainly does deserve some criticism.
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Still, I think what’s really happening is an end run around the FDA. A less partisan article would say the FDA. Sure, that’s in the executive branch, and so part of “Trump’s administration”. But it more directly tailors the issue so that we can fix it. It’s not as if Trump himself made an order to prevent these from being made. It’s more specifically “regulators”.
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Antibody tests should be useful to determine the actual prevalence of the disease in the community. Giving best estimates for all the missing cases that aren’t being testing. Maybe this is what you call research. On a personal level it is liberating to know you already had the disease. From a public health perspective one could envision only allowing people who had the disease interact with high risk populations. I don’t think that is happening though.
I defy you to prove a single Trump failing, ha ha. The media lost its mind when Trump said young people were “immune” to the disease. I knew exactly what he meant (they die at hugely lower rates) but as usual the media took his words literally in order to prove he was maliciously lying or something and denounced him in unison without any charity with what he likely meant.
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He should speak more accurately but he just doesn’t care about the literacy critics out there. I simply ignore him and I don’t know anyone who listens to him on this subject. This was just another case of bad faith fact checking, snore.
Tom Scharf (Comment #188815): “Antibody tests should be useful to determine the actual prevalence of the disease in the community. Giving best estimates for all the missing cases that aren’t being testing. Maybe this is what you call research.”
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Yes. But that does not require millions of tests. 10K random tests per week should be plenty.
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Tom Scharf: “On a personal level it is liberating to know you already had the disease. From a public health perspective one could envision only allowing people who had the disease interact with high risk populations. I don’t think that is happening though.”
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That would make sense *if* the antibodies were long lasting. But they are not. So what if you had the antibodies at some point in the past and I don’t have them? If the antibodies are required for protection, then maybe you are no longer are safe. And if T cell response is enough, then maybe I am safe.
Tom Scharf,
Prove? Some failings are a matter of opinion. I think his incessant self-promotional tweeting is a failing. I think his rather incomprehensible statements are a failing. You might like them or even consider them strengths.
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But since these are opinions, there can be no ‘proof’.
MikeM
We don’t know they are not. Moreover, even if they aren’t memory T-Cell response would likely be sufficient. There is evidence that exists.
lucia (Comment #188821): “We don’t know they are not.”
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Reports that I have seen have been saying the antibodies last for about two months. But it looks like there have not been many studies and they had small sample sizes.
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lucia: “Moreover, even if they aren’t memory T-Cell response would likely be sufficient. There is evidence that exists.”
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Yes, I said that. But what has that got to do with antibody tests?
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A positive antibody test says that you may or may not be immune. A negative antibody test says that you may or may not be immune. The only differences that I see are that the odds are better in the former case and that the former might produce a dangerous false sense of security.
Tom Scharf
Sure. But that’s not the only valid goal during an epidemic. Reducing transmission is a valid goal. In our particular circumstance, if we can reduce it a lot that will reduce the number who die or are debilitated before we have a vaccine. With enough cheap testing Ro could be driven so low we could achieve near eradication. (Cheap antigen tests with fast turn around times actually have promise in achieving both goals I described. Expensive PCR tests do not. )
The Supreme Court has already ruled states are not bound by FDA rules, in a case involving patents if I remember correctly.
States can distribute or sell tests without FDA permission.
The only avenue for the FDA might be they can go after the manufacturer.
MikeN,
Ok. I see your point on the antibodies. I read quickly and only connected with “only letting people with antibodies interact”. So my mind jumped to the idea that the purpose was to identify immunity.
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Cool about the SCOTUS decision! We’ll probably learn more about precisely what the FDA allows. After all: the states are buying these and presumably the state us using them. We’ll see where that puts things.
BTW: This articles says the tests the states are buying are authorized for sale:
https://www.medtechdive.com/news/7-states-ally-to-buy-covid-19-antigen-tests-bd-and-quidel-to-get-initial-o/582938/
Ok… perhaps not an endrun. (But not what the FDA has been promoting. )
https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-fda-provides-more-regulatory-relief-during-outbreak-continues-help
OK, so it looks like the spin in the Bloomberg article was just Orange Man Bad.
I don’t see what the big deal is or why the states need an interstate compact. Maybe somebody can explain what I am missing.
Earlier, I mistook the anitigen test for an antibody test, whereas it is a test for the viral proteins. So it would seem to be a valuable tool for screening. With a delay of several days for PCR, the value of the test is largely lost.
I’m finding other articles that don’t have that spin. In fact: it appears the governors are using precisely a permission granted by “Trump’s” FDA in this situation. It’s true TRUMP isn’t buying the kits.. but.. well… yeah. Spin.
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I’m not sure why they need a compact. Perhaps it’s got to do with financing or turning this into a huge purchase encouraging the companies to ramp up production.
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Some other articles are suggesting that the big sale is leading for these companies to arrange licensing to allow more manufacturers to put together test kits. If so, the “big” points may merely be:
(1) Formal use of these tests is ramping up which will cut time. (Good thing in my view.)
(2) The purchase will create a big economic incentive to companies to create these fast (and fwiw cheap) tests.
(3) Governors are acting. (Yay federalism!! 🙂 )
(4) These will soon be deployed in 7 states.
(5) With luck other states will follow.
The article doesn’t put in the other points that are circulating in articles promoting the use of these types of fast cheap tests. But I can’t help connecting those dots. Because these are the tests that can stem epidemics or keep us safer while waiting for a vaccine. I’m not going to slam PCR tests– they are good for clinical use. But these fast cheap tests are what we need and we need them now.
Oh– other reason for compact: We’ve seen states get slammed for making their own decision. Maybe the governors feel the need to present a group action to avoid having someone slam them for using “less accurate” tests.
“ First, we are putting in place a policy for states to take responsibility for tests developed and used by laboratories in their states…â€
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Yes, take responsibility. If the newly available tests help, then the states can take the credit as well. I think there is tremendous resistance at the FDA to not control ‘everything health care’, but they probably recognize they would lose at the SC.
Blue states were big on creating compacts on reopening. Nobody wanted to be first because the media would leap on the first one out for killing grandma.
Tom Scharf,
“… because the media would leap on the first one out for killing grandma.â€
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Unless the governor’s name is Cuomo or Murphy, who killed lots of grandmas (and grandpas). I don’t think Democrats anywhere are afraid of attacks by the MSM so long as they don’t cooperate with Trump in any way. It is a bit like the communists in the old Soviet Union not being afraid of Pravda…. the US MSM is the propaganda arm of the Democratic party, nothing more.
Interesting, your site not coming up on a duck duck go search had to get in through WUWT.
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Relevant to this discussion.
“Ohio’s DeWine Seeks to Reassure Residents on Covid-19 Test Accuracy After Conflicting Results
Governor received a positive quick antigen test result at a White House visit., and then two negative results from a more sensitive test
The second test was a PCR test, which De Wine’s office said was “extremely sensitive, as well as specific, for the virus.”
PCR or polymerase chain reaction tests are considered the most accurate kind available on the market, but demand has often overwhelmed supply, leading to delays. These tests detect genetic material related to the virus, while antigen tests look for protein fragments found on or within the virus.”
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In India, the ICMR conducted an independent two-site evaluation of the SD Biosensor kit.
The results revealed that the kit had a very high specificity, or the ability to detect true negatives, ranging between 99.3% and 100% at the two sites. The sensitivity of the test, or its ability to detect true positives, ranged between 50.6% and 84%, depending upon the viral load of the patient. The higher the ability to detect true negatives, the more reliable is any positive result.”
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???
My slight interest in PCR testing goes back to the days of getting a good test for chlamydia infections which was extremely hard to detect.
The test works by duplicating a piece of RNA or DNA 40 times in a row. What initially was a single short segment of DNA can be amplified to about 100 billion copies after 40 doubling cycles.
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Rapid tests on the other hand tend to detect the target proteins by a build up as the tested material flows through bound antibody.
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PCR is very quick and very accurate.
Rapid tests of non RNA/DNA can be done more quickly but lacking the multiplying effect of PCR cannot be as accurate.
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Testing, as the Guru Bill Gates has said, is basically worthless.
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Ask what are we trying to achieve?
and What population group are we trying to achieve the result in?
Ask how long we have had the tests to be able to access them??
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Antibody tests are best reserved for long term epidemiology studies, they involve taking as blood sample. Most people will not volunteer to this without a reason.
They have a minor place in confirming true infection after a couple of weeks. IgM antibodies arise early, 1-2 weeks and disappear early 6-8 weeks. IgG antibodies arise more slowly 2-6 weeks but persist for life albeit they can drop to very low barely detectable levels after moths to years but are programmed to appear and work with future infection.People mistake this for waning immunity which is not correct.
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Large populations with low numbers of cases will have a large number of false positives, much more so with rapid tests. So early random testing in an outbreak only cause fear and terror in innocent people.
Large populations with high cases will have a lower false positive rate but will have even more false positives. Knowing you are infected when half the people around you are infected will have little impact on how many people you infected before you had your test and give no insight into whether you are actually just in the early stages of the infection.
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There are advantages.
It makes you look as if you are doing something. Very important for political parties.
It means you can compare your actions to others in a positive political way.
And it helps reduce the chance of catching an infection if you are the President [very sensible].
In the health setting of Nursing Homes and hospitals it would help speed up detection of Carers and patients with the infection and help reduce the risk of spread in that extremely high risk area.
angech,
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In Illinois, the effective turn around time for PCR tests taken by people reporting to testing sites is 2 – 14 days. I know you can get a test back faster if you are admitted to the hospital, but it’s taking lots of time “in the wild”.
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What I’d like to achieve is getting infectious people isolated before the infect others. This can’t be done if the turn around is 4 or more days. For the most part, false positive rates in the rate we are seeing with antigen and LAMP tests are acceptable. It’s not as if we shoot people who trigger positives. The “worst” is they might not be allowed to report to a work site (that might not be operating at all if we had no testing available.)
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A follow up tests can be applied and those who get false positives can be sprung. So the penalty for a false positive is small.
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A tests implemented to screen people and contain viral spread would be “doing something”. It wouldn’t be merely looking as if you are doing something.
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The big issue is not hospitals, or carers. It’s meat packing plants, food processing, retail businesses and so on. We need these running. Hospitals actually have facilities and protocols to deal with infectious diseases. Meat packing doesn’t and, moreover, can’t do it easily.
A massive experiment re lockdowns is underway in Sturgis, SD.
https://www.foxnews.com/us/sturgis-rally-roars-ahead-despite-covid-concerns
It seems they expecting half the normal attendance at the motorcycle rally, “only” about 250K.
Mike M,
I’d stay away from that motor cycle rally!!!
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Of course, I wouldn’t go even if there was no Covid. 🙂
Lucia,
“ I’d stay away from that motor cycle rally!!!â€
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Ya, but if you liked riding motorcycles as much as you like ballroom dance? Especially if you had a skull tattoo on your right shoulder. 😉
I’d be tempted. But, having said that, I didn’t sign up for “Heart of america” dance competition that would have happened this month. The live event got cancelled and they are trying to run an online event.
Not quite on-topic for this post, but it is related to Covid…
Look at what was done on the graph in this tweet
Pretty amazing anyone would put that out.
HaroldW,
Stupid, dishonest, or maybe both.
SteveF,
The graph is dishonest and the author thinks we’re stupid.
Wow!!! That’s an amazing example of graphs-that-lie! He’s at least stoooooopid. Either (a) he doesn’t know you don’t do that or (b) he does know, but he doesn’t know other people also know and will certainly make hay.
In both cases the person who made the graph and used it is stupid!
The guy who made the graph claims that the point is the slope, not the number of cases. But there is no indication of *when* the mask mandates went into effect. And there are good reasons why places with a high case load might be dropping while ones with a small load is not changing.
So maybe deliberately dishonest, but more likely just good old confirmation bias. He found a way to present the data that agreed with what he thought the result should be, so he just assumed that it showed that.
If you follow the links, the guy who made the graph is unapologetic and insists it is valid.
MikeM,
The graph doesn’t make point about the slope either. Among other things, it doesn’t tell us WHEN masks regulations started.
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Honestly, the graphs might suggest is that high case numbers is “the cause” and masks are “the effect”. In fact, that may well be true. No one puts in place mask rules if there is no COVID circulating. It would be totally pointless.
“tests implemented to screen people and contain viral spread would be “doing somethingâ€. It wouldn’t be merely looking as if you are doing something.“
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“What I’d like to achieve is getting infectious people isolated before the infect others. This can’t be done if the turn around is 4 or more days.â€
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I agree with your aims and sentiments.
I have In a small way been trying to help get some plans into place to deal with a Covid outbreak In our town.
Now we have one starting. The only thing I achieved was a heightened sense of awareness in the powers that be that may help a more rapid and effective response.
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It is impossible to get infectious people isolated before they infect others because the delay in getting results is not the problem.
How to put it.
Viral disease can be asymptomatic but infectious.
Anyone can have it.
Testing is expensive.
Testing asymptomatic people every day is therefore impossible.
Testing people more at risk very day is impossible.
Whether they are health workers or elderly or abattoir workers.
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Testing people with symptoms, temperature, cold, pneumonia, will confirm if they have it and allow lockdown of contacts and less ongoing spread.
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But you do not need a test to do this.
You could just lock down and isolate everyone with a symptom and their contacts without testing.
Which achieves the goal you want but is impractical.
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Having a quicker test does not mean you can avoid the lockdown as if symptomatic the test could be wrong and really needs a repeat anyway in 24 hours.Three if originally positive but second negative.
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PCR testing is available and technically very quick. The priority in Illinois should be to get more machines, more staff and a quicker turnaround time.
Testing is not the problem and not the answer.
The old glass thermometer, very cheap and reliable, go to bed for 14 days if you have a temperature, see no one and have Uber deliver food to the door, text your contacts and put the self isolation obligation on?
The deaths per million in Kansas is among the lowest in the USA. I guessing that most of those deaths come from the (few) densely populated areas, and the rest of the state is very low in deaths. It’s another example of politics twisting what should be a technical evaluation; make them all wear masks….. because we said so!
angech
It doesn’t need to be.
The math shows that even with error rates at level expected for cheap less-accurate tests, you can contain by testing often.
angech
Thermometers may be ok for clinicians. They are definitely not sufficient for identifying who needs to be isolated precisely because people are infectious before they show symptoms like elevated temperature.
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Your discussion reads like something a clinician would think. That’s fine. We need clinicians. But what we need for treatment is different from what we need to stem spread.
Lucia, angech,
This paper suggests that asymptomatic carriers infect (on average) less than one person, while symptomatic carriers infect (on average) 3 people. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7322154/
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They say that intimate contacts (eg household members) have transmission from both type of carriers that is not statistically different. Which I guess means those who develop symptoms carry a much higher viral load than those who do not, but given enough time and contact with an asymptomatic carrier makes transmission as probable for an asymptomatic carrier as a symptomatic carrier.
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But the problem is that by the time someone is symptomatic, the viral load has already started dropping. So while contract tracing may only make sense for people who developed symptoms, we still don’t know how long someone who ultimately becomes symptomatic is infectious prior to onset of symptoms. There remains a lack of useful information about the length of infective period, which makes developing sensible public policy more difficult.
SteveF,
That paper highlights why you can not craft a policy based on catching people based on symptoms. The fast turn around tests can catch people who have viral loads but are not symptomatic. However, you have to be testing asymptomatic people.
That’s the plan at UIUC. They’ll test 60,000 students and faculty several times a week. The first tests uses the cheap tests. Those who get positives (even false positives) will be quarantined. They will also be retested using the more expensive and more sentivity tests. The ones who turn out to be false positives will be released. But it means a large fraction of infections people will be quarantied whether or not they become symptomatic and before they are symptomatic.
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False negatives would be a problem in principle. But it’s thought the reason for false negatives are because you are technically infected, but your viral load hasn’t risen. So you are effectively not infectious yet. They’ll get caught on the next tests within 2 days– so they won’t infect many people.
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This is going to be done at UIUC. So we’ll see how it works. But the idea is to isolate the infectious. We know it can’t be done if we only test after people have symptoms because they will have already infected others.
Lucia,
200,000 tests per week at one school? I don’t know for sure, but I think motivating students to be tested 3 times per week may be a bit of a challenge, and certainly as much a challenge as getting them to show up for all their classes. I also wonder how compliant students with few or no symptoms (that could be 9 out of 10 positive cases) are going to be about quarantines. I wish them luck, but I will be surprised if it works out as planned.
SteveF (Comment #188880): “This paper suggests that asymptomatic carriers infect (on average) less than one person, while symptomatic carriers infect (on average) 3 people. … But the problem is that by the time someone is symptomatic, the viral load has already started dropping. So while contract tracing may only make sense for people who developed symptoms, we still don’t know how long someone who ultimately becomes symptomatic is infectious prior to onset of symptoms.”
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lucia (Comment #188882): “That paper highlights why you can not craft a policy based on catching people based on symptoms.”
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I think that SteveF makes a very good point that lucia has missed. We don’t know when or for how long people are infectious. Viral load is *not* a measure of infectiousness.
Viral load measures viral DNA, dead or alive, in your mucous. You are not infectious unless the virus is alive and able to get out of you and into others.
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So consider the following two tentative facts, tentative since they are based on very limited data. First is that asymptomatic people are much less contagious than symptomatic people, rarely transmitting the illness to those who they do not live with. Second is that symptomatic and asymptomatic people have similar viral loads (https://www.bbc.com/news/health-53665008). Together they imply than symptoms are important to transmission.
Duh. If you are coughing and sneezing with a runny nose, you are way more likely to transmit to transmit the virus than if you are not.
So it is quite likely that presymptomatic people are not a big problem, except in situations where transmission is especially favored.
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How is it that we don’t know the patterns of infectiveness? At least some states have been doing contact tracing since March. The CDC d@~^ well better have been doing so, as well as collating and analyzing all the data from the states. By now they ought to *know* the extent of asymptomatic and presymptomatic transmission. It is a disgrace.
MikeN,
I didn’t miss that. But I still think that only means that testing before someone is symptomatic is what is necessary. I’m pretty sure that when load is on the way up at the beginning of an infection, the viral load represents live virus. Dead virus doesn’t multiple and rise. Exhaling, spitting or somehow depositing live virus is how we think the virus passes. So: the load of live virus is what matters. If we catch and isolate people whose viral load is high and on the way up we will dramatically reduce spread.
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Catching them after the have symptoms is pointless. As you point out their viral load might just be dead RNA.
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So as far as I can see, this is precisely why tests need to be early and often if used to stem spread. Later tests can be useful for clinical diagnosis or treatment (which is what doctors need.) But they are useless for stemming spread.
Except then the pre-symptomatic soon become symptomatic. If you only tests after symptoms start, they spread before they are tested. If you isolate them while their viral loads are rising, you have them away from people during the critical period when they are most infectious. That’s the purpose of frequent testing.
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I could see objection to the idea of isolation if it was equivalent to invasive surgery like breast biopsies after false positive mammograms or surgery for prostate cancer that turns out to not be required. But 24 hour isolation or even 48 hour isolation at home, a special dorm room or so on — with access to the internet, netflix isn’t any worse than what we been effectively imposed on everyone in Illinois in March. It’s what lots of people are more or less doing. This is a way to let us generally relax quarantines by knowing who has a high probability of being infectious when they are infectious.
Looks like all of the populous states that had a “second wave” of cases are now well past peak in cases, and at or slightly past peak in deaths. So for the whole of the USA, cases have peaked (a second time) and deaths as well (the second death peak far lower than the earlier peak). The ratio of deaths to cases in the second peak looks to be ~1/4 the first peak. Part of that is more testing, but part is likely due to a change in the age of the population with symptomatic illness.
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The pandemic looks to be finally winding down in the USA, with total deaths when it is over likely near 200,000, or a bit over 600 per million population. My swag: under 200 deaths per day by mid October.
lucia (Comment #188892): “Exhaling, spitting or somehow depositing live virus is how we think the virus passes.”
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Except that we don’t know the main transmission mechanism. The virus is not all that contagious. Coughing etc. must dramatically increase the rate at which the virus is expelled into the environment. So coughing might well be necessary to transmit the virus with any efficiency unless conditions for transmission are highly favorable, such as within a home, or a meat packing plant, or a crowded enclosed space where people are shouting are singing.
Mike M.,
You left out restaurants. A superspreader transmission in a restaurant has been reported. The infection followed the flow of air in the room with the exception of two people at an upstream table closest to the transmitter, which can be explained by turbulence. Maybe there was shouting and singing, but I doubt it.
If the virus is not all that contagious, how come there appears to be a drastic drop in influenza in the southern hemisphere while COVID-19 continues to spread rapidly? That would imply that SARS-CoV-2 is more contagious than influenza.
Trump is being accused of not doing much ..
However that is how the constitution breaks down Federal and State rights .
The Federal government is not the agency that controls shut downs with in the states.
Some states have done well, some have not….just as it is to be expected.
Opponents of the president hope to force him into usurping state rights so they can accuse him of dictatorial practices.
He has been very careful to allow states to bury themselves .
If Federal help is requested, then he is allowed to pick up the ball that was dropped by the States .
In the matter of federal property, he is obligated to protect it . It is not state property or responsibility in any state .
This is why Trump can not order schools to open without declaring a national emergency.
So he is accused of not helping or being a dictator. All based upon the political fancies of the accuser .
DeWitt Payne (Comment #188895): “You left out restaurants. A superspreader transmission in a restaurant has been reported.”
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One event? Symptomatic? How close and for how long?
There have been events in restaurants. Hardly surprising you have people close to each other for an extended time with a great deal of possibly loud talking.
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DeWitt: “more contagious than influenza”.
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Maybe the Wuhan virus spreads more easily in a virgin population than influenza spreads in a population in which everyone has had the disease, probably multiple times and half the population has had a recent vaccination. But even that is not clear. We are six months into this epidemic and the number of cases seems to be in the same ballpark as a typical flu season, most of which happens in just a few months.
——-
Addition: It certainly seems that the Wuhan virus spreads differently than the flu with a small fraction of people responsible for most of the transmission:
https://www.nytimes.com/2020/06/30/science/how-coronavirus-spreads.html
The reason is far from clear. The speculation in the article seems plausible, but why would the flu not be the same?
MikeM
.
The superspread restarant I’ve read about was in China. They had a window air conditioner unit that directed air across tables. People downstream of the infected person got sick.
How much does a test cost?
No one says.
Who makes them and how are they made?
No one says
How many laboratories making them now have live virus sitting around to help make the tests and test the tests and how is it stored and how safely is it stored?
No one says.
–
Steves point
60000 tests once a week on asymptomatic kids and staff?
The cost is not only the test.
Line up to do the test.
People, now at high risk, to do the test, in PPE.
Wages,
People to dispose of the POP , wages.
People to do the quick 2 hour tests, wages
People and time to contact all 60000 on results, large wages.
Positive result?
Wages.
–
Maths, 1 person dies every three days naturally in a group that size .
120 a year.
Covid likely to infect 1 % of the school population death rate in students of that age.
Death rate in that group 0.1%??
0.6 of a student dies per year.
–
Yes, I know the maths is totally wrong and any preventable death is wrong.
angech,
Articles I’ve linked here give ranges of costs. From my recallection:
* ingredients for PCR tests are about $40. A test typically bills out at $100 to insurance companies.
* ingredients for a LAMP tests are about $0.07. These typically don’t bill out to insurance companies because they are currently not approved by regulators for… reasons. Actual off the shelf tests could end up anywhere in the price range depending on what regulators end up requiring.
* I haven’t seen the cost of antigen tests to detect infection. But they typically are described as “cheap” (the way LAMP tests are desecribed).Actual off the shelf tests could end up anywhere in the price range depending on what regulators end up requiring.
* I haven’t seen the cost of tests to determine immunity.
I refer to the PCR tests as “expensive”.
angech
It’s going to be done. UIUC doesn’t have infinite resources. They likely have figured the cost issues out.
Angech
The main problem is that students being ill for two weeks is also costly. It’s really hard to catch up during the semester.
Lucia,
“The main problem is that students being ill for two weeks is also costly. It’s really hard to catch up during the semester.â€
.
Sure, for some kids, in some courses. But not always. I knew a guy who showed up first day, mid-term exam, and final exam. Lectures? Forgetaboutit. Studied on his own, and aced every class he was in with me. Ended up in physics, and last I knew headed for grad school. Kinda smart. Yes, some kids in STEM would struggle with a 2 week loss, but most kids are in fluff majors; they could keep up easily.
Here is a summary of a very interesting Swedish study on T cell response that is yet to be published:
https://sebastianrushworth.com/2020/08/08/what-is-the-best-way-to-measure-rates-of-covid-immunity/
.
0/37 samples from blood donors a year ago had T cells.
53/54 people who recovered had T cells. 50 had antibodies.
26/28 family members of the recovered group had T cells; the group was limited to family members who themselves were never sick. But just 17 had antibodies.
9/31 blood donors back in May had T cells, just 4 had antibodies.
Small samples, but still very interesting. It indicates that antibodies under count the number exposed and that the T cells are from the Wuhan virus, not one of the old coronaviruses.
The previous post Rushworth mentions at the start of this post talks about his observations during the epidemic. He works in a Stockholm ER.
Mike M,
I think it is clear that the covid (Wuhan) virus is enough related to other coronaviruses that there is considerable cross-resistance among those who have had a “common cold†coronavirus in the recent past. It is enough different to pose a much greater risk to seniors (and those with other serious health issues). But otherwise, there is nothing special about the virus.
.
A few places subject to a combination of extreme crowding conditions and extremely stupid politicians, like NYC, will suffer higher death rates (like 1:600 of the population), but in most places, the rate of death will not pass 1:1600 of the population. “Young countriesâ€, with very low median age, will hardly see a blip in fatalities. After the pandemic passes, most people in the States will not personally know someone who died from covid 19. So it is not the black death, even if the MSM screams that kind of rubbish constantly,
SteveF
True. Not the black death.
SteveF My swag: under 200 deaths per day by mid October.
Good for you for taking a stab. My swag is that rising herd immunity isnt as important as preventative measures like shutting down bars, masks, testing and isolating etc., and consequently cases will rise again as measures relaxed but maybe only up to 500 a day. I love to be proved wrong though and that Swedish study is very interesting. Time to scale the sample size.
Phil,
Cases and deaths are rising in Illinois where I live. We’ve been easing on shut down measures.
SteveF (Comment #188907): “I think it is clear that the covid (Wuhan) virus is enough related to other coronaviruses that there is considerable cross-resistance among those who have had a “common cold†coronavirus in the recent past.”
.
Is there evidence for that? I think I saw something about T cells in pre-epidemic blood samples, but I am not sure about that and the Swedish data implies otherwise. There are people who never knowingly had the disease, don’t have antibodies, and do have T cells, but that could be due to an asymptomatic infection.
lucia (Comment #188911): “Cases and deaths are rising in Illinois where I live.”
.
In areas that already have had a lot of cases, or downstate where there have not been many cases? Real question, I am curious.
MikeM,
I haven’t looked at every county. I looked at cases and deaths for the state as a whole yesterday.
I look at deaths in the region Pritzker dubbed “NorthEast” when we first went into stay at home or whatever you want to call it. DuPage, Will, Lake and Kane were way up last week. Last week, weekly average deaths in one of these counties were up 500%, another 200% and so on) Cook’s
.
I’ll have to add some lines to code to look at all the other regions. Unfortunately, that means I need to figure out which fips are which counties. (It’s not that hard. It’s just a task I haven’t done and … I have a few other things I want to do today.)
MikeM
I think an article I read said blood drawn before the epidemic did not have the Tcells they were looking at.
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What little I’ve learned about Tcells, I’ve learned during the course of this epidemic. So I have no idea whether Tcells from other corona viruses would be exactly the same and so detected by this test or just somewhat similar and not. I also don’t know if “similar” might possibly be cross-reactive and give some protection.
.
The article didn’t discuss this question that occurred to me. So… dunno.
Mike M,
The Swedish data does not suggest anything about other coronaviruses, but rather that many people develop T-cells which target the covid-19 virus without ever having symptomatic illness, nor generating a measurable level of antibodies.
.
There was one study where the reactivity of pre-covid T-cell populations to different parts of the civid-19 virus was evaluated. A substantial fraction of blood samples (>35% IIRC), either taken before the virus started spreading in late 2019 or from places were no cases had been detected, carried T-cells reactive to some conserved parts of the covid-19 virus.
.
A separate paper was published several years ago about an “outbreak†of virus illness in a nursing home which killed several residents and sickened staff. Blood tests taken at the nursing home were positive for antibodies to the original SARS virus (not covid), but it turned out the antibody test for SARS was cross reactive with antibodies for a “normal†coronavirus that causes colds… that virus spread in the nursing home, not SARS. This again suggests significant similarities across coronavirus types.
SteveF,
I think that may clarify. From what you say, it sounds like the Tcells from SARS would be sufficiently similar to those for Covid to achieve some degree of cross-reactivity. But a test that looked for an exact match to Covid would not find COVID t-cells.
.
Then, it’s possible those who had SARS would be functionally immune to Covid. But (and I’m guessing here) if the inhaled Covid, their body might now make Covid t-cells even though the SARS t-cells were also responding. Of course, I’d need to talk to someone who really knows biology to find out if this is (or maybe) the correct interpretation of the two tests.
Lucia,
As far as I know, there has not been any study to evaluate the resistance of survivors of the original SARS virus to covid-19. It might be difficult to do, because that population of survivors is small. What has been studied is the continued presence of T-cells within that population which remain reactive to the original SARS a decade after the illness. Which is a positive indication of durability of the immune response to coronaviruses; a long acting vaccine seems possible so long as the virus does not mutate too quickly.
.
The cross-reactivity of existing T-cell populations (common cold coronavirus) with covid-19 is a plausible explanation for people who appear immune to covid-19, even though they have not contracted the covid-19 virus. I am sure this will be evaluated and published at some point. If in fact common cold coronavirus infers some resistance to covid-19, that is an even stronger indication of likely success of vaccines.
SteveF
Yep. And possibly, the T-cell response from Covid vaccines could also reduce some cold symptoms caused by some other Corona viruses! I know most colds are rhinoviruses, but being lowered susceptibility to the Corona group in general wouldn’t be a bad thing.
Lucia,
On a recent thread, Mike M linked to a study suggesting common cold corronavirus illness recurs on average about once per decade in individuals, suggesting about a decade of resistance (on average) from an infection. Let’s hope an eventual vaccine to covid-19 is as long lasting.
SteveF,
A decade would be great. Heck, since I get flu shots once a year, a bit more than a year would be pretty good!
Mike M
https://sebastianrushworth.com/2020/08/08/what-is-the-best-way-to-measure-rates-of-covid-immunity/
The 4th comment was from a person called A.L.
“The presence of T cells that recognize the viral antigens isn’t surprising. The confirmation of such cells existing also does not prove functional immunity, where the cells are able to control infection- that is pure speculation, and no such data exists in this paper. There is no follow-up of such individuals to see if they are protected by virtue of these reactive cells, and for how long they would be protected”
Nic Lewis at Climate etc “Why herd immunity to COVID-19 is reached much earlier than thought ” also discuss T-Cells with views similar to the Swedes.
–
To be clear,
IgM and IgG circulating antibodies are what gives immunity to viral infections.
That is why we give vaccines.
T cells have a role to play in modulating viral disease, not preventing it.
T cells are always reactive after a viral infection and will show reactivity to that virus. Being reactive in no way confirms or confers a lasting immunity to that virus,
–
In passing I note that people keep referring to patients with no evidence of IgG antibodies.
There are two reasons.
One they did not have Covid or whatever in the first place,
Two the IgG fades away quickly when it is not needed in some people but Can be turned on like a flash of lightning if the virus is reintroduced.
–
I seem to be constantly knocking people but just want the science right.
lucia,
AFAIK, you need annual flu shots because the various influenza virus strains mutate rapidly and there are so many of them that annual shots are necessary. And even then, they have to guess which strains are going to be most prevalent because it takes several months to prepare mass quantities of vaccine. They frequently guess wrong.
https://www.cdc.gov/flu/prevent/keyfacts.htm
Elsewhere in the article, it says that getting a flu shot in July or August may not give as much protection for the later part of flu season as getting a shot in September or October.
angech,
Everybody is for the science being right. But your comments seem to me inconsistent with each other (AKA, they don’t make any sense).
.
“Two the IgG fades away quickly when it is not needed in some people but Can be turned on like a flash of lightning if the virus is reintroduced.”
.
Are you suggesting people raise T-cells active against covid-19 without ever having been exposed to covid-19? Are you suggesting that it is possible for the immune system to have such T-cells without ever having generated antibodies to covid-19, or are you suggesting the antibodies they once had (when they fought the virus) faded to the point that they could not be detected via the blood test used? (Not rhetorical questions, real questions.)
.
It seems obvious that post-infection “IgG fades away quickly when it is not needed…… turned on like a flash of lightning if the virus is reintroduced.” People couldn’t harry a lifetime’s worth of IgG at high levels to many different pathogens (hundreds? thousands?), but immune memory still mostly protects them from re-infection. It seems to me reactive T-cells are a strong indication of existing immune memory of previous infection. Are you suggesting the reactive T-cells exist but immune memory does not? (Not rhetorical.)
DeWitt,
I know that’s why we need them. My view that a year would be great is because I know there is nothing especially inconvenient about getting a shot once a year. I already do it.
Angech
I’d be happy with a vaccine that only “modulates” viral disease, since “modulate” appears to mean “make symptoms less severe and/or speeds recovery.” If it reduces symptoms and speeds recovery enough, people would seem immune. It would require daily testing to monitor viral loads to see that person had become infected.
.
This sort of vaccinne might not allow us to eradicate the virus. But we’ve only eradicated small pox, but the measles vaccine is useful nevertheless.
This paper:
https://science.sciencemag.org/content/early/2020/08/04/science.abd3871
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Was released earlier as an un-reviewed pre-print. It has now been reviewed and published. Abstract:
.
I think the reviewers made them couch the potential range of resistance to covid-19 due to earlier common-cold exposure as more speculative than in the pre-print. But it is still a very interesting paper.
SteveF (Comment #188924): “There was one study where the reactivity of pre-covid T-cell populations to different parts of the civid-19 virus was evaluated. A substantial fraction of blood samples (>35% IIRC), either taken before the virus started spreading in late 2019 or from places were no cases had been detected, carried T-cells reactive to some conserved parts of the covid-19 virus.”
.
That agrees with what I thought I remembered. But the Swedish study, as described by Dr. Rushworth, says 0%. Even with a smallish sample, that is not the least bit consistent with 35%.
.
I went to the blog article and followed the link to a preprint of the paper (https://www.biorxiv.org/content/10.1101/2020.06.29.174888v1.full). Quite the alphabet soup. I did not try to hard to decipher it, so I might be misinterpreting what they did.
.
It looks like they tested the blood samples against bunch of different peptides found in the Wuhan virus. Then they looked for peptides that gave a response in people who had the disease but not in the old blood samples. They used those to define a Wuhan specific T cell response.
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So they effectively defined the old samples to have a 0% response; but it seems that those sample did respond to some of the peptide sequences. That resolves the difference with the study that SteveF refers to. It makes sense for the purpose of looking for an acquired immune response from the current epidemic. But it does not address the question of a possible preexisting immune response as a result of prior coronavirus infection.
.
If T cells respond to snips of protein from a virus, does that mean that there will be an immune response to that virus? I don’t know. If the T cells are a result of exposure to that specific virus, then I would think the answer is yes. But what if the T cells were produced in response to a different but similar virus? That is what I don’t know.
Looks like Chicago was “mostly peaceful” last night, ha ha.
Tom.
Oh. Yeah.
Jim predicts store fronts are going to be redesigned on Michigan avenue.
Lucia,
Granite walls from the ground to the 4th floor and virtually impenetrable steel doors make perfect sense wherever government refuses to suppress rioters, looters, and criminals in general.
Here is another bunch of doctors challenging the official diktats on hydroxychloroquine: https://aapsonline.org/
It does seem that, in spite of their impressive name, the Association of American Physicians and Surgeons is rather small (~5000 members) and rather political (very conservative).
SteveF,
It will that or those beautiful roll down steel doors or something. Some swanky stores may also start only allowing selected people to shop by appointment. That happens in Rome. In fact, some jewelers in small stores in Chicago already require it.
Lucia,
Good thing you are not too close to Chicago. It is totally out of control, and Mayor Lightfoot is not likely to get it back under control. The looters seem to favor stores that sell big-screen TV’s. Why am I not surprised? Because they are just criminals looking for high value items to steal. If Lightfoot is not careful, the criminals will effectively be in charge of the city. But with personal security, at least she he can still arrange for a haircut.
The hydroxychloroquine question is one I think looks like worst of the cultural wars. I think Trump was completely irresposible to push it as he didnt have solid scientific support for his assertion when he did so, more like a lot of hope.
But that doesnt make him wrong about its effectiveness.
However, I now see one side anti any pro-HC data because they couldnt bear the possibility that Trump was right about something. And the other side doing the complete opposite.
Is this not a completely insane way to view a scientific question? Great environment for doing objective science in – not. I am suspicious of any HC study being done in the US. To what extent is it a search for truth, versus a shot being fired in the culture wars.
Mike M,
The two papers are looking at different things: one looks at covid-19 specific T-cells before and after the pandemic (in Sweden), especially among people without symptomatic disease but with known exposure, and the other looks at the apparent cross-reactivity of T-cells to other human corona viruses and covid-19. The former suggests antibody screening greatly underestimates the extent of infection, and so extent of progress toward herd immunity. The later indicates that previous exposure to other human coronaviruses (common cold coronaviruses) may infer a significant degree of resistance to covid-19, and so a wide range of “native susceptibility” to covid 19 in the general population.
.
Both are very interesting and important from a public policy POV, I think, and both invite further research work.
Phil Scadden,
“The hydroxychloroquine question is one I think looks like worst of the cultural wars.”
.
On at least that we completely agree: the HCQ battle is the ultimate corruption of science by politics. The data is clearly less than 100% conclusive. To dismiss it out or hand, or to endorse it without reservation is nuts. Conclusive data on HCQ will (sadly) only become available in September and October, after the pandemic has mostly subsided in the USA and the culture warriors have moved on to a different battlefield.
If Mayor Lightweight is going to contend for the title of Feckless Mayor of the Year, she will have to up her game. It is not just that the reigning champ, De Blasio, will be tough to take down. Over the weekend, a block party in DC turned into a shootout, leaving a teenager dead and 20 others injured. Mayor Bowser was shocked:
She was not referring to the shootout. She was referring to the block party.
MikeM,
“ She was not referring to the shootout. She was referring to the block party.â€
.
She is an idiot; what more can you reasonably expect from her? When you can’t say anything bad about violent criminals, you are not part of the problem, you are the problem!
SteveF,
The culture warriors will not, if they can help it, allow positive data on HCQ to appear before November 4. If it got out that there were at least tens of thousands of preventable deaths so far in the US from COVID-19 just to make Trump look bad, the Presidential election could turn around overnight.
The results in Switzerland of first withdrawing and then returning to the use of HCQ look pretty conclusive to me as far as reducing the death rate. It’s so strong that running a double blind test against a placebo now looks immoral to me.
Well .. here’s an interesting take by our arbiters of truth and justice.
Florida reports record number of COVID-19 hospitalizations
https://www.nbcnews.com/news/us-news/florida-reports-record-number-covid-19-hospitalizations-n1236286
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““These are devastating numbers,†Dr. Sadiya Khan, an epidemiologist and assistant professor of preventive medicine at Northwestern University’s Feinberg School of Medicine, told NBC News.
The blame, Khan said, should be laid at the feet of the Florida leaders who downplayed the danger early on and who have been slow to impose mask mandates and other public health measures.
“In Florida there has been this ongoing controversy about the severity of the coronavirus crisis,†Khan said. “There has been a politicization of the issue of wearing masks. This should never have happened, and now we’re seeing the results.â€
Miami Mayor: “New York could definitely teach Florida a thing or two about this pandemic,” Gelber wrote.””
.
OK then. Never mind that case rates are down 40% in the past few weeks or today’s numbers are the lowest since June or … our local paper today:
https://www.tampabay.com/news/health/2020/08/10/florida-adds-4155-coronavirus-infections-93-deaths/
“In mid-July, there were at any given time about 8,700 people in Florida hospitals whose primary diagnosis was COVID-19. Last week, the average number of hospitalized patients on a given day was about 8,200.”
.
Whatever … it doesn’t matter. This particular issue is curious and likely some data processing issue. I cannot even find the alleged information they are reporting. FL only very recently started reporting specific hospital data. The unbiased public health “experts” who are taking cheap shots and the reporters who print them have access to the same dashboard they point to which would show this selective blast doesn’t align with reality. Good thing they aren’t part of the politicization process because, you know, they only do “science”.
Mike M,
I read that WP article earlier and it was just bizarre. 21 people shot, 1 killed, over 100 rounds of ammunition fired. The focus of the article was on whether the party should have been shut down due to pandemic laws.
https://www.washingtonpost.com/local/public-safety/shootings-in-district-surge-as-officials-confront-mass-shooting-that-killed-1-wounded-21-at-block-party/2020/08/10/6d5446f4-daff-11ea-8051-d5f887d73381_story.html
Tom Scharf,
The fact the public policies in Florida are not PC is the only thing that matters. That NY, NJ, and a bunch of other ‘good’ states will end up with three times as many deaths per million among the elderly is utterly irrelevant to the SJW who would prefer a subservient populace…. and lefty leaders like them directing everything that subservient population is allowed to do. The specific policy issue doesn’t matter, they are always for more government control and less personal liberty. It is the nature of the left.
.
I note that there have been record purchases of guns in the last few months since the corona panic and the the rise of criminal behavior since the SJW riots and widespread looting in many cities. IIRC nearly 10 million guns have been purchased this year. That is not a coincidence….. and it is not criminals who are buying the guns.
SteveF (Comment #188954): “… previous exposure to other human coronaviruses (common cold coronaviruses) may infer a significant degree of resistance to covid-19 …”.
.
I know that. But on second thought, I don’t understand it. The proteins in the Wuhan virus are largely the same as the proteins in the common cold coronaviruses. The adoptive immune system learns to recognize proteins, so it makes sense that, having encountered one coronavirus, T cells might show a response, at least in a test tube, to peptides from a different coronavirus. Is there some reason to believe that the test tube response to peptides implies an immune system response to the virus in the body? I can see where that *might* be so, but I don’t know that it *is* so.
.
If that is so, it leads to a puzzlement. The proteins in one strain of influenza are largely the same as the proteins in other strains. So it should be that T cells that have learned to recognize one strain of influenza should be cross reactive with other strains. But it appears that exposure to one strain influenza provides no protection against other strains.
Mike M,
” The proteins in one strain of influenza are largely the same as the proteins in other strains.”
.
Sure, and there is no doubt that helps protect most people from severe illness; research has shown that the first flu strain a person encounters as a child has a very strong influence on lifetime susceptibility to that and related strains. Influenza is known to mutate very quickly, so that makes the protection from earlier infections less than perfect (we don’t yet know exactly how fast covid-19 will mutate, but we will within a few years).
.
I note that influenza kills lots of people every year, especially among the elderly. Very new strains (like the 1918 and the bird flu) are always worse. IMO, covid-19 is much like a virulent (novel) stain of flu, but one that kills almost exclusively elderly, unlike the flu which often also kills the young. Exactly how much resistance previous exposure to common cold coronaviruses gives to covid-19 is not known, but I expect soon will be.
.
Covid-19 will probably end up killing 2 or 2.5 million worldwide (out of ~7.8 billion, so ~0.03% of the global population). That is not a global catastrophe…. nearly 1% of the global population dies every year. The real catastrophe is the economic and social damage the policy response to the pandemic has done.
MikeM
I’m not sure that’s true. It’s true the vaccine is formulated to be specifically protective against the strains anticipated to be in circulation in a particular year. But that doesn’t mean they necessarily provide no protection against other strains. They would presumably at best provide less protection. Doctors would not be able to confidently state they provide any. But that’s not necessarily the same as being able to say they provide no protection. Among other things: that question may simply be unstudied. So no one knows.
.
SteveF (Comment #188935)
angech Everybody is for the science being right. But your comments seem to me inconsistent with each other.
.
“Two the IgG fades away quickly when it is not needed in some people but Can be turned on like a flash of lightning if the virus is reintroduced.â€
–
“Are you suggesting people raise T-cells active against covid-19 without ever having been exposed to covid-19? Are you suggesting that it is possible for the immune system to have such T-cells without ever having generated antibodies to covid-19, or are you suggesting the antibodies they once had (when they fought the virus) faded to the point that they could not be detected via the blood test used? (Not rhetorical questions, real questions.)”
–
We may have a misunderstanding here or I might be a bit old on the science?
“Lymphocytes are divided mainly into B and T cells. B lymphocytes produce antibodies – proteins (gamma globulins) that recognize foreign substances (antigen) and attach themselves to them. … T lymphocytes are cells that are programmed to recognize, respond to and remember antigens.”
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The Immune system as I understood it usually forms antibodies from B cells. Initially IgM short lasting acute protection which changes to IgG long lasting protection. There is also IgA involved in allergic reactions but a topic for a different discussion.
T cells generally do not form antibodies.
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To recap, T cells are unimportant in fighting new infections, They are not antibodies. The antigens they recognise are produced by all sorts of infected cells and tell the T cells to help activate the processes to get rid of them.
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The body has a lot of different mechanisms to help prevent unwanted infection but sustain needed infection [bowel flora etc] including a thick keratin skin layer externally and an acid chamber internally. T cells reacting to cell antigens and B cells producing antibodies to viral or bacterial antigens are only two of the various ways our white blood cells protect us.
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True immunity is antibody Immunity, The IgM disappears and the IgG does interesting things. In some illnesses and vaccinations it hangs around permanently at detectable levels in most people, Say Rubella and measles.
In others it hardly seems to form ir disappears quickly like in Hep B vaccination. People sometimes have to have a 4th or 5th vaccination to produce detectable IgG and it wanes quickly. It also wanes quickly after a lot of natural viral infections.
This does not mean it is not present or active or activatable.
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You stated “People couldn’t carry a lifetime’s worth of IgG at high levels to many different pathogens (hundreds? thousands?)” but this is clearly incorrect. They can and do. What seems an enormous number to you is very small at the cellular level where there are billions of cells. If our bodies could not do this we would not be here.
What happens is that the memory IgB cells reside in the lymph nodes carrying their protective IgG coding and then activate [massive production and divide massive increased production every hour or so until the infection is under control. Hence the development of palpable lymph nodes from only 2 mm in size to 2 cms in size in tonsillitis and glandular fever etc.
I would call going from negligible circulating or undetectable antibodies to billions of antibodies in hours and then thousands of billions of antibodies in 12-24 hours by secondary repeated cell division as
”like lightning” in a biological sense..
–
To answer your question.Not I.
Some people are claiming magic properties to T Cells having an immune memory to other viral infections with overlap that help them fight off covid.
This suggests immunity without ever having been exposed to Covid itself.
Such immunity could be due to a number of factors [as in the cases of people who claim justifiably that they never catch the flu]. Whatever the reason it is not due to T Cells whose immune memory is to the body’s own cells producing antigens that tell the T cells they are sick and need to be disposed of.
Not to any specific virus.
Sorry to be so long winded Steve. The level of discussion and interest here is excellent. I do go on too long. Happy to discuss or accept any corrections to my understanding and not trying to be rude.
angech
You wrote this
I don’t see how “tell the T cells to help activate the processes to get rid of them” is consistent with “T cells are unimportant in fighting new infections”. If the memory T cells are present when a virus invades the body, then they can be “told” to activate the process to get the B cells to make antibodies, it seems to me that that ought to help fight the virus that has just invaded your body.
.
Is this wrong? Or what am I missing? (Real Qs.)
If this exists, it would be similar to Cowpox giving immunity to people who were never exposed to smallpox. We know that happened.
.
I have no idea if that cross-protection involved T cells. But we know it sometimes happens. It would be very convenient in the case of Covid. I think health experts and individuals should be cautious about believing it exists. But I don’t think the word “magical” would be appropriate. Cross-reactivity does exist for some diseases. We’ve know this a long time.
lucia (Comment #188981): “It’s true the vaccine is formulated to be specifically protective against the strains anticipated to be in circulation in a particular year. But that doesn’t mean they necessarily provide no protection against other strains. They would presumably at best provide less protection.”
.
It is routinely claimed that the flu vaccine is an average about 50% effective, sometimes quite a bit better, sometimes quite a bit worse. And there should be memory B cells around from prior infections and vaccines. So I think something is missing from the simple explanation.
—-
SteveF (Comment #188980): “Sure, and there is no doubt that helps protect most people from severe illness;”
.
Fair enough. Maybe that is why most flu infections are claimed to be asymptomatic and most of the rest have only mild symptoms.
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SteveF: “research has shown that the first flu strain a person encounters as a child has a very strong influence on lifetime susceptibility to that and related strains.”
.
I did not know that.
.
SteveF: “Influenza is known to mutate very quickly, so that makes the protection from earlier infections less than perfect”
.
But the poliovirus is an enterovirus and those viruses, closely related to rhinovirus, mutate very quickly:
https://en.wikipedia.org/wiki/Enterovirus#Virology
and, specifically for polivirus:
https://en.wikipedia.org/wiki/Poliovirus#Origin_and_serotypes
.
SteveF: “we don’t yet know exactly how fast covid-19 will mutate, but we will within a few years.”
.
From what I have seen, the two long-known human coronaviruses have very stable genomes, as viruses go.
——–
p.s. – I am not trying to be disagreeable; I am trying to understand something I don’t understand.
angech,
I think you miss the point I was trying to make: the presence of T-cells that recognize cells infected with Covid-19 is as good a proof as there can be that the person was infected with covid-19, and beat back the infection (yes, with IgG), and so for sure still has immunological memory of the infection.
And that is the whole point. If someone has T-cells active to covid-19, but no detectable IgG circulating in their blood, they are very likely resistant to covid-19 infection… unless there is a substantial mutation of the virus. And even in that case, it is likely what illness they got would be much milder than that suffered by a naive 85 year…. which often leads to death.
.
Formulation of sensible public policy depends on understanding progress toward herd immunity. If many people who contracted the virus and had few or no symptoms have T-cells active to the virus, then they are part of the resistant population. It is not just those still circulation reactive IgG who are resistant. Which is why the Swedish study linked to above is important for public policy. If Sweden has 15% of its population with measurable IgG to covid-19, another 30% with T-cells reactive to covid-19, and 30% with some cross-resistance from earlier common cold coronaviruse infections, then the decline in cases and deaths (with no masks, no restaurant closures, no lockdowns, no school closures for kids below 16) becomes much easier to understand. (https://www.worldometers.info/coronavirus/country/sweden/)
.
WRT cross-reactivity: As Lucia correctly points out, cross reactivity of immune responses to related viruses is not just well known, but was used to completely eliminated smallpox. For there to be cross reactivity of immune response between other coronaviruses and covid-19 would not be at all surprising… what would be surprising is if there were none. We do not know how long the resistance to covid-19 will last after infection (or after a vaccine), but the fact that there is likely some cross-reactivity from earlier common-cold coronavirus infections is a very good sign that immunity is at least reasonably long lasting.
There does seem to be a process going on here where verified infection rates get to around 2% of the population and the virus peaks. So maybe ~20% of the population gets detectable levels of covid and the virus peaks and diminshes. It’s pretty clear nobody understands why. Here is a roundup on some possible theories from the WP.
https://www.washingtonpost.com/health/2020/08/08/asymptomatic-coronavirus-covid/
Mike M,
“But the poliovirus is an enterovirus and those viruses, closely related to rhinovirus, mutate very quickly”
.
Sure, but multiple polio vaccinations protect people for a very long time, if not their entire life.
Russia wins the vaccine race, US media immediately and unanimously condemns them without any evidence either way like this is supposedly bad news. If Russia wants to vaccinate their entire population “too early” that is fine by me. That will validate the efficacy of the vaccine. Side by side stories in the US media about devastating death tolls and the evil Ruskies going too fast on the vaccine produce whiplash. As I have posted before, Russia has some serious expertise in virus … errr … “research”.
Tom Scharf,
Well the WaPo is very slow on the uptake, but at least they demonstrate a limited capacity to learn. Now if they could just stop it with the SJW charade; I won’t hold my breath waiting.
Trump could cause the heads of the entire progressive/liberal/SJW class of nincompoops to explode simultaneously by asking Putin for some of the new vaccine…. and trying it himself. 😉
.
Conspiring with the Russians to save himself from covid-19! How horrible!
Ha ha, Trump takes the Russian vaccine. Hilarious. That would be the epic troll move of all time.
Tom Scharf
Me too. It won’t make me prefer their method, but they have a system of government that makes certain times of decisions. It tends to view things from a collectivists point of view, so individuals may be put at risk to have the whole better off.
.
That’s not our system. I don’t want it to be. But I’m not going to scold or condemn them here. The fact is: We don’t know the risk/reward balance.
Lucia,
“We don’t know the risk/reward balance.”
.
No, but if Putin’s daughter really received multiple doses of the vaccine (as he suggested in his news conference), there is a good chance it isn’t going to kill a lot of people. Of course, we don’t know if we can believe Putin about his daughter receiving the vaccine.
.
I still think Trump should ask for some of the Russian vaccine! 😉
SteveF,
Yep. If she’s received it.
I think I may have been infected in February. How likely is an antibody test to detect this?
Mike M,
Impossible to say. If mild symptoms, less likely.
I think I may also have been infected in early June…. three days sore throat, slight fever and slight headache; stayed away from everyone but my wife and 18 month old grandaughter. I am not going to spend the $150 for an antibody test.
MikeN,
IMO, the probability range is from slim to none with the probability decreasing with time since recovery.
SteveF,
A lot of blood banks will do an antibody test for free when you donate, if you’re eligible to donate.
Off-topic: Biden has chosen Kamala Harris as his running mate.
mark bofill,
Harris is the least bad person he could pick after eliminating all men and white women.
.
Still, she has plenty of baggage from her younger days, like sleeping with Willy Brown to get no-work, high pay “commission” placements (and his support for elective office), and later aggressive prosecution as California AG.
.
During the Kavanaugh hearings she was over-the-top dishonest and obnoxious. Her handlers may get her to tone it down. If not, she is not going to be someone people want to contemplate as ol’ uncle Joe’s replacement when he is diagnosed with dementia 6 months or so after taking office.
Steve,
I agree. Biden could certainly have done worse.
.
A couple months till the first debate, three months till the election. I am intensely curious to see how this all plays out.
.
[Edit: I probably shouldn’t say this. It shouldn’t matter. At all. Still. Kamala Harris is the whitest looking black woman I’ve seen in some time. I think my skin tone is darker, and I’ve always identified as white. Shrug.]
mark bofill,
It wouldn’t matter to me if you were purple.
Lol. You can’t be colorblind if black lives really matter.
https://www.deseret.com/opinion/2020/6/4/21279264/george-floyd-race-protests-black-lives-matter-why-you-cant-be-colorblind
According to Kendi, color blindness is a mask to hide racism.
—-
All that said, I fully agree with your sentiment Steve. Racist that I am. 🙂
I probably should have explicitly identified my sarcasm instead of saying lol. When will I learn…
mark bofill,
“ According to Kendi, color blindness is a mask to hide racism.â€
.
According to SteveF, Kendi is an idiot, no matter his skin color.
~grins~
Something else we agree on.
Thanks Steve.
A quick scan of the headlines shows the Russian Vaccine apoplexia has now reached 12 on a scale of 10. I find it very funny. There is no published data, no information about side effects, antibody titers, dose rates, or anything else, yet apoplexia ensues from the usual subjects. Those same people who would think nothing of throwing 20 million people out of work and disrupting the lives of most every student in the USA based on very incomplete information about the virus.
.
These people need to get a grip and remember they don’t have all the information they need. Putin could have a useful vaccine. Time will tell, but I doubt Putin would risk being very wrong if the existing data is not pretty solid. I wonder if those now raging about all the lives Putin risks by going to large scale immunization will take note if the Russian vaccine saves 50,000 Russian lives. And a comparable number die in the West waiting for complete trials.
WSJ https://www.wsj.com/articles/the-putin-vaccine-gambit-11597188160
Yep. Possible.
Lucia,
The Russians have announced trials for several thousand people in Mexico (leftist government), Brazil (right wing government), and several other places. I doubt all those involved would go along with an outright fraud. Chances are good it is a real vaccine. How well it works is a very different question. The description of the vaccine (based on placing a covid 19 gene in adenoviruses) is something the same company has done for a couple of other vaccines. We’ll see what happens. Count on companies working on vaccines to ‘redouble their efforts’ and make announcements soon. As a group their stock values dropped on the Russian announcement.
“I don’t see how “tell the T cells to help activate the processes to get rid of them†is consistent with “T cells are unimportant in fighting new infectionsâ€. If the memory T cells are present when a virus invades the body, then they can be “told†to activate the process to get the B cells to make antibodies, it seems to me that that ought to help fight the virus that has just invaded your body.
Is this wrong? Or what am I missing? (Real Qs.)”
–
In a new infection there has to be a new antigen/s.
If the antigens are the same it is not really a “new” infection.
The body reacts to a new antigen through a number of mechanisms that detect and then help to build a specific antibody to that virus.[It may well be possible to have multiple antibodies to multiple new antigens].
The B cells then produce increasing antibodies which help neutralize the virus enabling the other body cells to ingest and destroy the virus antibody complex.
T cells are activated later, possibly in part by this virus antibody complex. The memory for the T cells comes from after the B cells and antibodies are activated.
The T-Cell function includes destroying cells with high viral loads which they can only do after they are instructed to recognize the antibody/viral complex.
If they do destroy the cells before there are antibodies around they are not stopping the disease, merely helping spread it to other cells.
–
“T cells are unimportant in fighting new infectionsâ€. does not mean they do not have a role, just that it is never primary in a new infection and cannot do anything helpful in fighting a new infection
angech,
Ok. Then I guess I’m not sure what point you are trying to make in context of the previous discussion. But no one is saying the T-cells fight absolutely new infections.
Two ideas have been introducted:
1) T cells retained after an infection with Covid may give long term immunity or Tcells from from a related corona infection infection may give some protection against Covid. The latter would be a virus that is sufficiently similar that there is cross-reactivity (like cowpox giving immunity to small pox.)
2) The covid t-cells found in Swedes who do not show antigens suggests many many people in Sweden may now have some immune even though they never showed symptoms and tests do not show antigens.
So if by “new” you mean “absolutely new” (as opposed to a re-exposure by someone previously infected but who recovered), then I accept what you are saying as true. But I don’t see how it’s important in context of what other people are suggesting about what t-cells found in populations (like Swedes) means.
Not long ago, I saw a piece by a doctor, writing for Forbes I think, arguing that we should skip phase 3 vaccine trials. That would seem to be the route the Russians are taking. A few days later he wrote another piece admitting he was wrong, having been educated by his readers. But as I recall the reasons, most are not an issue if you control the media and don’t care if you kill a few of your citizens.
—–
Found the articles:
https://www.forbes.com/sites/stevensalzberg/2020/08/02/start-vaccinating-now/#58a6cd8acf6e
https://www.forbes.com/sites/stevensalzberg/2020/08/03/i-was-wrong-we-cant-skip-phase-3-vaccine-trials/#15c6d48a2ae7
Does anyone here know if we have antibodies in our blood to, say, measles? The antibodies themselves don’t last more than a few months, so if we have antibodies, we must still be making them. But the plasma cells that make antibodies only live for weeks, so we should not have any of them, unless we are still making them. But from what I can find, making plasma cells requires the pathogen. So what gives? I am guessing that it is the last bit that is wrong and that in some cases we keep making new plasma cells even after the pathogen is gone. But why would we?
Memory B cells can lie dormant for decades, then get reactivated. But they should not be making antibodies while dormant.
————
Maybe I just found my answer: https://pubmed.ncbi.nlm.nih.gov/18716625/
Thank you Mike M.
To be precise humans can sustain B memory cells to viruses for many decades after exposure-well into the tenth decade of life.
Normally they reside in the <2 mm size lymph nodes all your life, it is the ability to turn on and ramp up IgG antibodies that gives us our antibody defenses.
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1) T cells retained after an infection with Covid may give long term immunity or T cells from from a related corona infection infection may give some protection against Covid. The latter would be a virus that is sufficiently similar that there is cross-reactivity (like cowpox giving immunity to small pox.)
Thank you Mike M.
To be precise humans can sustain B memory cells to viruses for many decades after exposure-well into the tenth decade of life.
Normally they reside in the <2 mm size lymph nodes all your life, it is the ability to turn on and ramp up IgG antibodies that gives us our antibody defenses.
–
Lucia
1) T cells retained after an infection with Covid may give long term immunity
No not they way we normally talk about immunity.
Immunity is from antibodies from B cells. Proof?.
This is what all the virus manufacturers are working towards.
That is what making a successful vaccine means.
Nobody is working to make T Cell immunity.
–
T cells from from a related corona infection infection may give some protection against Covid.
No
T cells work at a different level to B cells.
They do not grab the invading virus like antibodies.
They do not prevent the virus from adhering to and entering cells.
What they do is detect cell surface changes and help initiate early destruction of that cell.
I guess cross reactivity would let them detect cells invaded by virus earlier if they detected cross reactive surface cell changes but it is all a bit of closing the stable door after the horse has bolted.
Context is important.
2) “The covid t-cells found in Swedes who do not show antigens suggests many many people in Sweden may now have some immunity even though they never showed symptoms and tests do not show antigens.”
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Herein the problems with this study hidden in their kaleidoscopic charts.
There is no Covid T cell as such.
No test for it. There is no T cell which has a marker specifically for Covid on it.
None.
T cells exhibit a range of switched on markers which vary with exposure to different viruses and bacteria.
Claiming that a particular pattern is unique for Covid is plain wrong.
Any Swede with a decent cold virus infection will have activated T cells.
If it is a related common cold virus it may well have 90% correlation with the pattern of Covid.
Yet here they claimed their sample group had 0 reactive T cell populations.
Baloney.
All people have T cell populations. Some of these must have been reactive to infections in the last 3 months yet they claim a pristine population group. Not possible.
–
The tests you mentioned should say show no antibodies, not antigens. Antigens are a sign of active infection which none of these people had when being checked.
Why do people have no antibodies?
Either they have never been infected [the control group]
Or they were misdiagnosed ie never had covid or, unlikely, the antibody levels had dropped to undetectable levels. Which begs the question again of were they really infected.
A good natural infection should leave detectable antibodies for months to years.
angech,
Did you actually read the two papers linked to above in this thread? From your comments, I am guessing you did not. Tell me if I am mistaken about that. And just to be clear: do you believe that infection with vaccinia virus provides protection against the related smallpox virus? If so, how does that happen?
angech,
I have the same question SteveF has. Did you read the paper? They don’t claim there is a t-cell with a marker for Covid-19 on it.
Off topic, but I think this short video (about 8 minutes) on the topic of “2+2=4” is worth sharing.
The odd thing about that is they make the ones who are against 2+2=4 be “conservatives” and she’s accused of being liberal for wanting to stick with what is the traditional view.
Lucia,
Yup.
I’d argue that the real life issue is the illiberal/progressive left vs. liberals and conservatives, not liberals vs conservatives. The liberals can’t quite bring themselves to say this. Look at the Harper letter; they still have to bash the right while trying to rein in the radicals. But still. What I think is really going on there is that the liberals are starting to realize that the radicals on the left have gone too far and are essentially taking over the liberal position.
I think the liberals have effectively conjured demons in their ongoing political struggle with conservatives by supporting the rise of radical illiberal progressives and eroding enlightenment values with the marxist / postmodernist / grievance study stew. The demons are turning on them, and they don’t much like it.
[Edit: But it’s still the conservatives fault. Somehow.]
I think I found the answer to one of my questions. Maybe you guys already knew this or maybe you don’t care or maybe you will find this helpful.
.
Although viruses mutate rapidly, there are highly conserved parts of their genome. It is not that those parts don’t mutate, it is that such mutations make the virus non-viable and are thus selected against. For example, the virus must have a protein that attaches to the cell surface as the first step in entering the cell. If small changes to a part of that protein make it impossible to attach, then that portion will be highly conserved. If an antibody attaches to a highly conserved region, then it does not matter how fast or how much the rest of the virus mutates; immunity will be long lasting.
.
Influenza attaches to cells via a protein called hemagglutinin. It has a “head” that is highly mutable and a “stalk” that is highly conserved. The head blocks access to the stalk and is what antibodies typically attach to. If a different strain comes along with a different head, the antibodies don’t work as well, if at all.
Researchers have made immunogens that induce antibodies that attach to the stalk, but it seems that in mice they only sort of work (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912658/). Maybe because they have trouble reaching the stalk on the wild virus.
mark bofill (Comment #189072): “I’d argue that the real life issue is the illiberal/progressive left vs. liberals and conservatives, not liberals vs conservatives. The liberals can’t quite bring themselves to say this.”
.
Indeed. My journey from liberal to conservative began when I realized that a key part of progressivism was the Totalitarian Left. At first, I thought they were mostly harmless academic kooks. But during Obama’s second term, I saw them rapidly gaining power and my transformation began to rapidly evolve, to the point that I voted *for* Trump (not just against Hillary) in 2016.
mark bofill,
“The demons are turning on them, and they don’t much like it.”
.
The extreme left always ends up eating its own, starting with the French Revolution. There is really no place today for a “classic liberal” within the “progressive” dominated Democrat party. The only thing that unites them is wanting to gain more political power. Oh, and wanting to get rid of Trump.
Mike M,
“Although viruses mutate rapidly, there are highly conserved parts of their genome.”
.
Yup, and those are the parts that are similar (conserved) between common cold coronaviruses and covid-19.
mark bofill,
To amplify a bit: look at the positions the Democrats have recently embraced: universal medicare/no private insurance/rationed health care, green new deal (with dozens of wacky policies), eliminating all nuclear power, wealth confiscation, 70+% marginal tax rates (at least for wealthy republicans), re-instating high (up to 90%!) estate taxes, eliminating the electoral college, confiscating all guns in private hands, packing the SC if needed to undermine the Constitution, permanent official racial preferences, limiting free speech, etc, etc. The list of lunacies is long.
.
The vision the Democrats have for the future is completely disconnected from existing laws, the plain meaning of the Constitution, and the country’s history of governance. They don’t like the way the USA is constituted, and want it to change so drastically that it effectively disappears… along with the personal liberties the Constitution guarantees. They do not care how that happens, and will undermine laws and the Constitution without the slightest hesitation whenever needed.
It is. It’s becoming too much. Rioting on the west coast cannot be objected to. It’s beyond the pale to advocate in an editorial that the National Guard should be called in. Prosecutors bring charges against those who hold guns in their hands to discourage unruly mobs from attacking them on their own private property. Rioters in Chicago declare that looting is a form of reparations. [Sorry, I should have said, the sacred Black Lives Matter movement declares this] The list goes on and on and on. 2+2=22, indeed.
Maybe if Trump thrashes Biden soundly in this election, the Democratic Party will take a long hard look at the madness. But I doubt it. It’s too late in a way. There are already generations of people who’ve been indoctrinated in the nonsense; these people aren’t going to just abandon their nonsensical ideals.
Ah well. This too shall pass. But I don’t envy my kids and grandkids the mess their going to have to sort out.
The Russia vaccine discussion in the media is just bizarre. I guess I missed the people who are saying “that’s great news, there is some risk there, but let’s investigate and test it ASAP to see if it works”. Most articles don’t even provide any information on the product or how it compares to other vaccines being developed. They are just Russia is evil, can’t be trusted, end of story.
.
I’m no fan of Putin but they sure put astronauts in space first and have some of the world’s greatest chess players, etc. A complete dismissal of their efforts for political reasons is not justified.
.
As for them effectively skipping phase III trials, this seems like a good idea in many ways. I have yet to see a.single.article, not a.single.effing.article discuss the trade off between early vaccine use and all the people who are going to die waiting for phase III trials to complete. There might be a vaccine disaster that kills or maims some people, but if it saves 100,000 people by vaccinating 3 months earlier than otherwise, it is very clearly worth it.
.
It may be out of their Overton window, but it sure isn’t out of mine. When I asked this question seriously in another forum the answer was literally “but Nazi doctors!”. I am clearly missing something here. I cannot for the life of me even comprehend how this isn’t up for a serious discussion by our very serious people in the media. I may not trust Russia, but I also don’t trust Team Science entirely either. This is basically a CYA on their part while the death count notches up 1,000 people a day in the US.
SteveF (Comment #189076): “Yup, and those are the parts that are similar (conserved) between common cold coronaviruses and covid-19.”
.
Yes. But are those the parts that antibodies attach to? I suspect not, since otherwise the coronaviruses would not be a significant cause of the common cold.
“Rioting on the west coast cannot be objected to.”
.
The Sacramento Bee should do a rewrite of the Charlottesville protest to today’s journalistic standards. “The protest was mostly peaceful with chanting of slogans and singing about ethnic unity. Free food was passed out and a wall of white Dads lined up to protect the peaceful protest from radical leftists who were agitating the mostly peaceful protesters. A very small number of people not connected to the protest were non peaceful. The man alleged to have driven his car into the crowd motives are unknown, but he was likely running from the agitators. Protesters claim he was arrested by unmarked leftist police thugs. The mass majority of people interviewed rejected violence. A GoFundMe account has been setup to bail out the alleged wrong doer.”
A fine example of the new era of protest journalism en vogue today. This one is an absolute howler.
.
Looting in Chicago was a long time coming, some experts say
The uprising sent a clear message for one professor: “This put everybody on notice that folks have had enough.â€
https://www.nbcnews.com/news/us-news/looting-chicago-was-long-time-coming-some-experts-say-n1236303
.
“Despite the misinformation, the uprising is still a commentary on what it means to exist in an over-policed state, Stovall added. “These folks are frustrated to the point that anything put forward by police is unbelievable because of the history that the police department has had in those particular neighborhoods.â€
.
The police made them do it. … Sorry it took me a while to stop laughing before I hit the Submit button.
mark bofill (Comment #189078): “Maybe if Trump thrashes Biden soundly in this election, the Democratic Party will take a long hard look at the madness. But I doubt it. It’s too late in a way. There are already generations of people who’ve been indoctrinated in the nonsense; these people aren’t going to just abandon their nonsensical ideals.”
.
Visible minorities now constitute the (relative) right wing of the Democrat Party. As long as they mostly stay loyal to the party, the crazies will hold sway. But if/when minorities start to abandon the Democrats, the party will have to adapt or die.
Mike,
That sounds plausible to me, although I’ll kick it around some. It gets me thinking though.
Does the BLM movement actually enjoy majority black support? I think I’ve just assumed this. When you get right down to it, BLM stands for stuff I wouldn’t expect polls of black people to show support for. We foster a queerâ€affirming network. When we gather, we do so with the intention of freeing ourselves from the tight grip of heteronormative thinking, or rather, the belief that all in the world are heterosexual (unless s/he or they disclose otherwise). Really? In 2014 only 42% of black voters supported gay marriage. They never warmed to Buttigieg and his homosexuality may well have been a good chunk of the reason. Another example — 4/5’th of black people want police to maintain or increase their presence in their neighborhoods as recently as 2015, according to Gallup.
I don’t really know what to make of that.
The answer to my question appears to be *yes*.
https://www.pewsocialtrends.org/2020/06/12/amid-protests-majorities-across-racial-and-ethnic-groups-express-support-for-the-black-lives-matter-movement/
Maybe some of it is people mixing up the sentiment ‘Black lives matter’ with the actual platform statements of the organization.
One endpoint is what happens when old rich white liberals actually need to give up real power to earn the votes of the identity complex they so allegedly revere. Pelosi/Shumer/Biden/Clinton/DNC et. al. are still running the handshake deal of vote for us and we will have your backs. They do nearly nothing beyond lip service as the identity complex has no other choice. The identity complex will eventually feel sufficiently empowered to kick these old white people to the curb based solely on their identity, the BLM political party. The self created monster of racial grievances may eventually eat them too.
.
That must be hard to manage. Everyone in power on the left will take the knee if they don’t have to sacrifice money and power. It’s all a bit condescending and performative. Tax us powerful rich people and give it to poor minorities never seems to happen even when the left is in power, strange that.
.
For the right the best outcome is a split of the left based on their own grievance playbook. This is practically undiscussed in the media probably because it is their deepest fear.
Lucia,
I know I’m unobservant as all heck, I get that about myself. My wife will change something in the house and I’ll finally notice, be surprised and remark on it three years later.
How long has this site said ‘Where we talk about news. :)’?’ up in the title?
mark bofill,
I think changed it about the time I wrote the post “all covid, all the time”. It seemed to me we were mostly discussing… whatever.
re: The web page banner statement
Sheesh mark, that’s been there for …
uh …
… a while!
I like “Where COVID talk gets hot”
Thanks Lucia. Figures.
[Edit: Earle. :p ]
mark bofill
Alas, I’m sure they don’t mean it. Because if they did, then we wouldn’t need additional formal reparations. They were already taken by force!
Earl… I should change it to “Where Covid talk gets hot!” 🙂
Lucia,
I love it. That’s going to be my new response when people bring up reparations- the matter was settled in Chicago as far as BLM is concerned. Reparations are done.
The best take I’ve seen on Kamrade Harris as Biden’s running mate comes from Ben Shapiro: Biden should hire a food taster.
Mike M,
No need to poison him, they’ll just invoke Section D of the 25th Amendment within a year or so of him taking office, and Harris will become defacto president immediately, even if Biden resists being pushed out for a while. The guy shows obvious signs of dementia, and won’t be in office long if he wins election. A majority of voters recognizes Biden is losing mental capacity, but enough people loath Trump that Biden may still win.
Lucia,
“Where COVID talk gets hotâ€
.
Maybe, but the pandemic and all the associated political craziness has already peaked. Part of that is declining cases, but part is that with gradual return to more normal activities covid-19 just won’t matter very much. People will stop being so afraid of it. What won’t change is using covid-19 as a reason for the MSM to heap scorn on Trump (and all Republicans) until November.
angech,
I have the same question SteveF has. Did you read the paper? They don’t claim there is a t-cell with a marker for Covid-19 on it.
–
Lucia.
I did a search “do t cells fight viruses. The first hit entitled
“T-cells | Ask A Biologist”
addresses the points I have tried to make here.
People are confused between B cells and T cells.
B cells are probably the only ones that make antibodies.
This is usually what is called memory in immunology.
–
T cells do not make antibodies. They do not fight viruses directly.
From the web
“T-cells are a type of white blood cell that work with macrophages. Unlike macrophages that can attack any invading cell or virus, each T-cell can fight only one type of virus. You might think this means macrophages are stronger than T-cells, but they aren’t. Instead, T-cells are like a special forces unit that fights only one kind of virus that might be attacking your body.
More than one kind of T-cell There are two types of T-cells in your body: Helper T-cells and Killer T-cells. Killer T-cells do the work of destroying the infected cells. The Helper T-cells coordinate the attack.
Killer T-Cells and Antigens Killer T-cells find and destroy infected cells that have been turned into virus-making factories. To do this they need to tell the difference between the infected cells and healthy cells with the help of special molecules called antigens. Killer T-cells are able to find the cells with viruses and destroy them.
Antigens work like identification tags that give your immune system information about your cells and any intruders. Healthy cells have ‘self-antigens’ on the surface of their membranes. They let T-cells know that they are not intruders. If a cell is infected with a virus, it has pieces of virus antigens on its surface. This is a signal for the Killer T-cell that lets it know this is a cell that must be destroyed.”
–
“They don’t claim there is a t-cell with a marker for Covid-19 on it.”
“There is no Covid T cell as such.No test for it. There is no T cell which has a marker specifically for Covid on it. None.”
–
Exactly.
They come close. They pretend the T-cells are covid specific.
“Next, we utilized an activation induced marker assay (AIM assay, (25–27)) to detect virus-specific T cells in a new set of unexposed donors,”
The T-cells they test can react to a lot of things
–
“There are 25 million to a billion different T-cells in your body. Each cell has a unique T-cell receptor that can fit with only one kind of antigen, like a lock that can fit with only one shape of key. Antigens and receptors work a lot like a lock and key. Most of these antigens will never get in your body, but the T-cells that patrol your body will recognize them if they do.”
–
What they do is a variation of the
xkcd jelly bean comic – “Significant”
I see that one time out of the twenty total tests they run, p<0.05
, so they wrongly assume that during one of the twenty tests, the result is significant (0.05=1/20
Except instead of 20 jelly beans they have 129 peptide chains and claim significance.
–
I expect you will appreciate the mathematics at play here, much better than the astounding maths at WUWT "McIntyre on Kaufman et al 2020" [worth a look and a laugh]
How about “Where viral ideas are spread.”
… Nah. It makes me want to put my mask on while typing.
SteveF
Did you actually read the two papers linked to above in this thread? From your comments, I am guessing you did not. Tell me if I am mistaken about that.
–
I read Mike’s paper, that is how I was able to write
“angech (Comment #188932)August 10th, 2020 at 7:46 am Mike M
https://sebastianrushworth.com/2020/08/08/what-is-the-best-way-to-measure-rates-of-covid-immunity/
The 4th comment was from a person called A.L.”
Having been through it all.
–
I have, now read your linked paper.
– My comments were based on Mike’s paper.
–
I hope my comment to Lucia helps explain my views more clearly.
These guys work, very hard, in a laboratory running the same tests that have been used for decades and try to get a paper out of it. Fair enough.
The problems are at least twofold.
One they break the covid proteins down into segments and and test T-Cell reactivity to these protein segments.
The first mistake is a very serious one.
Protein recognition is 3 dimensional. The way the protein fragments fit into each other is vital to recognition.
Even more for the B cells which have to make interlocking antibodies.
But still a problem for the B Cells.
There are 20 amino acids used in the human body and incorporated into viral protein. The complexity of 26 combinations in a chain even a few hundred amino acids long is staggering.
Here they use a simple approach of splitting the proteins into segments.
No suggestion that the lengths chose is what the T cell wants to know.
T cells react to a lot of protein segments, could be covid could be corona virus, could be the egg nog I had for breakfast.
And they find matches.
Amazing stuff.
Color me unimpressed, Yes it has some possible veracity.
–
But even your paper, last paragraph, ditches this.
Quote
“These finding of cross-reactive HCoV T cell specificities are stark contrast to HCoV neutralizing antibodies,which are HCoV species-specific and did not show cross-reactivity against SARS-CoV-2 RBD (33–35). Based on these data, it is plausible to hypothesize that pre-existing cross-reactive HCoV CD4+ T cell memory in some donors could be a contributing factor to variations in COVID-19 patient disease outcomes, but this is at present highly speculative ”
–
Notice it is highly speculative, ie an educated guess.
Further the mention of antibodies [from B cells] did not show cross reactivity.
–
“And just to be clear: do you believe that infection with vaccinia virus provides protection against the related smallpox virus? If so, how does that happen?” Rhetorical but anyway,
–
You know Cowpox and Small pox share antigens that provoke antibodies [B-Cells] that provide immunity. HOC and Covid share an RNA lineage but not an antibody provoking antigen surface.
That is part of the reason that we have not made vaccines for the common cold yet.
–
Perhaps I should ask you if you believe in your heart of hearts that it is the T cells that are stimulated by the vaccines and provide the protection against Smallpox, Rubella, Measles, not the B cell antibodies.
–
Anyway I am coming across too heavy and pedantic like someone else we used to know so a short break is in order.
Have enjoyed your and Lucia’s take on the situation which is similar to Nic Lewis so you are both in very good company.
angech,
I’m not seeing how “The way the protein fragments fit into each other is vital to recognition” makes it a “mistake” to breakproteins into fragments and then recognize fragments. No one is claiming they recognized the while protein– just a fragment. After that, there is a chain of inferences, which is logic and so not specifically biology, chemistry or any science.
.
Sure. But that only means there are tons of combinations that make a particular fragment unique. (A full protein is even more unique.)
.
Sure. That’s why a series of tests and logical inference is required (and done.) Ignoring that extra info in the paper and analyzing it as if it was not done strikes me as an inadequate evaluation of what the paper did.
Of course it’s speculative. The “education” is having done a series of test and looking at the outcome. This is typical of science.
I have no idea.
I also don’t know that it matters whether T-cells are involved in vacinnes for these other diseases. What I do know is the NIH is writing articles like “Immune T Cells May Offer Lasting Protection Against COVID-19” So THEY seem to think Tcells are involved in protection against COVID.
https://directorsblog.nih.gov/2020/07/28/immune-t-cells-may-offer-lasting-protection-against-covid-19/
There are also articles suggesting some *new* vaccines under development prompt the body to make memory T-cells. The logic says:
1) If T-cells provide immunity to *Covid* and
2) a proposed Covid vaccine prompts the body to make these T-cells,
Then
3) that proposed Covid vaccine might prompt immunity to Covid.
Testing would be required. It might be a “breakthrough” because this isn’t how smallpox, measles etc. vacinnes work. But there is NO logic that says there *must be* one and only one way for a vaccinne to work!
.
angech,
I find you comments very confusing and hard to follow, in part because it is not clear what you are quoting, in part because you sometimes seem to be putting words in people mouths and in part because I find it hard to tell what your point is. You also seem to make pronouncements way beyond your knowledge.
.
angech (Comment #189140): “The problems are at least twofold.
One they break the covid proteins down into segments and and test T-Cell reactivity to these protein segments.
The first mistake is a very serious one.”
.
It appears that the epitope mapping is a standard technique, so I am not impressed by your dismissal of it. One or even a few peptides reacting would not be impressive, but a large number reacting is much more significant. I would think that those who work in that field have criteria that are used.
Also, the variable regions of antibodies are rather small and react to pieces of proteins.
.
You quote the last paragraph of https://science.sciencemag.org/content/early/2020/08/04/science.abd3871
OK, so prior exposure to other coronaviruses might provide some protection via the T cell response, but not complete protection since the new virus requires different antibodies. That is interesting to know. But I don’t get the triumphant tone with which you cite that.
The Wall Street Journal is examining the causes of the Covid-19 catastrophe and the bungled response that followed.
.
Part 1: A Deadly Coronavirus Was Inevitable. Why Was No One Ready?
https://www.wsj.com/articles/a-deadly-coronavirus-was-inevitable-why-was-no-one-ready-for-covid-11597325213
.
“When Disease X actually arrived, as Covid-19, governments, businesses, public-health officials and citizens soon found themselves in a state of chaos, battling an invisible enemy with few resources and little understanding—despite years of work that outlined almost exactly what the virus would look like and how to mitigate its impact.”
angech,
“I hope my comment to Lucia helps explain my views more clearly.”
.
No, your views remain as clear as mud to me.
.
As best I can figure, you dismiss the linked papers, both authored by specialists in immunology, as pure rubbish, and the authors incompetents publishing nothing but speculation. I hope you can forgive me if I doubt that is the actually true. You must also think Francis Collins, the head of the US NIH is something of a fool for writing about the importance of yet another paper about T-cells and covid-19 (this one published in Nature, July 2020):
.
“SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls”
.
The very first line in the abstract reads:
“Memory T cells induced by previous pathogens can shape susceptibility to, and the clinical severity of, subsequent infections.”
That sentence is referenced to a 2002 paper:
“Welsh, R. M. & Selin, L. K. No one is naive: the significance of heterologous T-cell immunity. Nat. Rev. Immunol. 2, 417–426 (2002).”
.
Welsh and Selin must ALSO be fools, right? It looks to me like you dismisses a whole field of research based on your own personal understanding of something you have only superficial understanding of.
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Color me unimpressed. Please provide links to research publications, preferably your own, which clearly refute all the rubbish being published recently in Science and Nature…. and back to 2002.
angech
I admit what I know about t-cells is from the web. But things you say seem to hinge on modifiers– which in the end appear to not be meaningful in the context of the discussion here. We are trying to understand whether, how or why memory t-cels might work.
I’ve highlighted “directly”, because that word seems to make your claim both true but irrelevant. If we take the word out, your sentence because untrue. But we are trying to understand if the fight not whether it’s directly or indirection.
.
So,ok… it seems t-cells fight indirectly by killing infected cells. From:
https://www.genscript.com/antibody-drug-development-news/memory-t-cells-how-are-they-formed.html
.
.
So: I think it seems pretty established T cells fight infection. Whether that is “directly” or “indirectly” is pretty unimportant to the current discussion of t-cells.
.
You’ve also made much of antibodies recognizing angtigens. But, evidently, t-cells also work through antigens. T cells kill cells “after recognizing antigens”. These antigens evidently appear on the surface of infected cells. (This is from wikipedia. https://en.wikipedia.org/wiki/T_cell )
.
Also, evidently at least some vaccines work by generating memory t-cells
From https://www.genscript.com/antibody-drug-development-news/memory-t-cells-how-are-they-formed.html
.
The next is my speculation:
My inference: if viruses A and B cause infected cells to exhibit the same antigen the memory Tcells that trigger when they see virus A might also trigger on cells infected virus B. Because it’s triggered by the same antigen not by the whole virus. So this will kick off the same process to kill off cells. What the details of that process are doesn’t really matter: it’s been triggered and the cell will be killed. This should fight the infection. (Obviously, I’m speculating. The question is whether this seems plausible.)
.
OTOH: if some shared antigen for virus A and B is not one that triggers the Tcell, the memory t-cells from A won’t work to protect against B. One might also speculate that the collection of t-cells from A won’t give full protection against B because, perhaps one creates t-cells that trigger against a whole bunch of antigens from A, but only a fraction of those work with B.
.
All of this would explain cross-reactivity, and immunity based on memory t-cells rather than by causing the body to create antibodies that float around forever. There is tons of stuff out there all agreeing that t-cells themselves help fight viruses. (So do anti-bodies. But this doesn’t seem to be either/or. )
.
I certainly admit to having no knowledge of my own and know that it’s possible that these resources I found on the web are totally wrong. But there seem to be multiple ones, they appear to agree and there seems to be lots of peer reviewed research coming out all of which seems to suggest that memory t-cells can confer immunity, that these trigger on antigens.
.
Indians will be enthusiastic to vote for Kamala.
I wonder how much this will be tempered by her using an incorrect pronunciation for her name.
My local paper reprinted an LA Times editorial today:
Trust the progressive LA Times to completely miss the point and manage to get in a dig at Trump at the same time. The point being that Biden needs a strong VP because he is extremely likely, if elected, to be the first President removed from office under Section 4 of the 25th Amendment.
DeWitt,
I suspect it is true that Trump would never have picked a strong woman running mate. OTOH: Neither did Obama or Clinton or…..
.
I do think if Biden is elected, Kamala will be our first women president. The irony is that she’s is soooooo the opposite of what “defund the police” people ought to be supporting if they really don’t like overly strong policing that steps on toes. Oh. Well…. 🙂
Lucia
MikeN,
I doubt it will make much difference as Indians already vote heavily for Democrats.
The irony of her selection is that her give name, Kamala Devi, is another name for the Hindu goddess Lakshmi, the goddess of prosperity.
DeWitt,
“The irony of her selection is that her give name, Kamala Devi, is another name for the Hindu goddess Lakshmi, the goddess of prosperity.”
.
As you say, irony always increases.
Obviously people are so unbelievably shallow as to only vote for people who have similar ethnic origins to themselves. VP’s don’t win or lose elections. They don’t matter. Perhaps if Biden shows up without pants and starts drooling heavily during debates then it might matter.
The DOJ completed it’s investigation of Yale’s admission policies.
“The investigation concluded that Asian American and white applicants are only one-tenth to one-fourth as likely to be admitted as African American applications with comparable academic records.
“There is no such thing as a nice form of race discrimination,” Dreiband said in a separate statement. “All people should be treated with decency and respect and without regard to the color of their skin.”
.
The Supreme Court is going to be forced to rule on this yet again. This “give an inch take a mile” blatant discrimination by academia is going to need to be struck down. Progressive admission committees simply can’t be trusted to do this fairly. Remove race from admission applications and allow discrimination based on economics.
Mask theater is getting absurd. NPR: Joe Biden: For The Next 3 Months, All Americans Should Wear A Mask When Outside
https://www.npr.org/sections/coronavirus-live-updates/2020/08/13/902257311/joe-biden-for-the-next-3-months-all-americans-should-wear-a-mask-when-outside
.
What is bizarre here is the picture showing Biden/Harris wearing their masks walking in, and then taking them off to talk. “All Americans” should wear a mask when outside also presumably means they should wear them inside as well, maybe even when speaking at length in public.
“We absolutely need a clear message from the very top of our federal government that everyone needs to wear a mask in public, period,” he said.
.
He said, not wearing a mask. The media makes no mention of this contradiction.
Tom Scharf,
“ This “give an inch take a mile†blatant discrimination by academia is going to need to be struck down.â€
.
Won’t happen for one reason: Roberts; probably the single most dreadful SC justice in my adult lifetime. There have been many who signed on to even more horrible court decisions, but unlike Roberts, they were all pretty up front about it….’The living Constitution must be re-interpreted in light of todays political needs’ is incredibly destructive and foolish, but at least honest. Roberts’ many feckless decisions to maintain unconstitutional rules and laws betray every principle he ever claimed to stand for. I do not know how the guy faces himself in the mirror each morning.
Thanks Steve and Lucia for stimulating me onto looking further into what is around.
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The answer to Covid 19 lies in part in the development of successful vaccinations. [plural].
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This is normally injecting the body with an antigen derived from the virus coat or capsid though there are other ways being trialed.
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As I said it is complicated. There are B cells.There are a lot of different T-Cells with a lot of different roles.
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This was very good “NEWS FEATURE 28 April 2020
The race for coronavirus vaccines: a graphical guide
Eight ways in which scientists hope to provide immunity to SARS-CoV-2 .”
“More than 90 vaccines are being developed against SARS-CoV-2 by research teams in companies and universities across the world. Researchers are trialling different technologies, some of which haven’t been used in a licensed vaccine before. At least six groups have already begun injecting formulations into volunteers in safety trials; others have started testing in animals”
–
If you want to be safe you need to have a vaccine which will give you Ab, circulating Antibodies, to corona virus from B -cells.
Full stop.
–
Antigen presenting cells APC’s detect the virus.
They stimulate T helper cells [Have not seen them mentioned at all in the discussion on the T-cells that actually attack infected cells.
They do this by presenting bits of the virus to the T helper cells.
These cells activate the B cells.
They produce the circulating antibodies.
Note there can be more than one.
The Antibodies attach to and neutralise circulating virus.
No more cells are infected and the virus is beaten.
Takes up to 2 weeks.
–
They T helper cells also prime the T cells all the articles are about.
This means they can then detect and destroy infected cells [including the poor helper T cells. Each cell killed releases a shower of viral particles which can further infect the body cells but the Antibody production from the B cells is ramped up enough to neutralise it all.
–
Note the implied problems here.
T cells that are reactive to previous corona virus infections can only attack infected cells.
There are no antibodies to corona virus itself.None. Each infected cell that is destroyed showers millions to billions of viral particles into the blood stream where the APC cells are trying to respond to the new virus with no antibody protection yet.
T cells can recognise parts of corona virus, sure.
You can show this in a 100 ways with T cell reactivity, fine.
But the essential part of immunity is nit destroying infected cells and promoting more rapid spread.
It is by developing circulating antibodies.
This seems so naively and basically true that I worry when ither logical minds cannot see it.
–
Go the Russians. Go USA. Go the Australian CSIRO. Go the Chinese. Get those vaccines out.
Steve F
“Please provide links to research publications, preferably your own, which clearly refute all the rubbish being published recently in Science and Nature…. and back to 2002.”
I have backed up my assertions with [ir]refutable logic.
Please do not use this argument.
” you dismiss the linked papers, both authored by specialists in immunology, and the authors publishing nothing but speculation.”
They said it Steve, in their summary.
Did you read it?
Quote
“These finding of cross-reactive HCoV T cell specificities are in stark contrast to HCoV neutralizing antibodies,
which are HCoV species-specific and did not show cross-reactivity against SARS-CoV-2 RBD .
Based on these data, it is plausible to hypothesize that pre-existing cross-reactive HCoV CD4+ T cell memory in some donors could be a contributing factor to variations in COVID-19 patient disease outcomes,
but this is at present highly speculative â€
–
Plausible, Possible, highly speculative.
–
angech,
The problem with your comments is that you seem to be telling us that memory t-cells giving partial immunity is implausible, and impossible. So your posts seem to contradict the paper’s closing. In contrast, everyone else is saying it’s plausible and possible. (I agree it’s speculative. That’s not what the argument is about. We all know we are speculating here.)
.
Now maybe you don’t think you are telling us the cross-reactivity giving immunity is implausible, and impossible”, but that’s how it sounds.
.
So, direct question, are you saying “pre-existing cross-reactive HCoV CD4+ T cell memory in some donors” giving partial immunity is implausible, and/or impossible? Or do you think it is plausible or possible?
angech,
I believe your picture of the immune response by T-cells is partial. The Nature paper I referenced above shows the presence of both CD4+ and CD8+ T-cells reactive to protein segments found in covid-19 among >50% of people never exposed to covid-19. This short article: https://www.immunology.org/public-information/bitesized-immunology/cells/cd8-t-cells
suggests “CD8+ T cells (often called cytotoxic T lymphocytes, or CTLs) are very important for immune defence against intracellular pathogens, including viruses and bacteriaâ€, and goes on to explain how the cell inhibit virus production. They do not suggest (as you have multiple times) that CD8+ cells only make a virus infection worse by releasing many virons in the process of killing an infected cell, and say the CD8+ cells release cytokine proteins that attack virons.
.
People who are trying to actually understand the progress of the covid-19 pandemic (not the politically motivated virtue signalers flaunting their masks) are faced with clear data which shows herd immunity effects become important long before enough people in a truly naive population have been infected, and that indicates substantial resistance among many in the population who have never been exposed to covid-19. The multiple published papers on T-cells are all concluding it is plausible (and certainly possible) earlier exposure to other coronaviruses has produced this population of resistant people. And cross-reactive T-cells are in fact present in more than half the unexposed population. You seem to be rejecting that possible explanation for resistance for no good reason I can see.
SteveF
Thats how it sounds to me, It sounds like angech is saying this mechanism for resistance is impossible. But then he sums up with the quote that says “plausible, possible speculative”, which he seems to think agrees with whatever he is arguing.
.
Logically, if angech is claiming it is impossible then “plausible, possible speculative” in the closing of that paper flatly contradicts his position. So I’m hoping angech clarifies what his actual claim is.
.
Angech has certainly given a blizzard of details about the immune system. But it’s now unclear what his claim about the possibility that cross-reactive t-cells could give some degree of immunity is.
SteveF
wrt to this:
https://www.immunology.org/public-information/bitesized-immunology/cells/cd8-t-cells
.
If I read correctly, it appears the mechanism by which those t-cells eliminate virus in the body (a) does not involve antibodies in anyway and (b) does not involve B cells.
.
(Those virons happen to be inside infected cells. So wrt to angechs previous claim of not killing “directly”, one might say the virons are killed “indirectly”– by killing cells. But inside cells is where virons multiply. So this would seem to be a pretty hefty contribution to immunity. If looked at using the mathematics of an SEIR model, that would be reducing the Ro…. as as we know if it’s reduced enough, the virus would be eliminated. So “indirect” killing would be enough)
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angech (Comment #189168): “But the essential part of immunity is nit destroying infected cells and promoting more rapid spread.”
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Do you have any evidence for that remarkable claim?
.
I am inclined to agree with lucia (Comment #189181): “If I read correctly, it appears the mechanism by which those t-cells eliminate virus in the body (a) does not involve antibodies in anyway and (b) does not involve B cells.”
——–
angech (Comment #189168): “This seems so naively and basically true that I worry when ither logical minds cannot see it.”
.
In science, that which is naively obvious is often flat wrong. A little knowledge is a dangerous thing.
——
SteveF (Comment #189176): ” The multiple published papers on T-cells are all concluding it is plausible (and certainly possible) earlier exposure to other coronaviruses has produced this population of resistant people.”
.
Not entirely. It has also been proposed that prior exposure to other coronaviruses might make the disease worse via antibody dependent enhancement:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102551/
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SteveF: “clear data which shows herd immunity effects become important long before enough people in a truly naive population have been infected”.
.
That is one possibility. The other is that there is a wide range of R0 values in a population, in which case the average value is much smaller than the initial value, so that herd immunity is reached must sooner than might be estimated from the initial rate of spread.
——–
angech (Comment #189168) : If you want to be safe you need to have a vaccine which will give you Ab, circulating Antibodies, to corona virus from B -cells.
Full stop.”
.
Only if the vaccine is safe. A big risk of coronavirus vaccines is antibody dependent enhancement:
https://en.wikipedia.org/wiki/Antibody-dependent_enhancement#In_coronavirus_infection
No where close to being a biologist, but I think Angtech’s point is the CD8’s are coded for specific viral peptides being surfaced and held by the MHC’s that the identify the cell as being infected with a foreign entity. As described in Lucia’s link. This triggers the T-Cell to release the toxins. The question is are the fragments that caused the reaction in blood samples close enough to what would be exposed in a real world infection. IOW If the fragment had two of five structures, that could be enough to trigger on the samples, but the missing three could block the fit and match in the real world. You also have to deal with which parts of the peptide are being held by the MHCs and therefore not exposed to the T-Cell. I would hope that the fragments were selected to be a useful match, but I haven’t seen anything stating such.
AndrewP,
As far as I can tell, in context of this discussion that would be a sub point.
.
I want to know angech’s point or claim at a more fundamental or “big picture” level.
.
What I want to know is this:
Is angech claiming that cross-reactivity in t-cells, especially memory t-cells cannot possibly result SARS, cold or other corona viruses confering immunity to Covid-19 cells?
.
Angech should be able to give a yes/no answer because it would, presumably, be his “big picture” point which all the other details and sub-points would support.
It shouldn’t require a paragraph discussion of immunology at least for now
.
So I’d like to see a yes/no answer to the question highlighted above. Ideally, I would like to see that as the only information in a message. As in
“My answer to lucia’s italicized question is _______?”
.
The, if he wants to add more to support why he thinks the answer is yes or no, put that in a different message.
MikeM
I agree with you there are other possible explanations for the infection spread seeming to plateau sooner than expected based on the SEIR model for spread in a homogeneous, 100% susceptible population that doesn’t change it’s behavior such that R0 itself changes.
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So that would indicate that we can’t be sure what the true explanation is. The true explanation might be more pedestrian: People are wearing masks and self isolating. If so, we will expect another wave or wavelet if they all stop self-isolating suddenly. (And then we can argue about Sweden. . .)
.
But that, of course, doesn’t resolve the question vis-a-vis angech which is what is his “big picture” claim about whether memory t-cells left from past infections that are cross reactive could confer immunity. He’s giving a heck of a lot of (somewhat confusing) details to support some big picture claim. But I honestly cannot for the life of me figure out his claim about anything important to spread and immunity of the population as a whole.
.
As far as I can tell, his big picture claim is that t-cell cross-reactivity from other corona viruses cannot result in partial immunity to covid-19. I want to know his direct answer to whether he thinks this or not. (No more explanation of “why” they answer is yes/no. I want to first read if his answer is ‘yes/no’ on this big picture.)
lucia,
My impression of what angech is saying is that he thinks T cells don’t kill infected cells until the infected cells have produced a large number of virons and are close to dying anyway. I doubt that is correct. If, OTOH, T cells can kill infected cells very early in the process of virus replication then, as you say, the internal Ro will be smaller, possibly much smaller, than if there were no T cell reactivity.
Tom Scharf,
Wearing a mask outdoors is, AFAICT, nearly pointless, much like wearing a mask while driving in a car by yourself. Everything I’ve seen is that transmission in the open air is insignificant compared to transmission inside structures. If masks are to be significantly effective, then they must be worn inside, and especially when talking.
The 1918 flu maxed out at around 33% of the population (showed symptoms). I think we would have seen at least some large pockets of very high covid infection rates by now. There is very likely something limiting transmission beyond social distancing. Some self limiting factor.
.
I imagine we will know what these things are in the next couple years. One lesson to learn here is that the rate of discovering what these things are needs to be accelerating DURING the pandemic. This is not an academic exercise when 1K people are dying a day in the US and we have no idea who is susceptible and who isn’t. Perhaps these things just can’t go faster, but color me unconvinced of that.
I’ve been reading about “not enough testing” being done lately, specifically when commenting on declining case numbers in some hot spots. I think we are in a different situation now where declining test numbers is actually now a sign of declining infections. AFAICT everyone who wants a test can get a test in most hot spot areas, so this is just a sign that people are less symptomatic than they were previously.
NPR has an article on contact tracing. One of the first ones I have seen.
https://www.npr.org/sections/health-shots/2020/08/14/902271822/13-states-make-contact-tracing-data-public-heres-what-they-re-learning
.
“But in reality, public health workers don’t have that level of success. In New Jersey, these data show that public health workers reached only 44% of new cases within 24 hours, and nearly half of those reached refused to provide contacts.”
.
Louisiana has a list of where outbreaks were happening (bar, food processing, industrial setting):
https://ldh.la.gov/index.cfm/page/3997
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North Dakota: Community spread 3281 cases, household spread 1368 cases.
.
Very interesting data, it boggles my mind why this isn’t being farmed and disseminated.
Tom Scharf,
One of the reasons I like the ratio of positives to test is that it’s more robust to changes in number of tests. If cases in the population are declining then the positivity ratio will likely go down. (I know there are issues though. . .)
.
But yes: the number of tests taken could go down because (a) the number of people with symptoms go down (b) the number who think they are exposed go down and (c) the number of people who are worried goes down. (c) is affected by the past few days case numbers!
DeWitt
According to SteveF’s link, the process by which T-cells kills the infected cells appears to kill the virons inside the cell before it kills the cell. If so, to prevent multiplication in the body, the T-cells would only need to kill the infected cells before the virons escape the cell. My impression is live virons only escape the cell when the cell dies. If this is true and the T-cells do kill the virons inside the cells before it dies, then they are dead before escaping. So it wouldn’t matter if this happens “early” or “late” in the life time of the infected cell. It only matters that it happens before live virons are released.
.
To avoid my question to angech getting lost while he’s probably asleep in australia, I’m going to repeat this to angech:
Is angech claiming that cross-reactivity in t-cells, especially memory t-cells cannot possibly result SARS, cold or other corona viruses confering immunity to Covid-19 cells?
I’m looking for a yes/no answer for now. (I don’t want long details explaining why it’s yes or no. Just is his answer yes or no.
.
Lucia,
“If I read correctly, it appears the mechanism by which those t-cells eliminate virus in the body (a) does not involve antibodies in anyway and (b) does not involve B cells.”
.
Yes, and that is why I think angech is pretty much lost in the weeds. It is plain from that brief article (and many other independent sources!) that CD8+ (killer T-cells) do destroy virus particles at the same time they kill cells infected by viruses.
.
Of course, having circulating antibodies to a viral pathogen is probably as important (or even much more important) for resisting an infection, but to simply dismiss cross-reactive T-cells as irrelevant to explain apparent resistance to symptomatic covid-19 illness (or dismiss that cross reactivity as just wild, unfounded speculation) is, IMO, quite beyond bizarre.
.
Apparently the editors at Science, Nature, and other journals, agree that it is worth publishing… and important enough to the body politic to take down the usual paywalls.
Hospitalizations are down 20% from the recent peak, which matched the 60,000 max in April, and are now below the level of a month ago.
Daily cases are also down. I think Texas and Arizona reintroduced partial lockdowns.
Daily deaths have not dropped, and are still over 1000 per day.
Mike M,
“That is one possibility. The other is that there is a wide range of R0 values in a population, in which case the average value is much smaller than the initial value, so that herd immunity is reached must sooner than might be estimated from the initial rate of spread.”
.
Sure, but what we actually see is the same pattern for the pandemic quite independent of specific cultures. Where things have gotten really ugly (New York, New Jersey, Massachusetts, Milan, etc) has always been where the rate of infection exploded, and lots of very elderly people were not protected and became infected, leading to very high average death rates. The many “second wave” peaks in cases across the USA (and “second wave” peaks in other countries) have not produced the same high rates of death.
.
Yes, it is possible something as simple as a wide range of behaviors generates a wide range of Ro values, but it seems to me more likely there is a range of susceptibility to the virus due to previous exposure to related viruses. It could, of course, be a combination of both.
Mike N,
The pandemic is coming to an end in many places, including most of the USA and Europe. How long, drawn out, and economically/socially destructive the decline of the pandemic will be remains to be seen. Much, unfortunately, will depend on lefty politicians who don’t really want it to end… so I am not sanguine: the end of the pandemic could be very slow and unnecessarily painful and damaging.
So… New Zealand. I guess that amazing lockdown strategy is getting a dose of viral reality. Still, nothing another few months of lockdown can’t solve I suppose.
DaveJR,
I don’t know if you saw the link in a previous thread, but even quarantine and isolation are not guaranteed to prevent outbreaks.
https://www.realclearpolitics.com/articles/2020/08/07/the_myth_that_lockdowns_stop_pandemics_143899.html
The more effective the lockdown, the bigger the subsequent epidemic. In the absence of a vaccine, herd immunity is the only way an epidemic will subside. To put it another way, flattening the curve doesn’t necessarily reduce the area under the curve.
“My answer to lucia’s italicized question is yes.
Is angech claiming that cross-reactivity in t-cells, especially memory t-cells cannot possibly result SARS, cold or other corona viruses confering immunity to Covid-19 cells?
Immunity
Means immunity.
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T cells are part of a very complicated immune process.
They help with some aspects but they never confer immunity.
–
The discussion of their role is even more complicated because there are different types of T cells with markedly different functions. Most of the papers and discussion are not on memory T cells but I am happy to discuss them with the rest.
–
Immunity is not just an antibody response.
In the current context, that of any naive population, with all the natural immunities ignored the question is can T cells with all their abilities, provide immunity to covid 19?
The answer is no.
–
No matter how many antigens the T cells can memorise or react to
( their two main functions) the T cells can never develop antibodies to the virus, they can never stop the virus entering cells and they can never destroy the virus * ( I will look at Steve’s latest article which apparently says otherwise). It is not their role.
THree comments, slightly abridged for brevity are wrong
” This short article: https://www.immunology.org/public-information/bitesized-immunology/cells/cd8-t-cells
say the CD8+ cells release cytokine proteins that attack
–
“SteveF’s link, the process by which T-cells kills the infected cells appears to kill the virons inside the cell before it kills the cell. If so, to prevent multiplication in the body, the T-cells would only need to kill the infected cells before the virons escape the cell. My impression is live virons only escape the cell when the cell dies. If this is true and the T-cells do kill the virons inside the cells before it dies, then they are dead before escaping.”
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“. It is plain from that brief article (and many other independent sources!) that CD8+ (killer T-cells) do destroy virus particles at the same time they kill cells infected by viruses.
–
None of these statements are correct.
Apart from the fact that I could not see the word viron in the article.
Cytokines do not attack virons or virus particles. They are proteins that stimulate many reactions including promoting natural viral resistance on the cell surface. Some of them actions are to slow or prevent viral production and replication in the cell itself but not to attack or destroy the virus. They only kill the cells.
Saying that the article says attacks the viron, do kill the virons inside the cell, do destroy virus particles is not correct.
–
Once we get away from the idea that T cell actions on their own can kill or destroy the virus we realise that immunity is not a crossreactive T cell property.
–
By the way does anyone wonder why and how the papers all refer to possible previous exposure by the subjects to the SARS virus conferring T cell “immunity to Covid”. An incredible comment seeing that According to the World Health Organization (WHO), a total of 8,098 people worldwide became sick with SARS during the 2003 outbreak. Of these, 774 died. In the United States, only eight people had laboratory evidence …
I could postulate that prior exposure to related common cold corona virus meant that 50% of the population already had T cell resistance to SARS so it died out.
“Based on these data, it is plausible to hypothesize that pre-existing cross-reactive HCoV CD4+ T cell memory in some donors could be a contributing factor to variations in COVID-19 patient disease outcomes, but this is at present highly speculative â€
–
Plausible, Possible, highly speculative. The authors words, not mine. The opposite would be plausible, possible not speculative
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Would prefer people to discuss Klinesmith, 1 down 298 to go?
–
angech,
Resistance does not necessarily mean complete immunity. From a practical POV, resistance which leads to no illness in spite of exposure is no different from immunity.
.
We know that a large fraction of exposed individuals never suffer symptomatic illness, even though they are by definition “naiveâ€, since they could not possibly have had previous exposure to covid-19. We also know from the published articles about T-cells, as well as many other sources, that many people who develop antibodies suffered few or no symptoms at all, yet others with the same age and health status become very ill.
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We are left with only two plausible explanations: 1) previous exposure to related coronaviruses provides some degree of resistance, or 2) some people have “natural resistance†due to their genes. As far as I am aware, nobody has published anything supporting natural resistance to covid-19, save for a somewhat lower risk of covid infection for people with blood group O (about half the population in the States).
angech,
From the short linked article:
“ Granzymes are serine proteases which cleave the proteins inside the cell, shutting down the production of viral proteins and ultimately resulting in apoptosis of the target cell.â€
.
Are you suggesting that is simply wrong?
angech
In that case, your position is flatly contradicted by the paper you cited to support it. You correctly summarized that sentence with “Plausible, Possible, highly speculative.”. But you are using that to support “implausible, impossible”.
.
I’m rather surprised you don’t see that that paper utterly contradicts your position.
Since angench defined immunity “means immunity”, I thought I’d post the definition of immunity
.
“: the quality or state of being immune especially : a condition of being able to resist a particular disease especially through preventing development of a pathogenic microorganism or by counteracting the effects of its products — see also active immunity, passive immunity.”
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It sure as heck sounds like T-cells “resist a particular disease” and also “prevent development of a pathogenic microorganism”. It does this by killing cells infested with developing virus.
.
It also appears that in 2018, the NIH thought memory T-cells can confer immunity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046459/
.
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The reason we are reading so many articles discussing memory t-cells conferirng immunity is that’s what researchers think they do. That’s the actual goal of some vaccine makers. It appears to be a new basis for vaccines working– but it is thought t-cells confer immunity. Or if angech doesn;t like taht word, “protection against disease”.
.
They are now finding t-cells are cross reactive to various viruses. This should not be surprising because (just like antibodies) they react to antigens, not the whole virus.
.
As far as I can tell: angech’s position is mistaken.
SteveF (Comment #189208): “Resistance does not necessarily mean complete immunity. From a practical POV, resistance which leads to no illness in spite of exposure is no different from immunity.”
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Exactly. It is not black or white; infection can produce a wide range of illness from no symptoms to death. Coronavirus is hardly unique in that regard. From what I can tell the same applies to all the respiratory viruses: Influenza, rhinovirus, adenovirus, parainfluenza, enterovirus. I think I am missing one.
——-
SteveF: “We are left with only two plausible explanations: 1) previous exposure to related coronaviruses provides some degree of resistance, or 2) some people have “natural resistance†due to their genes.”
.
That seems to be readopting the black/white view. All people have a degree of natural resistance via the mucosal and innate immune systems. It may be that those are sufficient to deal with a small initial infective dose but that a larger initial dose of virus requires a T cell response and an even larger dose is not successfully dealt with until the blood stream is flooded with antibodies.
.
Not coronavirus specific: From what I have been reading, there is a fighting-the-last-war quality to antibodies. It takes several days to start producing antibodies, by which time many infections are on the wane. Then the level of antibodies in the blood stream keep increasing for several weeks, long after the infection is gone.
MikeM/Steve
It meets the dictionary definition of immunity. There is an “or” in the definition “or by counteracting the effects of its products “.
.
The ‘effects’ of a viral infection are basically the symptoms. So, merely not getting symptoms is “immunity” at least as far as the dictionary is defined. I don’t know angech’s definition other than “immunity means immunity”.
lucia,
There are multiple definitions of immunity and the dictionary definition need not be the same as the medical definition. For example, from the Wiktionary definition of immune (https://en.wiktionary.org/wiki/immune#Adjective):
and for immunity (https://en.wiktionary.org/wiki/immunity#Noun)
I think that is how angech is using the term.
But then, for ‘immune’ there is also:
I think that technically an acquired resistance to a pathogen is ‘partial immunity’.
I haven’t been following the the T cell discussion, but here is NYT story:
The Coronavirus Is New, but Your Immune System Might Still Recognize It
Some people carry immune cells called T cells that can capitalize on the virus’s resemblance to other members of its family tree.
https://www.nytimes.com/2020/08/06/health/coronavirus-immune-cells.html
The Portland protests are endless entertainment. After the DA decided not to charge the majority of protesters arrested unless the charge was for a violent crime, the state police decided to leave.
https://www.washingtonpost.com/nation/2020/08/14/protests-live-updates-oregon-police-leave-downtown-portland-after-da-declines-prosecute-most-protest-related-crimes/
.
“The Oregon State Police is continually reassessing our resources and the needs of our partner agencies and at this time we are inclined to move those resources back to counties where prosecution of criminal conduct is still a priorityâ€
MikeM,
I’m fine with the idea there are multiple definitions. But I think it’s fair to say that we can expect people in a blog post are allowed to use any one of them. So angech’s “immunity means immunity” is clearly not clarifying anything.
.
If angech means something very precise and his idea that it doesn’t give immunity is based on that very precise definition– one not shared universally by dictionaries– it’s incumbent for him to say that and then explain how given his definition (which is not universally shared), it doesn’t confer “immunity”.
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In fact, it’s not clear that groups like the NIH agree with his view on even that. But… maybe they do.
.
After that, we can then move on to other questions which is “does it give what he would call partial immunity (and which some dictionaries call “no adjective immunity”)? Does it give resistance? Does it do anything at all?
.
Without an actual definition of “immunity”, then we really can’t have a clear discussion.
So my question is whether there is any such thing as total immunity. Can’t you always overwhelm the immune system with a large enough dose? Real question. That would mean that all immunity would technically be partial.
And to somewhat nitpick: “Immunity is immunity” seems to me to be some sort of logical fallacy. I lean toward begging the question, i.e. assuming your conclusion. But it might be something else. It certainly fails as a definition.
DeWitt Payne (Comment #189220): “Can’t you always overwhelm the immune system with a large enough dose?”
.
Cool question. My guess is that the answer is yes in theory but no in practice. With a new virus, it takes several days for the B cells to evolve to the point of producing antibodies. By that time, the virus population in the body must increase enormously. I would think that would be far beyond any real world initial dose other than maybe injecting a syringe full of virus incubated in laboratory.
Don’t know if any of you are interested in Big Ten football or a study upon which the cancellation was partially based. In any event, a Michigan cardiologist said the study was statistically flawed and should be retracted. If so inclined to opine, I would be interested in comments from those way more statistically than I am. https://twitter.com/venkmurthy/status/1294406748678365191
Then there’s this from the WSJ:
Related Lancet article:
https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(20)30198-X/fulltext
Wrong person, place and time: viral load and contact network structure predict
5 SARS-CoV-2 transmission and super-spreading events
https://www.medrxiv.org/content/10.1101/2020.08.07.20169920v2
Model based so take it for what’s it worth. 10% of the positive cases are responsible for 80% of the spread. States that likely window of contagiousness is half day. Super spreading happens when someone is in a place where they have multiple close contacts at just the wrong time in their infection.
“So… New Zealand. I guess that amazing lockdown strategy is getting a dose of viral reality”
Yes, pain, but as health ministry constantly said, it was always a case of when, not if and so certainly prepared. The bummer is that outbreak in relatively densely populated South Auckland, in Pacifika with church-going multigeneration families. Auckland is in level 3 lockdown for two weeks and rest of the country is in level 2. Rest homes are in level 4. It is a healthy dose of reality. The director-general of health has been rabbiting on for weeks that testing rates were too low because people didnt think they needed to, and the contact recording was extremely slack. That has sure changed.
Still, the contact tracing army is doing it’s job well. The really interesting question is finding the source. Every positive test since Feb has been sequenced. No match to anything found in quarantine. The first case was worker in cold store dealing with imported frozen goods. It would be interesting if that was source. China has found live virus on frozen chicken imported from Brazil. Still a long shot. Australia is also sequencing so it will be interesting if can find match there.
If that’s the source: wow!
Lucia,
“If that’s the source: wow!”
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Interesting, yes, but the answer is always the same: herd immunity.
Phil Scadden,
Let’s hope, for the sake of the people in NZ, that an effective vaccine becomes available sooner rather than later. Otherwise, it will all have been for naught. Sweden, of course, doesn’t really need a vaccine.
Viruses, like facts, are difficult things to avoid indefinitely.
Yes, a few smallish countries/city-states probably can isolate themselves sufficiently to avoid the immediate covid-19 pandemic while waiting for an effective vaccine. The question is if that is a practical strategy for most countries…. I am guessing it is not.
.
The China model may work as well… throw anyone in jail who does not comply with strict isolation…. but that is not going to work outside totalitarian regimes. The desire for liberty is, like viruses, a difficult thing to avoid indefinitely.
SteveF,
Well, I’m sure Russia will let them buy “Sputnik V”!
Lucia,
Would work…. save for that the government of NZ needs to make Trump look bad. I mean, if you buy into the whole Trump-is-a-Russian-puppet ideation, then you can’t buy from those evil Russians. OTOH, the Russian vaccine, if it actually works, will be available long before other vaccines, so maybe Phil should practice his Russian accent.
SteveF,
I have to admit…. my view of Trump has nothing to do with my reluctance to stand first in line for a vaccine that has not gone through phase 3 testing. I know that I can perfectly well continue to have an utterly inactive social life for quite a while with no great harm to myself!
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I’ll be happy to be first in line for vaccines that have gone through phase 3 testing. Others… not so much!
All for herd immunity but preferably by a well tested vaccine. meanwhile, we stick with stomp and dance. More of the Korean,singapore, Vietnam, Taiwan type model though. Can learn a lot from Taiwan on the border control.
” save for that the government of NZ needs to make Trump look bad.” Um, we do? why?
It would be “wow” if frozen goods were the source but it is regarded as very long shot – and very hard to establish. Still waiting on genome matching from cases linked to cool store of same company in Australia. So far, despite all the testing, all the cases are linked except 2, which are probably linked but still under investigation. Early days though and we just hope the testing orgy doesnt find another cluster.
Lucia,
“In that case, your position is flatly contradicted by the paper you cited to support it. You correctly summarized that sentence with “Plausible, Possible, highly speculative.â€. But you are using that to support “implausible, impossibleâ€.
I’m rather surprised you don’t see that that paper utterly contradicts your position.”
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I knew what you were doing with that question and took a lot of time to consider whether I could do a simple catch Y/N answer.
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Doing Italian at the moment which is opening up new vistas in my English.
-”Utterly contradicts” is a pretty blanket statement, no nuances.
Plausible is a fairy floss word. [used in that paper]
It does not mean something is correct. In fact the gist of it is often to imply the opposite, as in giving a plausible excuse for missing work, It does not mean that it is correct only that it seems correct and may well not be correct.
Possible is even worse, if possible, in that anything can be said to be possible with no guarantee that it is even or ever likely. [this is the word I used originally. It is not in the paper. My view, condensed into one word at your request did not leave me much room and gave two bad options].
This is one of the main faults with papers dressed up as science as I feel you and Steve F would agree,anything can be put forward as possible.
In this case it is an actual science paper with valid methodology but as they say is highly speculative.
Highly speculative means could, possibly, maybe right but is highly likely wrong.
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I hope you would agree that those 3 words should not be used as proof for or against any opinion.
–
The body has developed a mechanism for dealing with viruses over millions of years.
Viruses have developed mechanisms of coping with immune defenses over millions of years.
The body developed B cells to provide circulating antibodies to neutralize and eliminate most viruses.
This is the way what we normally refer to as immunity develops.
This is the method Edward Jenner used in 1796, after he inoculated a 13 year-old-boy with vaccinia virus (cowpox), and demonstrated immunity to smallpox.
In 224 years we have never developed a true T-Cell “vaccine” ie a way of stimulating T Cells to stop viral infections on their own.
I doubt it is possible.
We have worked out how B cells and then T cells work, some of the earliest work was done by fellow students, researchers and friends of mine at the Monash Medical Centre at Prince Henry’s hospital in 1974-80 and obviously continued on from then.-
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I do not want to denigrate the views of people here who in part are reflecting a greater argument in the community over the modes of transmission of Covid, herd immunity and whether there are factors that might reduce the risk of the pandemic and let us come out of our shelters.
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The ideas can be practical, plausible or wishful thinking.
Some even seem to be suggesting against vaccination.
It would be great if prior similar infections give us an innate immunity.
T cells help the immune response in many ways but that is my point. They help the Immune response in various ways.
Cannot do without them.
But,
They do not cause immunity.
They cannot cause immunity.
No matter how cross reactive they are and how quickly they can pull immune processes together they are not the component that determines immunity.
Without B cells and their Immunoglobulins the most cross reactive T cell in the world is useless at stopping a viral infection.
Phil Scadden,
Your prime minister has called herself a “democratic socialist†and “progressiveâ€. She is the political opposite of Trump, and thinks capitalism is an abject failure because it does not ensure there is no poverty.
angech
Yep.
No. It’s not. Possible also is not a “floss” word.
Absolute nonsense!
Nope. Yes/no was precisely what I wanted you to condense to.
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If learning Italian is doing this to your English comprehension, you should stop learning Italian!
.
Wrong.
angech
Paper after paper after paper contradicts your view of whether t-cells can clear virus. Here’s one study on t-cells in ebola infected mice. It includes test on B-cell-deficient mice.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC368745/
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I know you will keep providing your description of what you think t-cells do and do not do. But empirical evidence shows that t-cells can clear infections even in the absence of B cells.
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In this study, it was the memory t-cells that saved the mice from re-infection. The remaining B-cells and antibodies did not save them.
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There is a reason we are seeing paper after paper after paper discussing t-cells. Perhaps in the past people didn’t know t-cells can kill virus by themselves w/o B-cells. But the evidence suggests they can (and do).
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I used my editor superpowers to insert the link to the paper inside the comment above. (Superpowers are required after the ordinary time limit is past.)
Lucia,
“Perhaps in the past people didn’t know t-cells can kill virus by themselves w/o B-cells. But the evidence suggests they can (and do).â€
.
I think that pretty well sums up the discussion. Researchers generally publish unexpected results. Journals like Nature and Science focus most often on those same unexpected results. Which was why the Steig et al paper on uniform Antarctic warming (when most on the ground thermometers said otherwise!) made it to the cover of Nature; turned out to be rubbish, due to poor methodology, but it was very unexpected rubbish.
.
All the papers on T-cell based resistance, could turn out, like Steig et al, to be rubbish, but that seems to me very unlikely based on the number and quality of the papers; evidence for resistance to covid-19 from previous exposure to other coronaviruses grows, even if it is unexpected. Your linked paper suggests that CD8+ T-cells can alone protect against ebola virus.
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The ‘search‘ in research is always for explanations for unexpected or conflicting data. Research on covid-19 is no different. There is growing evidence of a wide range of individual susceptibility to the virus among naive populations, and people are searching for explanations.
angech (Comment #189243): “In 224 years we have never developed a true T-Cell “vaccine†ie a way of stimulating T Cells to stop viral infections on their own.”
.
That demonstrates nothing. For something like 80% of that time, we did not even understand the roles of T cells. That something has not been done does not show that it can not be done. In fact people are trying to make T cell vaccines:
https://www.nature.com/articles/nm1212
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In angech’s posts, it is difficult to find statements that are clear, correct, and non-obvious.
Mike M,
That is a very good link; I hope angech takes the time to read it, and Lucia’s link as well. But maybe not… research that shows you are mistaken can more easily be dismissed as ‘fairy floss’.
.
Lucia’s paper (ebola in mice with different parts of their immune systems deactivated) seems to me to suggest that CD8+ T-cells which recognize and kill infected cells do not themselves completely clear the virus…. they just suppress its rapid growth, and keep the mice from being killed. As soon as the CD8+ cells were eliminated, all mice died, but removing B cells and CD4+ cells did not make them die from the virus.
.
So, perhaps having CD8+ cells which recognize covid-19 infected cells slows the viral multiplication enough for the normal immune response to clear the virus…. often without symptoms.
MikeM,
Thanks for the link to the nature article (from 2005– so there should be enough time for people to say it’s nonsense if it is.)
https://www.nature.com/articles/nm1212#Tab2
One problem with angech’s “support” for his claim is he seems to believe that Bcell and Tcell immunity must be mutually exclusive. Even if his friends at Monash learned a lot about how B-cell immunity works back in the 70s, there is no logical reason to think B-cell immunity is the only immunity that exists.
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The 2005 nature article tells us B and T cells immunity are not mutually exclusive:
.
.
So, evidentlty, there are plenty of people “out there” who do not think “we” figured out that t-cells can’t confer immunity back in the 70s. People did not just stop the research.
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Another problem is that angech seems to think that saying “smallpox” vaccine somehow argues that t-cells can not confer immunity. But, in fact, smallpox vaccines do create t-cells.
.
.
Like it or not, you can’t prove t-cells don’t or can’t confer immunity by point to the success of a vaccine that creates memory t-cells. It may be they don’t. But this is simply not empirical evidence against the notion that t-cells can.
.
The time it takes to develop vaccines is also not evidence against t-cells being able to give immunity. Jenner did not know why the vaccines work. He didn’t know an antibody from a B cell from a T cells.
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The 2005 nature paper discusses why it is difficult to develop a t-cell vaccine. That would explain the time it’s taking. But none of these difficulties supprot angech’s claim they can’t give immunity.
.
This seems to be a list of the difficulties.
.
* Response is variable in individuals. This means it’s more difficult to create a vaccine that protects everyone who has it. That’s a big flaw in a vaccine. It does not mean that angech’s claim about t-cells are right.
* Testing individuals for response is more difficult (which would make development more difficult. It is not an argument that t-cells don’t give immunity.
* there are safety issues (which is actually something shared with all vaccines. But these are newer… so…)
* pre-existing immunity (to something?) might limit how well a particular vaccine works.
* some vaccines might work, but currently, the protocol regulatory agencies use to determine protection is creating antibodies. (Using something called “logic†one should know correct established protocol does not actually govern biology. So this does NOT mean that only antibodies give protection. )
Angech, I’m sorry, but even if your fellow students worked on immunity in the 70s, you are really giving nothing to support your claim t-cells cannot confer immunity. There is tons of stuff out there– discussing mechanics, discussing empirical evidence in animals and so on. The research community is working on it.
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It may be that we will never manage to develop a pure t-cell vaccine– for reasons above. But even that is not evidence against the idea that t-cells themelves can give immunity. The mouse paper I linked is empirical evidence they do. No refering back to your buddies at Monash in the 70’s can over come that. (Things that could overcome that are people showing that research group screwed up in some way.)
SteveF (Comment #189254): “Lucia’s paper (ebola in mice with different parts of their immune systems deactivated) seems to me to suggest that CD8+ T-cells which recognize and kill infected cells do not themselves completely clear the virus”
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I don’t think that is correct:
So killer T cells (CD8) were sufficient to clear the virus, perhaps with help from the innate immune system.
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SteveF: “As soon as the CD8+ cells were eliminated, all mice died, but removing B cells and CD4+ cells did not make them die from the virus.”
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Not sure what you mean. They vaccinated the mice and showed that protected the mice. Then they vaccinated mice, altered their immune systems, and reinfected the mice. If CD8 was depleted the mice died, but they survived with CD4 and/or B cells depleted.
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Killer T cells don’t just kill the infected cells. They inject an enzyme that cleaves all proteins encountered, thus destroying both the virus particles and the cell itself. The scorched earth approach to immune response.
It does seem unlikely that such an approach by itself could totally eliminate the virus without causing excessive collateral damage. But maybe it does, or maybe a bit of help from the innate immune system is enough to finish the job.
Mike M,
The paper goes on to say that even though the mice survived with only CD8+ T-cells, they did not completely clear the virus… the virus was suppressed, not eliminated.
SteveF,
Only suppressing the virus should be enough to subsequently give the rest of the immune system time to completely clear. But merely not getting symptoms meets the ordinary definition of “immune”– and would be adequate for most people’s health. (It might not allow us to wipe out the virus from the planet… but that’s not what normal people mean by “immune”.0
.
In that paper the researcher used B-cell deficient mice. Ordinarily, mice would not be B-cell deficient. So perhaps the B-cells would be able to clear what is remaining. But in the paper, the T-cell deficient mice with operational cells did not clear the virus. So the empirical evidence is that in this case of ebola, the T-cells by themselves gave functional immunity to disease. The B-cells were unable to do that.
.
It’s likely having both help. But angech’s claim about T’s and B’s is disconfirmed by this mouse paper. And no amount of saying this is impossible based on 70s research makes this paper go away. (Angech also hasn’t engaged this paper.)
.
Angech’s claim that T-cells cannot confirm immunity seems almost certainly wrong based on post-70s research.
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Of course, this mouse paper doesn’t tell us anything about cross-reactivity. That’s in other papers.
lucia (Comment #189255): “Jenner did not know why the vaccines work.”
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It seems that we still don’t fully understand how vaccines work, specifically we are still working out why and how some vaccines produce antibodies for a lifetime. From a 2018 paper (https://www.frontiersin.org/articles/10.3389/fimmu.2018.02673/full):
Emphasis mine. The long lived plasma cells appear to have been discovered in 1997.
lucia,
IIRC, HIV inspired a great deal of research and new information on the immune system. 1970’s research is rather beside the point.
Mike M,
Yep.
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Biology, especially medical applications, have been studied intensely since the 50s. There have been enormous advances in what we can even test. Obviously no one would be discussing features of DNA vs RNA before the 50s, not how different sorts of RNA viruses differed. Many of the laboratory tests being used now simply didn’t exist.
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Even now, much of what we know has to be based on inference. The difference is we can do more precise test. I mean… it had to take time to create Bcell and Tcell compromised mice! Without them, it’s really, really hard to infer which type of cell– gives functional immunity in a particular circumstance. With them, one can figure out if either one, the other, neither or both confer immunity. Without them, you have a less testable hypothesis.
Heck, according to wikipedia, we didn’t even know t-cells are regulators for b-cells until 1971.
https://en.wikipedia.org/wiki/Lymphocyte_T-cell_immunomodulator#History
The idea that we somehow knew everything about the roles of B and t cells in immunity in the 70s- 80s is absurd. Even if someone thought they did, empirical evidence like the mice study above would need to be explained in light of what we thought we knew. As far as I can tell, the mouse empirical evidence doesn’t make any sense if t-cells cannot confer immunity on their own.
Well, knock me over with a feather; here is a main stream media article challenging the conventional wisdom on the Wuhan virus:
https://www.msn.com/en-us/news/technology/covid-spread-cant-only-be-explained-by-whos-being-bad/ar-BB17VlsC
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The article goes on to highlight work by modellers who have the nerve to think that conclusions should be evidence based. They are finding that what matters is not masks and such but herd immunity, with the second wave outbreaks being in places that did not have much of a first wave. Sadly, they are encountering political push back within the world of science:
Mike M,
I saw that article. I don’t think the author appreciates the social danger of writing such things. She is making lots of enemies on her left.
MikeM,
I like the fuller quote!
This “maybe it would make people do X” was also used in mask advice. Back when “the experts” said we should not wear masks, the claim was maybe masks would make people less careful about washing their hands, social distancing and touching their faces. You had to be trained to wear a mask.
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At the time I thought…. “well… maybe the constat reminder of having a mask on would make people more careful about washing their hands, social distancing and not touching their faces!” (I actually thought and still think wearing a mask makes me more vigilant about social distancing and not touching my face!)
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I also think I remember reading about doctors lying about steroids long ago. The “official” word was they don’t work to build muscle. Well…. body builders figured out that was a big fat lie pretty quickly because they work really well. So they doctors admitted they work but said they were “bad for you”. Then the word was that they previously lied because they thought people would use them if they knew they worked. Well.. uhmmm… they did anyway, because they worked.
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After that, mds wondered why people kept using them. Well… combination: 1) they worked and that’s all that mattered to some people and 2) some athletes didn’t believe doctors claim they were “bad for you”. (And heck, some might not be as bad for you as claimed. Some may be worse. )
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But regardless these “people might misbehave if they knew the truth” reasons for hiding information or lying are generally counter productive.
Science specifically shouldn’t be filtering the facts because of how it * might * be interpreted and how people might change behavior. I’ll tell you on thing that does change behavior, learning science is manipulating the facts to try to change your behavior. I know examine science pronouncements, especially when there is an obvious taint of regulated group think involved, to be less reliable.
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Example. Global warming isn’t as bad as we thought it might be. Haven’t read that article from the usual suspects lately, have you? They actually narrowed the future temperature range slightly a while back and it was treated very oddly. Of the very few who covered it, it was caveated to an extreme. Sea level rise is continuing on its “not 2M” levels for the last decade to zero notoriety. Etc. Food science is terrible with this as well.
Covid outbreaks weren’t examined through a moral lens until the outbreaks started happening in the south. The coverage is basically the NE was a victim of the disease itself, the south is a victim of their own bad behavior. The majority of this is just white elites battling between each other for virtue points, it’s all very tiring and repetitive.
Tom
Yep.
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Yep.
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That’s one reason some people really don’t like people suggesting part of the reason for the declines is natural. Those who recover are no longer susceptible. That automatically decreases the rate of transmission. Also: the asymptomatic transmission that was so dangerous on the upswing means there are quite a few “no longer susceptibles” than you would expect based on how many people actually got sick.
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Now: I don’t know that we’ve reached herd immunity in NY or Sweden or anywhere. But it doesn’t make me angry for people to discuss it. I also don’t think the idea we might have is going to send everyone in NY to pitch out their masks and rush onto the streets in a wild throng. (Although, protesting does seem to be enough to result in the wild throngs in various places!)
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My view: it might be reduction in susceptible people that is sufficient to slow transmission. It might be masks and distancing. It might be both. I’m not going to crowded dance halls yet– because it might be masks and distancing. Plus the transmission rate is hardly zero in Illinois. So it doesn’t matter what the reason is. It’s prudent for me to distance. OTOH: I am taking private lessons.
Tom Scharf (Comment #189268): “Covid outbreaks weren’t examined through a moral lens until the outbreaks started happening in the south.”
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That is not so. The moralizing started in March. When Georgia started to relax restriction back in April, it was called an experiment in human sacrifice. But when cases started to rise in red states, the moralizers kicked into high gear, screaming “We told you so”.
Lucia,
“But regardless these “people might misbehave if they knew the truth†reasons for hiding information or lying are generally counter productive.“
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The implicit idea is that some people believe they are best qualified to judge what other people should do. It is one of the fundamental principles of ‘progressive‘ politics….. force my values, priorities, and beliefs on you because I don’t like your values, priorities, and beliefs. “They should just not be allowed to make their own choices†is the always the ‘progressive’ response when people (like bodybuilders taking steroids, gun owners, and many others) continue to do what they want instead of what progressives think they ‘should do’. Progressive politics always reduces personal freedom and liberty; it is a defining characteristic.
By many measures white elites do produce better results. Better educated, healthier, etc. Perhaps eating kale salads, running 4 miles at 6 am, maintaining a stable and financially secure family unit, reading to your kids for an hour before bedtime, and instilling certain cultural values everyday produces superior and measurable results. Fine.
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There are plenty of fine people who do this type of stuff and don’t feel compelled to advertise their superiority in a condescending way to the rest of the world. They just don’t happen to be on Twitter or write for the NYT, ha ha.
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Many of these superior folks feel compelled to tell others to help others improve their lives through argument, this is almost tolerable. Many of these folks are just signaling their superiority to lesser groups to their peers, this is much less tolerable. Some of these folks think lesser groups should be legally compelled by the state to improve their lives by adopting elite behavior, this is completely intolerable.
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For the most part these groups are easy to discriminate. There are of course a wide range of debatable actions between “you must send your kids to school for education” and “Big Gulps are banned”.
Tom,
I think some ‘elites’ currently think it’s just fine to forbid big gulps, but it’s out of bounds to suggest that it’s better to be married before having kids. . .
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I’m not big into moralizing in general. But there are life habits that do help people prosper. Education, employment, stable personal relationships (which are fostered by marriage) and so on and so on. Even though circumstances of fate do affect prospects, many of these are at least partly choice.
Steve, while I agree that Ardern is political opposite of Trump, the idea that nz government would be making decisions on basis of making Trump look bad is ludicrous. She also leads a fractious coalition with the populist “nz first” party as her deputy. The closest we get to a Trump. Hmm, just bowed to pressure from opposition parties and postponed election till October.
SteveF,
This goes back a long way. Try Plato and his idea of philosopher kings, i.e. him and his friends. Some days I not only think Socrates got off too easy by being allowed to commit suicide rather than one of the more nasty forms of execution prevalent at the time, but that his whole school, especially including Plato, should have been done in with him.
Speaking of philosophy, there was a book review on early twentieth century philosophy in the WSJ recently. It didn’t really cast philosophy in a very flattering light, IMO.
[my emphasis]
Philosophers arrogant? I’m shocked, I tell you, shocked. /sarc
Well, We live in an era of propaganda and half-truths. Covid science is not the only field where gate-keepers tell us only what we “should” know. There was a recent retraction of a paper on police shootings. The authors said the paper was correct but they didn’t like having it accurately cited by Heather McDonald.
https://www.wsj.com/articles/the-ideological-corruption-of-science-11594572501?mod=hp_opin_pos_1
In my lifetime, I’ve never seen science subjected to such politicization. It’s as if the twitter mob is becoming a secret police force to root out “error” and “non-compliance.” The twitter attacks on John Ioannidis have shocked even me. He is very nonpolitical.
David Young,
“ The twitter attacks on John Ioannidis have shocked even me. He is very nonpolitical.â€
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There is no upper bound to the evil which those on the extreme left can do…..and will do if allowed to. The crazy left is the reason guns are selling at a record rate.
Thanks everyone for putting up with my postings. It is appreciated.
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I read Mike’s article, one of several good ones he put up.
Hmm. After 20 plus years of T cell research.
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“The evaluation of the ability of T cells to control infections is still in its infancy. A major limitation for this new approach is the complexity of the assays used to score responding T cells and the failure of these assays, as currently used, to provide a single correlate for protection.â€
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Since CDC Basics of vaccines still defines a vaccine as producing antibodies “A vaccine stimulates your immune system to produce antibodies, exactly like it would if you were exposed to the disease. After getting vaccinated, you develop immunity to that disease, without having to get the disease first.“
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“ In fact people are trying to make T cell vaccines:
https://www.nature.com/articles/nm1212
In angech’s posts, it is difficult to find statements that are clear, correct, and obvious.â€
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Maybe, but,
The very words T cell vaccination are misleading Since they do not and cannot lead to antibody production
“T-cell-inducing vaccines – what’s the future
Sarah C Gilbert“
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Immunity has been redefined as to not having symptoms. I disagree.
My concept of immunity is not being able catch the infection In the first place. A pre infection state.
People who catch the disease but do not develop the symptoms are lucky, not immune. They still can pass it on to there loved ones. They have no way of knowing that they will be immune. It is a post hoc definition of immunity. The reason that they were asymptomatic was that they had a good and early reactive T cell response that kicked in and prevented the disease
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Is it ‘immune to’ or ‘immune from’?
In most cases, if you are immune to something, it has no effect on you—If you are immune from something, it cannot reach you.
angech
Which sounds like the opposite of your position. Your position is that we know they cannot give immunity. In contrast everyone else’s position is they might. The latter position is consistent with evaluation being in it’s infancy. Yours is not.
No one said it was “redefined” that way. In normal conversational usage, it’s always been used that way. See the dictionary definition above.
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But even if we were to use your definition you’ve just bumped it up to needing to define what “catch infection” means. Does it mean “never having the virus enter your body?” (It can’t mean that.) Does it mean getting past some initial stage of the immunity system? Does it mean the body has to make more antibodies but can just coast on antibodies currently circulating in the body?
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Real questions because you’ve just thrown out this idea, but there is no way for me to know what state we need to monitor to figure out if someone is “immune”.
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So what if they don’t know? This is irrelevant to determining whether you are immune. It’s useful to know if you are immune. But not knowing you are immune doesn’t make you “not immune”.
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Beyond that: there is nothing about the definition of “not displaying symptoms after exposure” that is post hoc. The definition is also not ad hoc, pre hoc or neo hoc. It’s only knowledge that someone is immune that is “post hoc” to observing them not having symptoms after exposure. But guess what? This “post hoc method is the standard protocol required by regulatory agencies for determing whether a vaccine confers immunity! Someone making a vaccine makes a persuasive explanation why it might confer immunity. You give the vaccine to people. They you allow people to be exposed. So the “post hoc” aspect of not knowing based on theory can’t be an impediment to defining immunity this way.
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Huh?
First, wrt “your immune to”: once again you are pushing “immune” back to things you are not defining. What do you mean by no effect? It seems you already decided it can’t just be “no symptoms”. OTOH, previously circulating antibodies from a vaccine eliminating the virus is still “an effect”. So if taken literly, you’re saying “no effect” means no one is every immune. Assuming my smallpox vaccination has caused me to permanently circulate antibodies, their kicking into action is “an effect”, so, taken literally you would be saying my small pox vaccine doesn’t make me immune!
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As for your “immune from”: Covid can’t really “get to” me in quarantine. Or perhaps it wouldn’t be able to “get to” me if I wore a hazmat suit. So it would seem quarantine or a hazmat suit would make me “immune from”. No one thinks that’s what immunity means!
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Look, with some luck, you ‘ve at least now realized that your position of certainty about what t-cells can do– based on 70s info– is not shared by current groups. I still don’t know what you think “immunity to” or “immunity from” means because you’ve kicked the can to other undefined terms. Worse, you are trying to make a “to/from” distinction that is incoherent.
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If you want to be very precise in what you mean by the term “immunity”, and what you mean is different from the various dictionary definitions, you are going to need to tell us your definition precisely. (See questions above.)
FWIW: As for when immune came to mean “has no symptoms”, the New York Times used it that way in 1938
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https://en.wikipedia.org/wiki/Mary_Mallon
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If angech has some other definition that ways Typhoid Mary was not “immune”, that’s fine. But then (a) angech has to describe it precisely and (b) he has to admit the other definition has been in common usage since before I was born (and possibly before he was.)
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angech,
Finally progress, I think.
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Putting aside the exact definition of “immunity“, what matters most for sensible public policy is understanding the circumstances which lead to passing the effective HIT and the pandemic declining to very low rates of illness and death. We are faced with clear evidence of herd immunity in places like Sweden which have not adopted mask wearing, closure of restaurants, schools, etc, in spite of confirmed cases plus % of people with blood antibodies being far below what would be needed in a truly naive population where everyone is susceptible to the virus.
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Resistance via T-cells generated as a result of infection with other coronaviruses makes sense in light of how the pandemic has actually proceeded.
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Places were the virus was very broadly spread before any ‘social distancing’ and lockdowns (like New York City, New Jersey, Milan, etc) have had the pandemic mostly die out, but at a terrible cost in elderly lives, while places like Florida, where the early spread was restricted by social distancing and public policies, had a much lower initial rate of confirmed cases, but a surge in cases when those public policies were mostly lifted. Florida now has as more confirmed cases than New York. The difference is in how many elderly will die in different places when the pandemic is over, where Florida will do much better…. because it better protected the elderly from the virus.
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My concern is not that the pandemic will die out (it will, no matter the specific public policies adopted), but what policies will minimize the cost in lives and economic damage. Understanding why the pandemic dies out is important to inform both current and future public policies. If people become convinced that only virtue-signaling mask theater and economic destruction keep the virus at bay, then we will have those nightmares in place indefinitely. Which is why real data about “existing resistance†is crucially important; people need to be informed of the real causes of the pandemic’s decline, and not terrified into doing things which accomplish nothing but cost much.
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There is little information available about how often asymptomatic (or mildly symptomatic) carriers actually spread the virus, and this is a crucial piece of the puzzle, since those carriers are far more common than carriers who eventually do become symptomatic. We do know that children, even though infected, rarely spread the virus to others. This, and simple logic, suggest that viral load may control the probability a carrier will spread the virus. Which is consistent with resistant individuals not being highly contagious…. but that remains to be proven.
“I think some ‘elites’ currently think it’s just fine to forbid big gulps, but it’s out of bounds to suggest that it’s better to be married before having kids”
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The incoherent elite, ha ha. The rule being you can’t criticize the lower class for bad behavior and you also deny they have any agency in improving their situation. You then place blame not on other right thinking elites, but some nebulous other class that oppresses these people who are victims. This oppressor class is composed of people who do not support the elites directly or do not sing the ever changing catechisms in sync. In order to be absolved you only need to support right thinking elites, no actual sacrifice is necessary. But beware, one high profile misstep and you are excommunicated to the oppressor class.
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The lower classes do have real disadvantages, but they also have agency. The incoherent elite along with all the usual elite people who want to keep their station have placed roadblocks so that lower class agency cannot be executed easily. The requirement for expensive college degrees (credentialism) and the secret handshakes to get into top tier colleges being glaring examples.
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What I fully support is the removal of any roadblocks that reduce agency for anyone, otherwise known as equal opportunity. The incoherent elite appears to dismiss this entirely, much preferring to blame the nebulous class of which nobody is an avowed member. The incoherent elite get to feel superior, virtue signal their peers, and maintain their and their prodigy’s station.
SteveF
Fortunately, in Illinois, our transition to different phases is based on concrete metrics like
* number of cases (absolute and rate of change),
* % positive test results.
* number of deaths (absolute and rate of change).
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As these go down, we progress to lighter restrictions. So the “theory” that the only thing protecting us is masks or distancing won’t keep us in semi-permanent semi-quarantine.
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It is true we might come out faster if the Governor or health authorities believed the “herd immunity” theory. But even though I think there is some evidence in favor of it, it’s not certain. So I can’t entirely criticize their position. Yes. In retrospect, it may turn out that we could have done fine with fewer restrictions sooner and so less economic damage. The problem is like it or not, there is doubt.
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From the gutter, this is admittedly a bit inflammatory. Portland last night. Mostly peaceful protesters call in their local security to investigate an alleged driver who might have tried to run someone over (no evidence this ever happened). The powers of de-escalation and community based policing ensues.
https://www.theblaze.com/news/portland-thug-kicks-man-in-head
If you define immunity as not getting the associated disease after being exposed to the infectious agent, which seems reasonable to me, then being truly asymptomatic after infection means you’re immune. You can’t know if you’re immune unless you have been exposed and your immune system has been challenged. So having antibodies doesn’t necessarily mean you had the disease, at least not if you never had symptoms. And, as pointed out by the Typhoid Mary case, you can be immune and still be a carrier or vector.
lucia (Comment #189290):
Not sure that is true. If the criteria are sufficiently strict, you could have a near steady state in which the conditions are not met and have little chance of being met in the foreseeable future, leading to a semi-permanent semi-quarantine.
I think a big factor in how one sees this is whether one believes that the state has a significant capacity to control the virus. If you think that the state has significant control, then the Illinois approach might make sense. But if epidemic progression is a result of random chance combined with localized herd immunity, then the purgatory that SteveF predicts is likely.
The disease is going to progress based on the number of contacts citizens have between each other. The exact mode and probability of transmission is still in dispute (this is shameful) but there is little doubt that more human interactions increase the probability of transmission.
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The lock down argument is basically based on knowing very little about transmission then only blunt tool remedies are allowable. The actual remedy is to go get better data and design less restrictive lock downs that are much more effective. There are approximately zero people in the media advocating this.
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The virus may be contagious enough that partial noncompliance to social distancing and masks is enough to keep it going. Therefore state power must be used to enforce compliance. What is missing here is actual evidence that this specific noncompliance is what is really keeping the virus going. This is assumed, not proven, and nobody is trying to prove it.
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The data is there. Pay 100 people to interview 100 people each in an ocean of infected people and you will have 10,000 data points. Then better decisions can be made. Until then it is speculative how effective lock downs, masks, et. al. actually are.
+1 Tom Scharf
The sad part is that this is peak polling season–all the administration would have to do is look at what they’re doing and scale it up.
Lucia,
I read the the requirements for moving to less restrictions.
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All I can say is: good luck.
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Pritzker is planning on waiting until the population is vaccinated and completely immune before any return to normal. This is obviously not going to happen for a very long time. What I think is more likely is that there will be de facto easing and return to normalcy when people just refuse to go along with Pritzkers rules…. as already happened with the sheriffs and police chiefs some time ago. Pritzker will save face by agreeing to modify the rules when this happens, as he did before.
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Meanwhile, he will do nothing about looting and violence in Chicago.
Mike M,
“But if epidemic progression is a result of random chance combined with localized herd immunity, then the purgatory that SteveF predicts is likely.”
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And that is what is actually happening. NYC is long past herd immunity, but outside the city (eg up state) there remain susceptible individuals…. so a slow drip of new cases which will go on for a long time. Look at Worldometers for New York…. flat number of new cases since mid June, near 800, but deaths have fallen from ~75 per day to ~10 per day… yet there is zero talk of reducing restrictions in NYC….. falling deaths is not good enough, still too many new cases. The charade of masks will continue.
SteveF,
Yes. I’m sure there will be creeping non-enforcement when cases start to drop. It looks like we are at or near a top to the “2nd wave” based on state numbers. (I think it’s really an “Urban->spread out” feature. Not a “wave”. But it looks like we are near peak. We’ll see.)
Oh– SteveF,
Our phases apply to county by county, not the whole state. Kane and Will (I think) are getting pushed back. The rest aren’t.
Lucia,
“Our phases apply to county by county, not the whole state.”
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People will drive to the next county if they are unhappy with their own county rules. Maybe there will be road blocks. Maybe not.
They are, btw, doing 100% remote learning in the Lisle School district. I haven’t checked Naperville and so on. This is a killer for the sciences that benefit from labs! OTOH, maybe it will make the teachers do more direct instruction instead of having kids form groups and talk it all out.
SteveF,
There will be no road blocks!! They can raise the bridges in Chitown, but blocking all the surface streets into and out of every county would be impossible!
Lucia,
I was joking about the road blocks. People would not accept that level of enforcement if it were tried.
I think online learning will be a disaster overall. I’ve taken many classes online and at first I was surprised at how isolated and disconnected it felt. Very easy to just ignore without properly focusing. I just don’t feel this kind of environment will work well at all for children, especially if they don’t have their parents cracking the whip behind them the entire way.
DaveJR,
My youngest daughter has been doing virtual classes for a while. She loathes it, and says she can’t learn anything that way. There may be some (very good) students who are ok with it, but I think it is going to hurt a lot of kids.
DaveJR,
I’ve had mechanical engineering students report online is not good for them. I think it could potentially be ok for adultsif someone thought out the plan well in advance. But quite obviously, it was not possible for faculty to think it all out in advance last semester. For high school… not great. It varied a little depending on the teacher. I know from talking to one Mom that the teachers also got burned out toward the end of the year.
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For elementary….. I just don’t even see how it’s possible unless the kids also have an adult supervising and engaging at home.
The best students will do better or same with online learning is my guess, the worse students will do worse. Type A parents will see to it that they get it done, with learning pods (probably even better than normal) and other adaptations. The gap with lower students will very predictably widen and the usual suspects will declare this unacceptable with 100% of them forgetting they advocated for it all along. I read a large percentage of the lower than average students don’t even log in for virtual learning.
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Personally I do as good or better without a human teaching me. I can go at my own pace, etc. My wife is the opposite, she really needs someone there to (drone on) teach her. One of my daughters prefers online classes because she doesn’t particularly like human interaction, she gets that from her father, ha ha.
lucia,
The parents who are motivated enough to do home schooling seem to do a pretty good job on average. But they use different resources than public schools. And that probably isn’t possible for, say, a working single parent. Most parents aren’t that motivated or there would probably be a lot more home schooling. Public school teachers have neither experience nor training in remote learning, so most of them will likely botch their end.
DeWitt,
“so most of them will likely botch their end.”
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Maybe. I expect people will just realize that “on-line learning” is just not very efficient.
SteveF (Comment #189287)
“Putting aside the exact definition of “immunity“, what matters most for sensible public policy is understanding the circumstances which lead to passing the effective HIT and the pandemic declining to very low rates of illness and death. We are faced with clear evidence of herd immunity in places like Sweden which have not adopted mask wearing, closure of restaurants, schools, etc, in spite of confirmed cases plus % of people with blood antibodies being far below what would be needed in a truly naive population where everyone is susceptible to the virus.”
–
Well put.
lucia (Comment #189284)
The evaluation of the ability of T cells to control infections is still in its infancy.
“Which sounds like the opposite of your position. Your position is that we know they cannot give immunity.”
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Let me say the ability of T cells to help control infections is not in doubt even in its infancy.
Here is the crux of the matter, role definition.
Different cells play different roles in the bodies response to infection.
The overall position is summed up by describing many cells as part of the Immune system.
Hence the problems when I quibble over what is meant by Immunity and defer when people use it in a sense that is technically, in my opinion, mistaken.
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T cells are part of the innate immune system, along with neutrophils, Macrophages and lymphocytes etc.
The policemen of the the body.
This type of immunity we are born with, it reacts to and protects us from invaders. Prior to any and independent of the nature of the invaders.
None of them provide Immunity to viruses.
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Viruses are programmed to get around these cells and walk straight into bank and take out the money.
No matter how many guns or tanks or photographic ID’s you give to the police, read “Cross reactions” to other criminals..
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Immunity to viruses is a specific role given to the fraud squad. They sign up computer experts, even enroll ex hackers and fight the viruses on their own terms with antibodies [anti hacking software].
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In this alternate universe people are allowed to try different solutions when the fraud squad seems out of ammo. You can take the T Cells, big, solid policemen, the “Other Guys” and try to train them to fight viruses as well. But when you sit them down at the computer and say you try catch this cyber criminal and give them a new AK 47 or whatever to do it will they ever catch the criminal.
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My position is that we know they cannot do it [give immunity.]”
* The Other guys is a netflix movie, poor comedy, ninety minutes of your life you will never get back, but in the middle is an absolutely gorgeous misogynist scene when Mark Wahlberg meets Will Ferrell’s wife Eva Mendes. A true ‘There’s something about Mary’ moment. Priceless.
angech (Comment #189313): “T cells are part of the innate immune system, along with neutrophils, Macrophages and lymphocytes etc.
The policemen of the the body.
This type of immunity we are born with, it reacts to and protects us from invaders. Prior to any and independent of the nature of the invaders.
None of them provide Immunity to viruses.”
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That is just wrong. T cells are part of the adaptive immune system. Natural Killer cells are part of the innate immune system. They both fight viruses by identifying infected cells and triggering apoptosis which causes the cell to die and destroys its contents.
angech
The problem is you keep not telling anyone what your definition is! If you are going to quibble, you need to actually tell us what you define as “immunity”.
Well… metaphor. But I have no idea how this translates into whether or not t-cells give immunity.
Perhaps you can explain the mouse study where t-cells did protect mouse against infection but b-cells did not. The explain how this fits into your idea of immunity.
DeWitt Payne (Comment #189292) ‘So having antibodies doesn’t necessarily mean you had the disease, at least not if you never had symptoms.”
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Either one has had a vaccination which can give you antibodies,
or one has caught the disease and naturally developed antibodies.
Alternatively like with Covid and DNA tests one has been given the wrong results.
The disease is the Covid virus. The lack of symptoms, but developing antibodies means you have had a reaction to the virus, in this case a positive one not a negative one. Can one have a positive disease??
Yes, Sickle cell anaemia, is considered a genetic disease yet it confers some protection against malaria.
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Mike M. (Comment #189314)
angech (Comment #189313): “T cells are part of the innate immune system, along with neutrophils, Macrophages and lymphocytes etc.
The policemen of the the body.
This type of immunity we are born with, it reacts to and protects us from invaders. Prior to any and independent of the nature of the invaders.
None of them provide Immunity to viruses.â€
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“”That is just wrong. T cells are part of the adaptive immune system. Natural Killer cells are part of the innate immune system. They both fight viruses by identifying infected cells and triggering apoptosis which causes the cell to die and destroys its contents.”
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Thanks Mike,
You are right. I’m wrong in that regard in what I wrote.
always good to be corrected. [shiver].
Note that they do not kill viruses, they kill infected cells.
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“The adaptive immune system, also referred as the acquired immune system, is a subsystem of the immune system that is composed of specialized, systemic cells and processes that eliminates pathogens by preventing their growth. The acquired immune system is one of the two main immunity strategies found in vertebrates (the other being the innate immune system).””
Two main activities—antibody responses and cell mediated immune response—are also carried out by two different lymphocytes (B cells and T cells). In antibody responses, B cells are activated to secrete antibodies, which are proteins also known as immunoglobulins.”
B cells kill viruses.
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Remind me again of any T cell action specifically killing a virus??
Not it’s actions killing a cell containing virus.
Which is a pretty suicidal act if you do not have circulating antibodies around to mop up the billions of live virus particles.
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Anyone? specifically killing a virus??
Illinois has relaxed restrictions on restaurants for over a month now, including allowing buffets to reopen.
Relaxing rules doesn’t mean people will come and eat.
angech,
People have already engaged the issue of how t-cells killing cells can be enough to give immunity. So that’s not a new issue– it’s been addressed.
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Before anyone answers your question again: Can you explain the mouse study in which mice with no antibodies and no B cells but with t-cells survived infection by a virus? But those with B cells but no t-cells did not?
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The mouse study was posted some time ago. We’ve discussed how your theory cannot explain it quite a bit, and you keep not addressing this.
MikeN,
Yep. Jim and I aren’t going out to eat. We remarked on it at breakfast yesterday. We wondered out loud of one of our old breakfast joints would survive Covid. (Specifically: Omega in Downers Grove. The Fox in Lisle already closed, but that’s not really entirely due to Covid. The long time owners were approaching or past ordinary retirement age and were pretty much letting it run down slowly.)
(Note: The Fox closed Feb 26. So just before lockdowns. We stopped going there about 5 years ago. It was partly because Jim’s parents were moved into assisted living, but partly due to it’s declining attractiveness.)
angech,
I agree with Lucia; however you want to define immune, you need to explain how mice with CD8+ cells activated to ebola, but with no B cells (and no antibodies!), kept them alive when injected with ebola virus, but those without CD8+ cells died. It is a very clear case of protection from an otherwise fatal infection….. by T-cells. No amount of quibbling about definitions of immunity and the roles of different types of cells will explain this away. T-cells by themselves protected the mice. The logical extension to other viruses is obvious.
SteveF,
I think instead of by themselves, it’s more correct to say ” “With no B-cells or antibodies present, T-cells protected the mice. The logical extension to other viruses is obvious.”
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The reason I’m editing that is the empirical test doesn’t tell us the mechanism. Something else could have helped– we don’t know. But that something is not the B-cells or pre-existing antibodies. So this experiment is very strong counter evidence to angech’s position that seems to insist that immunity is only conferred by antibodies.
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I’m fine with the idea that there could be multiple processes for immunity. In fact, it would make sense since there exist many, many types of pathogens and the best process for thwarting one might be different from thwarting another.
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This is one of the reasons I am totally unconvinced by angech’s argument which seems to amount to explaining a mechanism for immunity but then makes the ginormous leap to the idea that the mechanism he described must be the only mechanism. That argument has zero basis in logic.
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And the empirical evidence clearly points to the idea that the B-cell/antibody mechanism is not the only mechanism for immunity.
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Now… it may be that angech’s view is that killing virus the the presence of pre-existing antibodies antibodies is the definition of immunity. If so, then of course, t-cells don’t give immunity. But in that case… well… who cares? What we want is to be able to avoid disease when exposed. T-cells seem to let that happen. If angech wants to dream up a new word that specifically means
“: the quality or state of being [new word] especially : a condition of being able to resist a particular disease especially through preventing development of a pathogenic microorganism or by counteracting the effects of its products without involving the presence of pre-existing antibodies circulating in the body— see also active [new word], passive [new word].â€
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Then I’d be happy if someone developed a vaccine that conferred this [new word]. I honestly don’t care if the ability to resist the new disease is achieved by having the body constantly circulate pre-existing antibodies!
The new word could be Timmunity.
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BTW, I think it is also very important to note the virus was not completely cleared when the mice didn’t have B cells or antibodies, just suppressed enough to protect the mice.
I am beginning to think that angech has no interest in learning. He admits he was wrong about killer cells, then goes back and reasserts his incorrect claim.
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For the record, killer cells (NK and T) kill viruses. They don’t just kill the cell and they don’t lyse the cell. They inject the cell with proteases that destroy all the proteins in the cell, thus killing the virus particles and the cell.
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Circulating antibodies are usually a good indicator of immunity, but they do not automatically confer immunity. People with HIV have circulating antibodies against HIV. Since those antibodies can not clear the virus, they surely can not prevent infection.
———
lucia (Comment #189326): “What we want is to be able to avoid disease when exposed.”
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Exactly right. Avoiding disease, or minimizing its effects, is what matters. The immune system has multiple mechanisms to accomplish that.
——-
angech seems to think that immunity means that your body has a fence around it that does not permit the pathogen to enter. Otherwise, there is no bright line between immune and not immune.
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If you are infected (see note) with a novel virus, the innate immune system is initially pretty much on its own, then appropriate T cells and plasma cells start to proliferate to fight the virus and the antibody level in your blood rapidly rises.
If you are infected with a virus for which you have memory cells, exactly the same thing happens, except that the adaptive immune system kicks into gear much faster.
If you also have circulating antibodies from long lived plasma cells, the same thing happens except that the innate immune system has a bit of help while the adaptive immune system ramps up. From what I can find, the level of circulating antibodies is typically not nearly enough to clear the virus on its own.
In all three cases, the viral load will initially increase. The difference is in the maximum viral load reached before the immune system gets the upper hand.
——–
Note: Among the definition of “infection” are:
(1) The invasion of bodily tissue by pathogenic microorganisms that proliferate, resulting in tissue injury that can progress to disease.
and
(2)The entry or placement, as by injection, of a microorganism or infectious agent into a cell or tissue.
I am using “infection” in the second sense. I am not certain that is the correct technical usage.
angech,
Apparently you are a believer in the Humpty Dumpty theory of language.
Being exposed to a virus and developing antibodies is not the same as catching the disease. A disease by definition (see above) has symptoms. If you didn’t have symptoms, you didn’t have the disease. We have many examples of people with antibodies who apparently did not have symptoms. IMO, that means they were [effectively] immune.
So ‘immune’ and ‘disease’ mean something other than the dictionary definitions when you use them. It would help if you defined exactly what you mean when you use those words.
SteveF,
Yes. Basically, the T-cells gave what one might call “functional immunity”. The mice did not get sick. Ordinarily, the mice would also have working B-cells. Even if none of the B-cells has “memory” and there were no appropriate pre-existing antibodies, you would expect that those would then kick in and help clean up remaining virus.
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But for all practical purposes, the pre-existing t-cells were “enough” to give the mice T-immunity which is pretty much just as useful asand functionally indistinguishable from “pre-existing antibody immunity”.
immune
adjective
Resistant to a particular infection or toxin owing to the presence of specific antibodies or sensitized white blood cells.[my emphasis]
Definition 1 of immune from here:
https://www.lexico.com/en/definition/immune
Do I need to post the definition of resistant as well? /sarc
The above definition applies to agents that are capable of infecting humans or whatever organism is of interest. If the agent is not capable of infecting humans, than humans are, of course, immune to it, like feline infectious peritonitis which is also a coronavirus. But if one restricts the definition of immunity to that, then we would need another word like ‘resistant’ to discuss SARS-CoV-2.
The Left has now decided that Susan B. Anthony was evil. Because Trump pardoned her and Orange Man Bad.
Maybe Trump should pardon Biden for any crimes he may have committed with regard to Ukraine and Burisma.
I like reading here, good discussions of not readily apparent factors of Covid. I have a stupidly basic question. How could University’s like UNC and ND not expect to find low numbers of positives (146 in ND case) when you put 20 to 30k students on campus? And they then turn around and shut everything down? It’s intrinsically obvious you’ll have at least that many cases.
I dropped off my daughter at CU Boulder for the semester at a stupidly expensive rental house because she had 1.5 out of 5 classes in person. I fully expect they’ll go totally remote after everyone gets there and they find 50 cases. That should happen in the next week.
Literally just asking if this is just a cash grab by University’s that can’t balance their budgets without it.
Jerry,
I have no idea! I know some universities are testing everyone on arrival and isolating those positives. UIUC will evidently be testing everyone (60,000 people!) twice a week or so, the isolating positives.
.
You are not the only one to suggest decreeing in person and then going online in a 1-2 weeks is a cash grab.
Jerry (Comment #189343): “How could University’s like UNC and ND not expect to find low numbers of positives (146 in ND case) when you put 20 to 30k students on campus? … asking if this is just a cash grab by University’s that can’t balance their budgets without it”
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I think you nailed this. People are not going to pay $50K a year or whatever for online classes. So the universities have made elaborate plans to “protect” students so as to get the parents to shell out tuition for the coming year. But they are not actually protecting students, they are protecting their revenue streams. Once the tuition money is safely in the bank, they will be free to cancel in-person classes.
———
Addition: I had not realized that this has already happened.
Mike M,
“But they are not actually protecting students, they are protecting their revenue streams.”
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That is certainty a big reason, but the secondary reason is that canceling classes is not (and never was) about protecting the students, who are not at serious risk… it is about protecting professors and administrators, many of whom are at significant risk, especially the most senior of them.
SteveF,
Yes. For the most part, cancelling classes is about protecting professors and administrators. Of course who gets sick is a bit of a crap-shoot. But college age students would largely be asymptomatic or have mild cases. The same can’t be said for mid-career or senior faculty or administration.
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Support staff would be exposed too. But I’m not going to kid myself and think that going online is for them. They, like “essential workers” are almost invisible to decision makers.
Mike M. (Comment #189328)
I am beginning to think that angech has no interest in learning.
“ killer cells (NK and T) kill viruses. They don’t just kill the cell and they don’t lyse the cell. They inject the cell with proteases that destroy all the proteins in the cell, thus killing the virus particles and the cell.â€
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Reminds me of the old joke about the guy holding a glass container of an acid that dissolves everything it touches.
Or to put it simply, how did the proteases not destroy the T cells and NK cells producing them?
Thinks.
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Here are these little fragile RNA particles with a protein coat so fragile that a mere touch of a protease can destroy it.
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The mechanism for viral retransmission has a mundane method.
Virus survives acids, proteases and all the natural immune defences and enters unsuspecting little cells. Multiplies. Then with billions of copies ready to go kills the cell itself. The virus is quite happy for the cell to be killed.
BTW lots of proteases floating around then as the dead cell remnants attract macrophages T cells NK cells etc which mop up the cell fragments by ingestion and more proteases. The virus? Happy as a rabbit in a briar patch.
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I think you will find the references to antibody attachment to a virus forms a complex that proteases can break down if you research it a little. not the virus on its own. That is how Ab works.
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Please provide any true reference to T cells killing virus directly
What, academia sacrifice for the pandemic? I roll on floor laugh out louding. We can’t have these essential workers left unpaid, who would be left to morally scold the immoral among us?
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Yes, let’s cut a deal. We will close the schools down as requested, and you don’t get paid for not working. Sacrifice for thee, but not for me.
angech,
At this point it seems to me you are just being stubborn. The role of Killer cells in limiting viral replication appears to be well known…. but apparently not by you. https://www.ncbi.nlm.nih.gov/books/NBK8423/
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You still have never addressed how mice with no B cells nor antibodies to ebola managed to survive inoculation with ebola, but all mice without T-cells died…. even though they did have B cells and antibodies.
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Failing to directly address this means you are just wasting people’s time. I am reminded of old dogs and new tricks.
angech,
I’m going to keep reminding you of this issue: Have you given a thought to the mouse studies in which t-cells protected the mice, but antibodies and B cells did not? Can you explain how your theory of immunity could be consistent with that empirical data. Because as far as I can tell, you continue to ignore that paper, which many of us have brought up and agree is inconsistent with your view about t-cells and immunity.
angech,
While we are at it, in response to this
Please provide a reference that says T-cellsneeds to kill virus “directly” to prevent disease. Killing is killing. Several of us have already pointed out that killing them indirectly should be sufficient. So your returning to this “directly” red herring is just reminding us that you just like to go off on tangents that take us away from the main point of discussion.
angech,
From my above referenced text book:
I’m not sure how cytotoxic T-cells are “effective against viruses” if they don’t reduce the replication of viruses…. by killing the cells in which the virus is replicating. Other references people have provided to you say much the same. Nowhere is there a reference saying killing of infected cells makes the infection worse by releasing lots of viruses…. just the opposite.
Europe is apparently heading into a second phase.
Covid-19 Appeared to Be Under Control in Europe. Now It’s Surging Again.
https://www.wsj.com/articles/covid-19-appeared-to-be-under-control-in-europe-now-its-surging-again-11597848444
.
“The seven-day moving average of reported new daily cases has more than doubled since the end of July in the five largest European countries, nearing 11,000. That is the biggest sustained rise on the continent since it beat back the virus’s initial spike in March and April.”
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Still a lot smaller than US but certainly enough for sustained and increasing transmission.
NYC releases results of 1.5M(!) antibody tests. 27% of residents test positive. Some zip codes around 50%, the lowest 13%.
https://www.nytimes.com/2020/08/19/nyregion/new-york-city-antibody-test.html
“The hardest hit ZIP code in the city — 11368 — was the one in Corona, a predominantly Hispanic neighborhood with many construction workers and restaurant employees. Many had to work throughout the pandemic, raising their risk of infection.
About 23 percent of residents in the ZIP code have gotten an antibody test.
That part of Queens has an especially high rate of household crowding, which may also partly explain the high positive antibody rate. Experts have said transmission within households is a leading driver of the disease’s spread.â€
“The accuracy of antibody testing varies widely. Moreover, most antibody tests were done for people seeking them out, which means that those who got tested are a self-selecting group and not a random sample.”
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Meanwhile in an alternate universe Cuomo declares grand victory for his performance at DNC, ha ha.
angech,
https://askabiologist.asu.edu/t-cell
https://askabiologist.asu.edu/cytotoxin
https://en.wikipedia.org/wiki/Natural_killer_cell#Cytolytic_granule_mediated_cell_apoptosis
That one is arguably ambiguous as to whether lysis might be induced, but context says otherwise:
https://en.wikipedia.org/wiki/Natural_killer_cell#NK_cell_receptors
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And that pretty much exhausts my patience.
Tom Scharf,
Yes, lots of cases (in some countries), but a relative handful of deaths. Different people are catching the virus….. and very few of them are dying.
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WRT Cuomo: He is personally responsible for many deaths among the elderly. Only a shameless scumbag would be celebrating this ‘victory’…. someone should keep reminding him how no other place on Earth has had as many deaths per million population as NY, and that NYC is even worse than the whole state. Yes NY “beat the virus”, but at a high cost in both lives and economic damage. Cuomo should be ashamed, not celebrating.
SteveF,
The Case Fatality Rate in NY is currently 7.2%. Connecticut is even worse at 8.7% The CFR in the much derided in the press Florida is 1.7% and Texas is 1.8%. The CFR for the US is 3.1% including the disastrous results in the northeast. Most of the deaths in CT were in Long Term Care facilities. New York, btw, did not count deaths as being from LTC facilities if the patients were transferred to a hospital before dying.
To be a little fair to Cuomo, some part of the problem with assessing how bad the situation was in February was caused by the faulty test from the CDC that took three weeks to correct. But treating Cuomo and NY as a model for dealing with the pandemic is ludicrous on its face. New York didn’t “beat the virus”, the virus beat New York.
Mike M
“That one is arguably ambiguous as to whether lysis might be induced“
Try this instead.
Cytotoxic T Lymphocytes and Vaccine Development
“Cytotoxic T-lymphocytes (CTL) are well-known elements of the immune response to virus-infected cells. [1–Remarkably, granulysin (in contrast to granzymes) has emerged as a fundamental mediator of microbial killing. The mode of action of granulysin appears to be through the disruption of membrane permeability [4]. It follows that granulysin has been found to insert into the microbial membrane through ionic interactions between the positively charged amino acid residues and negatively charged phospholipids. Insertion of granulysin in turn disrupts membrane permeability resulting in the influx of fluid into the cytoplasm and death by osmotic lysis.“
–
Further
“https://askabiologist.asu.edu/t-cell“.
Is not a paper, it is an opinion that pops up on google search without any substantive backing.
Not one other T cell kills virus comment or paper of any substance will you find.
Cytotoxic means cell killing not virus killing.
–
“And that pretty much exhausts my patience.â€
Fair enough, Mike M Sorry, in lockdown and have always gone on too much. Thanks for putting up those references.
You win on TKO.
You have all been very patient and put up with my contrarianism above and beyond call of duty. Enjoy the mainstream.
Thank you all.
DeWitt,
I’d be a lot more inclined to be “fair†to Cuomo if he was even the tiniest bit honest about what happened and why. It is his utter dishonesty that rubs. Yes, NYC was a disaster in the making…. but Cuomo and DeBlasio worked in the beginning to make sure it was the worst possible disaster. Everything they did was worse than doing nothing. They were working from a state of little knowledge (which history shows is absolutely typical for both), but they are also incapable of learning, because they are rendered idiots by their crazy lefty politics.
angech (Comment #189365): “Enjoy the mainstream.”
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Well, that is revealing. SteveF, lucia, and I have been telling angech that his views are contrary to generally accepted science and we have been citing generally accepted science in support of that. All without effect. Now angech reveals why: He is rejecting the generally accepted science. He might have told us that sooner and saved us all a lot of trouble.
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p.s. – I am only minimally annoyed since I learned a fair bit in the process.
angech
Well…. https://askabiologist.asu.edu/ is written by a team of well funded researchers at Arizona State University. In contrast, you’ve cited absolutely nothing that directly supports your view that the t-cells do not kill virus inside the cell when they kills the cell. So clearly, MikeM has found much more than you have.
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Out of curiosity, are you ever going to address the empirical evidence in the mouse study? Though asked repeatedly by a number of people here, you continue to ignore it. It strongly disconfirms your over all claim. People aren’t going to forget that evidence exists merely because you only want to try to argue about subordinate details related to one particular process in the immune system.
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I strongly suggest that before you go back into the weeds about biochemistry, you engage the mouse study!
angech (Comment #189365): “Try this instead.”
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The quote angech then posts may be lifted out of context, since killer T cells don’t just kill virus infected cells. But I cannot really tell, since he provides no way to find the source.
The good news: We have all been motivated to read a bit on immunity and how cross-reactivity of T-cells that target other coronaviruses might help explain the evolution of the pandemic.
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The bad news: arguing with angech has taken a lot of time for nothing. I am reminded a bit of the ‘skydragon’ crowd who would refuse to admit CO2 absorbs infrared near 14 microns, and also radiates in all directions at 14 microns, no matter how clear and strong the evidence. It wasn’t worth the effort with them either.
MikeM
Some fragments match this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896662/
Which is a paper that describes appears to be describing the “precise mechanisms underlying CTL killing of microbes“.
I don’t know where angech found his version, but it seems to be an edited version of this (the bold seems to match what angech quoted.)
(I used bold to highlight the parts in his quote.
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Overall: this paper does not contradict your source at asu.edu because it’s discussing a specific mechanims and in no way suggest that mechanism applies to viruses.
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If you scan to the paragraph following the final one I quoted, the paper actually distinguishes this behavior of CTL as being
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So…. the paper seems to be trying to warn the reader not to make the mistake angech seems to be making. That is: one should understand it is a specific mechanism, that applies in specific cases and is specifically not the mechanism for viruses.
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So it seems that once again angech is trying to lead us down an “either/or” path. That is when he finds one description of something a t-cell does, he concludes it’s the only thing it can do.
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Perhaps in angech’s world, people can chew bubble gum or they can walk, but they can’t do both either at the same time or even at different times!
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Anyway, perhaps angech found something else. If so, he could provide the link. But it looks like the paper I linked.
BTW, the NIH paper does describe other mechanisms by which t-cells kill other things. So quoting something that happens in a particular “bacteria” interaction most definitely does not support the claim they don’t do something else in other circumstances. So, if that is what angech was tying to do: Logic fail.
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More specifically: The t-cells seemed to bind directily to some Fungi, so there might be a some contact dependent killing in that case. However, there is evidence other things either also kill the fungi and that sometimes the t-cells can’t kill the fungi.
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Overall: this paper absolutely does not support angech’s view that t-cells can’t kill viruses. It is actually silent on viruses.
lucia (Comment #189372),
I am in awe of your search skills. I try to remember the maxim that one should never attribute to mendacity that which can be explained by incompetence. But if angech actually edited the text as he appears to have, then mendacity it is.
MIke M.
I used ” ” quotes on long strings. When I saw this… I thought there were an aweful lot of fairly long strings that match. Then I used the search in my browser to find several of them.
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Maybe angech found what he quoted somewhere. But what I found really changes the complexion of what he quoted. His quote made it read as if there was a paragraph discussing how t-cells deal with viruses. But it’s the opposite. It’s not only dealing with bacteria and goes out of it’s way to make sure the reader knows this is not the mechanism for dealing with other things.
SteveF (Comment #189371)
I agree with SteveF that at some point discussing a point of contention becomes a waste of time and band width, but I can see where those who continue the discussion can be motivated to dig deeper into the facts of the matter and bolster their arguments.
As an aside I have to allude to points being made here about blames and credits for politician’s reactions to the Covid-19 pandemic. I believe that from the polling on blames/credits the matter goes very much in favor of Cuomo and against Trump.
The states and locales in the US form of government have most of the authority when it comes to reaction to pandemics. In fact if Trump had attempted to directly control local and state governments in this matter he would have been near universally charged with some kind of fascist takeover. That is not saying that with Trump’s narcissistic tendencies and rambling tweets that showcase him that would not be a predictable impression of the public.
The Cuomo spin has to start with the impression that the initial and exponential outbreak of cases and deaths was out of his control. I have heard him reference New York as a travel center of the world and thus most susceptible to a very contagious disease and some vague remarks implicating the Federal government in the initial problem. Once the people being polled are convinced of that, Cuomo can stand ready to take credit for the steep decline of cases and deaths (admittedly from very high numbers) by putting in place the standard label restrictions on the population with which the majority of the populace agrees and also has not yet come to grips with the economic consequences of the those restrictions.
I see the spin on the upcoming election by the MSM and the Democrat party being the importance of Trump and his administration being blamed for the Covid-19 cases and deaths in the US and that somehow Biden should be seen running as a moderate and as such the fear of a far left upcoming government is ameliorated.
I see posters here pointing to these issues, but mainly pointing to the politicians and their supporters. The party mostly left out of these discussions is the public at large and how much of what seems unreasonable to some of us is swallowed by them. A big reason I favor minimal government is that these unreasoned ideas can be forced upon me and others whereas if they had to be submitted for voluntary acceptance and approval there would have to be a much large appeal to reason than emotional spin casting.
Once a decent set of antibody tests is available it seems the CFR/IFR should use that number as the denominator?
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27% test positive in NYC of 8.4M = 2.27M cases. 23,643 deaths. = 1.04%
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NYC had a major testing problem early so many more of their cases weren’t counted.
Trump owns the US pandemic, that is just the way the world works. When the economy hits record highs he gets credit even though he may not deserve it.
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For those who want to dig more than one inch deep though the question is what would the opponents have done and would that have made a material impact? The opponents have the advantage of hindsight when they profess what they wold have done.
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Realistically Biden wouldn’t have prevented the initial CDC f***up and would have been caught just as flat footed as everyone else … in the world. That’s just the way big slow agencies work when an unprecedented event happens.
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Any fair assessment (not likely to get this from any media source) will be able to look at multiple left controlled government responses (NY, NJ, CN, CA, NYC, Detroit, Baltimore etc.) and map that onto the hypothetical national response.
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My opinion is the virus won, end of story. Trump was a leadership disaster, as expected, but everyone else was just as bad or worse when outcomes are measured. US culture is such that we aren’t a very compliant populace to federal control. National lock downs enforced by state power would have made every city Portland.
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I thought the US would do better, it didn’t. The only thing important now is to learn the right lessons and do better next time.
Tom Scharf (Comment #189378)
Tom, I am in essential agreement with what you say here, but the full picture of the pandemic and its consequences for the US and the world has yet to be written. The remaining questions are (1) herd immunity and when and at what level it might occur, (2) the longer term economic damages, (3) level of second surges and (4) most importantly, what do governments do if an effective vaccine or prophylactic is not forthcoming and a second surge is significant. Not that the public will have retained much interest when all this plays out and it is written or even that the potential writers of this story will have retained sufficient interest to write about it..
Kenneth, Tom,
I agree that Trump mostly made a fool of himself with mildly to totally inaccurate statements in the daily news conferences, and that made a very bad impression on a lot of people. It wasn’t that he did anything terrible, and his administration did a lot of sensible things. But Trump just acted badly.
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An air-head like Cuomo (or his even lighter weight younger brother Fredo) can ‘do’ gravitas a lot better than Trump…. who doesn’t do gravitas at all. Trump’s many off-the-wall statements and tweets just embarrass and even offend many of his natural supporters. It is not clear to me if that embarrassment and offense are enough to make them vote for a demented old man with an unhinged lefty sidekick… who not doubt has already memorized the 25th amendment, section D, word for word.
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It will be an interesting election. Since at least the candidacy of George McGovern, there has not been so clear an ideological separation between the parties and their nominees.
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By the way, I trust the polls saying people blame Trump for covid even less than I trust the voter preference polls in battleground states. Lots of people really do not want to discuss their lesser-of-evils support for Trump with some stranger on the telephone.
Mike M. (Comment #189370)
angech (Comment #189365): “Try this instead.â€
The quote angech then posts may be lifted out of context, since killer T cells don’t just kill virus infected cells. He provides no way to find the source.
Sorry.
my bad.
“Cytotoxic T Lymphocytes and Vaccine Development”
angech,
Do you have a url? Authors? Etc. Googling is finding too many things with that title, and they don’t include your exact paragraph.
Lucia
“Out of curiosity, are you ever going to address the empirical evidence in the mouse study? Though asked repeatedly by a number of people here, you continue to ignore it. It strongly disconfirms your over all claim. People aren’t going to forget that evidence exists merely because you only want to try to argue about subordinate details related to one particular process in the immune system.”
OK. Happy to do so.
“lucia (Comment #189249)
angech They do not cause immunity.
Paper after paper after paper contradicts your view of whether t-cells can clear virus.”
–
Do they kill virus? No.
Here’s one study on t-cells in ebola infected mice. It includes test on B-cell-deficient mice.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC368745/
–
Paper comments
” All CD8 T-cell-deficient mice succumbed to subcutaneous infection and had high viral antigen titers in tissues, whereas mice deficient in B cells or CD4 T cells cleared infection and survived, suggesting that CD8 T cells, independent of CD4 T cells and antibodies, are critical to protection against subcutaneous Ebola virus infection”.
I know you will keep providing your description of what you think t-cells do and do not do. But empirical evidence shows that t-cells can clear infections even in the absence of B cells.
In this study, it was the memory t-cells that saved the mice from re-infection. The remaining B-cells and antibodies did not save them.
.
–
I think this is misunderstanding of the forces at play here and also what was done by the scientists in the experiment.
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1. The mice were all originally immune to Ebola virus due to vaccination – their words, {subcutaneous infection with an adapted Ebola virus resulted in a nonfatal infection associated with long-term immunity against lethal rechallenge] Long term proven immunity scientifically means antibodies.
2. Even though some of them were theoretically B cell deficient.
[Ironically a laboratory antibody treatment technique]
Long term immunity is due to antibodies so all one can say is that the so called B cell deficiency was not and could not have been complete*. Understandable as the treatment to deplete the B cells does not eliminate from the mouse with at least 20% levels remaining in the bone marrow.
This was the case at the start of the experiment so B cell levels would only have improved as the study went on!
I find it remiss of the authors not to mention this.
3.Four main groups survived rechallenge with Ebola.
-B cell deficient mice as expected because they still had the ability to produce antibodies. In part due to the logarithmic reproduction of B cells once TC8 cells tell them there is a threat to respond to.
-TC4 depleted cells. Because T cells do not kill virus, the B cells did it again with antibodies.TC4 cells.
– β2-microglobulin deficient mice
-Normal vaccinated mice.
4. Two groups died died, those missing C8 cells.
This was not proof that TC8 cells clear or kill virus.
Only that when you knock off the trigger for the B cells in either the B cell deficient or Bcell normal group the B cells striggle to get active.
Contrary to the arguments put forward for B cell for T cell effectiveness what it showed was that without the B cells being activated the virus could not be killed and cleared.
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Counter intuitive but correct in all facets of the T cell B cell controversy.
I think I have covered and nailed all the salient points to your satisfaction.
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“There is a reason we are seeing paper after paper after paper discussing t-cells. Perhaps in the past people didn’t know t-cells can kill virus by themselves w/o B-cells. But the evidence suggests they can (and do).”
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A conundrum.
T cell TC8 memory cells have no killing function.
It does expose a flaw in the methodology which if the authors see it here they might have to acknowledge in time*.
Cytotoxic T Lymphocytes and Vaccine Development
http://www.hindawi.com › journals › bmri
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Had looked at the paper but it was hard to reply to your query before in the right way to address your concerns. The time gap and subsequent discussions have helped immensely in trying to understand it as Mike M said.
T cells are very important in Immunity. play vital roles and are worth all the research. Their main lines of helping will be anti cancer and anti autoimmune disease. Some viral induced cancers may well be treated by T cells through their ability to destroy cells with viral markers.
“in response to this ” Please provide any true reference to T cells killing virus directly” Please provide a reference that says T-cells needs to kill virus “directly†to prevent disease. Killing is killing. Several of us have already pointed out that killing them indirectly should be sufficient.”
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If I said,
” Please provide any true reference to T cells killing virus directly or indirectly”
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I still think it would be hard to do so. Pointing out that killing them indirectly should be sufficient is not proving that it happens.
The T Cells do lyse the cells getting the virus out to where the antibodies can attach to them and render them disposable.
But that does not prevent disease.
blocking them forming in cells by transcriptase interference is modifying, not preventing the disease.
Recognising a part of them, on a cell membrane is different to actually grabbing the virus and breaking it into little bits, that is why the antibodies exist. If the T cells could do it on their own we would not have a discussion, or antibodies.
Maybe there is a mechanism, written down somewhere I have not noticed or been too slow to understand, that is why I am asking.
Mike M. (Comment #189374)
“I am in awe of your search skills. I try to remember the maxim that one should never attribute to mendacity that which can be explained by incompetence. But if angech actually edited the text as he appears to have, then mendacity it is.”
Thanks, Mike M. re 189360
Not offended. I took the bit relevant to your comment that seemed to claim TC4 cells worked mainly by inducing apostosis.
“The distinction between apoptosis and cell lysis is important in immunology: lysing a virus-infected cell could potentially release the virions, whereas apoptosis leads to destruction of the virus inside.”
You said
“That one is arguably ambiguous as to whether lysis might be induced, but context says otherwise:’
I presume you did say that?
So,as a mendicant [important difference], Could I ask you to state unequivocally that the main action in acute viral infection is indeed lysis, not apostosis? Thanks.
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Also You quoted a comment “Cytotoxins go directly inside the cell through this pore, destroying it and any viruses inside.”
Whereas a following article distinctly says it instead could potentially release the virions.
Wiki v ask a scientist is not exactly proof but since you quoted it
Release has a totally different meaning to kill wouldn’t you agree?
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I do think it is important for you to correct your comments if they need correcting
It now is clear, every specialist working in the field is wrong that CD8 T-cells inhibit viral replication and one anonymous person not working in the field is right. There is also a bridge in New York available for sale. angech, your critiques of the papers are contrary to what those references actually say, and this is the last comment in which I will address your wrong-headed analysis. Cio.
I think that at this point the only thing left is to ignore angech, since he refuses to engage in an honest manner.
angech
Their words do NOT say they were “immuneâ€. It says “associated with long-term immunityâ€. These don’t mean the same thing, and I doubt the authors were so careless with language to use “associated with†to mean something other than “associated withâ€. (Anyway, obviously, they weren’t all immune. Some later died.)
.
Simple googling contradicts this claim about the antibody treatment technique. The “internets†say Bcell deficient mice are mutants.
“Also Known As:muMt. Homozygous mutant mice lack mature B cells. “ (The paper says the T-cells were depleted by a lab treatment. Not B cells.)
I don’t think mutations wear out. So…. no, I don’t think Bcells levels would improve. Your theory that the B-cell deficient mice are not B-cell deficient sounds like it’s based on incorrect “factsâ€.
Your interpretation is unconvincing.
angech
Could you provide a link to the article This is not a linke to the article. In fact, it’s not even a link to the hournal.
Please provide enough informaiton for someone to find it. How about:
1) Title of paper.
2) First few authors names (one or two?)
3) Year of publication.
4) Link where the article can be found.
(4) would be enough, but you can’t seem to post actual full links The “bread crumbs” you leave aren’t sufficient to help me find the article. (And I’m pretty good at finding articles!)
Angech:
That’s what the bit he quoted said. You could go back to asu.edu and ask them!
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In contrast article that seems to match the one you posted (and may have severely edited) says the bacteria inside an infected cell die of lysis. So there is absolutely nothing in there to contradict the notion that an infected cells does not die of aptosis!!
.
We all thinks so to. So it would be nice if you could correct your own!!
Lucia,
I found this searching for “Cytotoxic T Lymphocytes and Vaccine Development”. It’s an introduction to what appears to be a single-topic issue of the Journal of Biomedicine and Biotechnology in October 2010.
[Also here.]
Edit add: Journal has been renamed. Currently known as BioMed Research International, per this page
Harold W,
Thanks, those links at least help us find the “Journal of B and B”. This does seem to confirm that angech’s quote must be a highly edited version of the actual material in the paper I quoted.
This is info from the top of the Journa;
Hindawi Publishing CorporationJournal of Biomedicine and BiotechnologyVolume 2010, Article ID 936549,1pagedoi:10.1155/2010/936549
It appears to be a link to the requisite gracious letter by the editors thanking authors for contributing on the topic. The main thing we learn is there is so much new information that the editors felt the need for a special issue to collect stuff together
.
A list of the actual substantive articles is here:
https://www.ncbi.nlm.nih.gov/pmc/issues/181617/
.
The paper at the NIH link I posted earlier seems to be to an article that was published in that issue:
J Biomed Biotechnol. 2010; 2010: 249482.
Published online 2010 Jun 23. doi: 10.1155/2010/249482
.
This does suggest that angech’s “quote” was a heavily edited version of what I posted. (Note angech, when you leave out text you consider “unimportant”, you should replace it with […]. That allows the reader to know you edited it and alerts them they might want to check. This is also why it’s useful to give enough information to allow them to find the article. Initially you gave none. )
.
It’s clear the paper I tracked down entering sentence fragments in google does not discuss how t-cells interact with virus. Also the “take away” point angech is trying to make (about lysis vs apotasis) is totally irrelevant to the discussion of how t-cells affect virus. It
(a) does not discuss the death or killing of the infected cell at all.
(b) it discusses the death/killing of the microbe inside the cells.
Here’s the key bit vis. a vis. angech’s attempt to rebutt MikeM’s cited article:
.
So in this particular mechanism, microbes (not virus infected cells) are said to die of lysis. This absolutely positively does not rebut the claim at the asu.edu site that discusses virus infected cells dye of apotosis.
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I admit the heavily redacted version by angech tended to give the impression– but even his version doesn’t say infected cells die of apotosis. Notice the “insert into the microbial membrane “. That was in the bit angech posted and gives away that it was not discussing anything inserted into the microbe infected cell. The membrane being penetrated was the microbes not the infected cell wall. The thing that died of lysis was the microbe, not the cell.
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It’s really hard to believe anyone could read that full article and think that angech’s did not severely distort what the authors said. Moreover, not inserting […] where material was left out is very bad practice. And not giving any reference in the first place and one to a different article later on is really not helpful. Angech, I really think you need to learn to edit more fairly and also give links so we can check everything you cite. Because this current practice is just wasting people’s time.
.
In the end, we are generally able to find the mistaken claims of fact in your comments. But it’s really tiring.
Note: I think I mistakenly thought the microbe was inside a cell. But, it might not be. The passage describes how the t-cells kill a microbe. (My mistake is not relevant to my point which is: this has nothing to do with how a cell dies. It describes how the microbe dies. )
WRT to the NIH paper discussing how TCells kill bacteria, they have a graphic
(A) shows CTL killing bacteria that are OUTSIDE a cell.
(B) shows CTL killing bacteria that are INSIDE a cell.
(C) shows CTL first killing an infected cell which releases bacteria. Then CTL kills them (the same way it works in A).
In all cases, CTL kills the bacteria with no apparent involvement of antibodies or Bcells. (Of course, this isn’t about viruses. But it does show direct killing of a pathogen without involvement of antibodies.)
lucia (Comment #189393)
angech
Could you provide a link to the article This is not a link to the article. In fact, it’s not even a link to the journal
Cytotoxic T Lymphocytes and Vaccine Development
http://www.hindawi.com › journals › bmri
Please provide enough informaiton for someone to find it. How about:
1) Title of paper.
2) First few authors names (one or two?)
3) Year of publication.
4) Link where the article can be found.
–
1 Cytotoxic T lymphocytes and Vaccine Development†is the title of the paper.
2 Editor. Zhengguo Xiao Guest Editors. Kim Klonowski Hanchun Yang
3. Publishing date. 01 Jun 2010
4. I just put the title into google when the page opens there is the title of the article and underneath the word “descriptionâ€
Hitting on this or the little arrow far off to the right brings up the whole article free to read.
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It is what I have consistently put in.
You did ask for a url which is what I thought the http was/is.
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To clear up a small matter .
Mike M used a quote first. In fact 4.
Trying to refute the fact that T cells have no known mechanism of killing a virus.
Directly or indirectly.
The proof is simple. It is in their name.
They are not called virus killing cells.
If indeed they could do this particular function they would be labelled virus killing cells, not cytotoxic or cell killing cells.
“A cytotoxic T cell (also known as TC, cytotoxic T lymphocyte, CTL, T-killer cell, cytolytic T cell, CD8+ T-cell or killer T cell) is a T lymphocyte (a type of white blood cell) that kills cancer cells, cells that are infected (particularly with viruses), or cells that are damaged in other ways.“
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Mike chose a quote to make a point.
I chose a quote that contradicted his quote.
That was the sole reason I used it.
That is why I asked if he stood by that quote, not the authors of the quote.
Either he does, in which case there is a contradiction he needs to resolve or he agrees with my contention.
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I am bemused by claims of selective editing etc.
I took a scientific fact from a scientific source and quoted it.
Is it wrong?
No.
Case settled.
Feynman said it years ago, one small fact destroys the theory.
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Attacking the motives or methods of the messenger that brings that fact is understandable if the fact is upsetting.
Can we stick to the facts?
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By the way thanks for clearing up part of the mystery, to me , of the b cell deficiency mice though it raises even more questions for the Sherlock Holmes amongst us.
Observations on the mice experiment.
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lucia (Comment #189249)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC368745/
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Apart from the fact that they have live Ebola virus in the laboratories in Atlanta, Georgia USA.
No Wuhan problems likely here.
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“Mice infected s.c. clear the virus and generate high titers of anti-Ebola virus IgG (Fig. ​(Fig.1),1), as do human survivorsâ€
From link 19 another interesting paper from the authors about a related trial.
Journal of virology 2001 “ Passive Transfer of Antibodies Protects Immunocompetent and Immunodeficient Mice against Lethal Ebola Virus Infection without Complete Inhibition of Viral Replication“
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Apparently if you as a mouse are given a small sub cutaneous dose 100 PPU you have time to develop IgG (NB) to the mouse Ebola modified virus.
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“Thus antibodies suppress or delay viral growth, provide protection against lethal Ebola virus infection, and may not require participation of other immune components for protection.“
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“We took advantage of the immune status of s.c.-infected mice to assess the ability of homologous IS to protect against lethal i.p. challenge with Ebola virus.
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Two take away from this.
Immunity does mean IG antibody derived immunity and is present in all the immunised mice.
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My take on B cell deficiency mice for what it’s worth (not very much obviously) Is that while they cannot react to form IgA or IgM they are still able to produce IgG when needed.
Hence their ability to survive except when they cells that prime them CD8 memory are absent.
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It is important to note that B cell deficiency does not mean no B cells, just that they lack working IgM and IgA. The B cells are apparently still there.
Furthermore they can produce working IgG when needed.
I could easily be wrong here, help from a microbiological immunologist would be handy.
The genetic modification is one that changes the order of formation of IgM antibodies around making them present but useless,.
A bit like having a TCD4 cell around primed to SARS but with no B cell activation to produce the needed Immunoglobulins to fight the infection ( never been exposed to the real virus).
But I digress.
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So called B cell deficient mice cannot be immunoglobulin deficient to the virus, something is working in them, B cells activated to produce a useful immunoglobulin, probably IgG or they would have all died from the initial sc dose small though was, in the first study you quoted.
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The authors do have a dilemma in stating the mice are B cell deficient, implying they lack the wherewithal to form antibodies, and at the same time saying that they are immunised and were immunised at the start of the study, which can only mean they did develop antibodies.
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Explanation anyone?
angech,
I think you are trying and trying and trying and trying to salvage your pov despite the copious evidence it is incorrect.
True.
Will comment further on this if people request clarification or discussion, practically I will stop.
Thanks for the opportunity to explore some concepts that are currently very topical.
Thanks to SteveF and Mike M for tolerance above the call of duty as I know I can be very aggravating and obstinate when my tunnel vision kicks in.
Can you put up an election post instead at some time?
I don’t know what to say about the election!
angech
The material you quoted is not from this 1 page paper written by editors. So yes: You consistently put in a paper that is NOT the paper from which you took the material. When you quote from a paper, cite the paper you quoted, not a different paper.
.
lucia,
I have a request. Angech has volunteered to shut up on this topic. Please let him.
MikeM
Good idea.