https://www.researchsquare.com/article/rs-35331/v1
Something for the forum experts to have a look at.
apparently up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity.
https://www.researchsquare.com/article/rs-35331/v1
Something for the forum experts to have a look at.
apparently up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity.
Richard Taylor
"William Tell could take an apple off your head. Taylor could take out a processed pea."
Sid Waddell
Thank you for finding this WP.Originally Posted by Witton Park
Whilst I will defer to the better knowledge of experts, as this is a serious research article, for those who are interested in knowledge about the virus there is much to read. For those without the time to wade through it I have lifted two parts, below in bold, one of which mentions the 81% figure WP mentioned
Using predicted or randomSARS-CoV-2--derived peptide pools, two very recent studies reported preexisting SARS-CoV-2-directed T-cell responses in small groups of unexposed as well as SARS-CoV-2 seronegative individuals, thereby suggesting cross-reactivity between human common cold coronaviruses and SARS-CoV-210,11
Notably, we detected SARS-CoV-2 cross-reactive T cells in 81% of unexposed individuals. To determine if these T-cells indeed mediate heterologous immunity and whether this explains the relatively small proportion of severely ill or, even in general, infected patients during this pandemic32,33, a dedicated study using e.g. a matched case control, or retrospective cohort design applying our cross-reactive SARS-CoV-2 T-cell epitopes would be required.
Does this mean that the 81% who have a T cell response are completely asymptomatic or that some are while others will just have a mild illness?
MikeT provided this link last week.
https://thorax.bmj.com/content/early...nl-2020-215091
This study found that 59% of people on a cruise ship tested positive for Covid-19. However, interestingly it also revealed that 81% of those people were asymptomatic. Perhaps, these people had T cells that could fight it off as above and would probably not be revealed to have had the virus in an antibody test.
Much is being made about the apparent explosion of new cases in the USA at the moment. However, the states that are showing the large increases appear to be those that got off relatively lightly early on in the pandemic, such as Texas. There is no such spike in New York, which as we all know was previously very badly affected.
Another example to look at is South Africa. It had one of the most stringent lockdowns in the world and early on too. South Africans weren't even allowed to buy alcohol or cigarettes. They successfully suppressed the virus throughout March, April and much of May. But much good it has done them now. As the lockdown has eased, cases are now rapidly growing.
I guess the point I'm getting to is does in the end the virus have to get to around 20% of the population, who don't have some sort of immunity and then after that it will naturally tail off of it's own accord? In which case, unless a vaccine comes along before this level is reached, is lockdown a waste of time? I don't know, but it seems possible.
I don't think your conclusion from the article is correct or valid. I think you are over-interpreting what the article says. Note, however, that I am not claiming any expertise, or even any significant level of competency, in this or any associated field. (Neither am I claiming that I fully understand everything that is written in the article!)
My purpose in making this post is not to make any claims as to what the conclusions from the article should be, but rather simply to make the case that (based on my understanding) the conclusion that "up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity" is not a correct nor valid conclusion to be made from the article. Certainly it is not, as far as I can see, a claim made anywhere in the article itself.
Here is a quotation from the second paragraph of the Discussion section:
"Notably, we detected SARS-CoV-2 cross-reactive T cells in 81% of unexposed individuals. To determine if these T-cells indeed mediate heterologous immunity and whether this explains the relatively small proportion of severely ill or, even in general, infected patients during this pandemic32,33, a dedicated study using e.g. a matched case control, or retrospective cohort design applying our cross-reactive SARS-CoV-2 T-cell epitopes would be required."
My understanding is that this does not mean that "81% have a had some T cell response to COVID". My understanding is that, on the contrary, these individuals have had NO exposure to SARS-CoV-2 / Covid-19. That's what the "cross-reactive" and "unexposed" parts of the quotation mean. My understanding is that "cross-reactive" means that these T cells have come about through exposure to something other other than SARS-Cov-2 (i.e., they are not SARS-CoV-2-specific T-cells). The 81% refers to the 185 individuals in the study who had NOT been exposed to SARS-CoV-2. Basically, my understanding is that what they are saying is that, of the 185 indiviiduals in the study who had not been exposed to SARS-Cov-2, 81% of them had been exposed at some time to something else which created T cells which are highly relevant and of interest in terms of the body's response to SARS-Cov-2 infection but which are not (obviously, because there has been no SARS-Cov-2 exposure) SARS-CoV-2-specific.
Neither does it mean that "lots of people have immunity" to SARS-CoV-2. It's possible that this is true, but the paper certainly does not say that this is the case. Rather, it specifically says that a dedicated study would be required to understand what the consequences of their findings are in relation to possible immunity from SARS-Cov-2 (see the quotation, above).
The study involved 180 individuals who had been exposed to SARS-Cov-2 and 185 who had not been so exposed. This seems a small sample to me if the objective of the study was to provide wide-ranging conclusions relevant to levels of infection and immunity. However, this was not the objective of the study. Rather, the objective was simply (!) to identify and characterise "SARS-CoV-2-specific and cross-reactive HLA class I and HLA-DR T-cell epitopes". (And, no, I don't claim to fully understand exactly what that means!)
Note, again, that all the above is based on my understanding. I would be happy to be corrected on any of my interpretations of what the article is saying (provided, of course, that sensible supporting evidence is provided).
I would suggest that it's also worth noting the comment at the top of the web page:
"This is a preprint. Preprints are preliminary reports that have not undergone peer review. They should not be considered conclusive, used to inform clinical practice, or referenced by the media as validated information."
It would be great if 81% of everybody had some resistance to covid-19 due to previous exposure to other corona virus’s and Prof Karol Sikora on Twitter was quite enthusiastic about this survey this morning too. I just think the high percentages infected in the two recent meat processing plant outbreaks (40% or so in Angelsea and 60% in Germany) tend to show that (even if some t-cell resistance is helping) there is still a high potential of catching and being able to spread the disease
I don't think the fact that so many caught the virus at these plants invalidates the idea that many people have some immunity to it. They will have tested everybody at these plants once it was established that there was an outbreak. But a large proportion will likely have had no symptoms. It would be very interesting to know quite how many.
Normally you would only go for a test if you were showing symptoms so we don't know how many people in the population have been exposed to Covid-19 and fought it off without realising it. They likely won't have produced any antibodies (because they didn't need to) so won't be picked up as being exposed to the virus by any antibody test.
The fact that so many people don't have symptoms is the main reason why it so infectious, many people won't realise they are passing it on.
It wasn't my conclusion. It was Prof Karol Sikora's. His conclusion as far as I am aware is not that 81% have immunity, but that many more than we are picking up from the anti-body tests.
40%? 50%? 70%...? who knows? But there's something in this.
It is early days absolutely, more work needs to be done. But it adds further information and it provides an explanation as to why a virus with a natural R assessed as over 3 and up to 5 that is rife in a population for 2 months at least before measures were put in place, only seems to have created 5-7% with anti-bodies.
Richard Taylor
"William Tell could take an apple off your head. Taylor could take out a processed pea."
Sid Waddell
Broadly speaking I think both you and WP are correct. Something is causing a lot of people who have been in contact with it to not produce anti-bodies, and the figures do not correspond with the accepted R(0) number. Until an expert comes up with a better theory to explain these irregularities, this makes a lot of sense.
I suspect that rural areas in Britain, that have had very few cases so far, will have sizeable outbreaks in the future, whilst areas like London, that have been badly hit, won't get it badly again (although there may be still be flare-ups).
In view of the all the demonstrations, raves, massing on South Coast beaches and football celebrations you would expect outbreaks breaking out around now in the areas where these people live. It will be interesting to see if this is the case, or whether the new outbreaks are confined to areas that have previously had very few cases. This will tell us if this is a valid theory, or just another blind alley.
Link to article from a couple of weeks ago that implies decline not due to immunity
https://www.imperial.ac.uk/news/1982...immunity-says/
Link to article from last week indicating herd immunity may come from a lower number of people infected than previously thought.
https://www.sciencedaily.com/release...0623111329.htm
I've also read articles that advise any immunity to this virus is short lived.
Guess we will just need to wait and see!
Imperial and oxford have made such wildly ridiculous and opposed predictions I am surprised anyone is still listening to any of them. Fantasy Ferguson resigned. He who said the swedes would have 50000 deaths if they pursued their policies. NOT.
Indeed WHO observations that some may get a second dose are far more likely to be a failure of tests.
A false positive, then later they get the disease. WHO were so invested in testing they have to say it was a double dose.
Having been vociferous in attacking government for lack of antibody tests, We now find BMJ saying that the tests are largely a waste of time. It says more about the medical professions penchant for self promotion and arguing regardless, than it does about COVID
One of the clear statements in wittons paper, is now generally accepted. That neither abbot nor Roche test are anything like as good as they claim. Even the test laboratory I used admitted it!
The first role of TCells is recognition of an invader ,so turning on immune response. Some are later involved in killing, helping etc, and later making antibodie.
The peptides in this study do indeed appear to trigger T cells in non covid patients. Far less than ex covid patients, but still significant.
Cross response is the norm we all rely on. It is why cowpox vaccine immunises against smallpox.
I think the future will show for example that South Korea succeeded despite their government action not because of it. After all - the Chinese hid it for weeks, and covid can progress assymptomatically. By the Time S korea acted they shut the stable door after the horse had come.
Could it be past exposure to other corona viruses tuning T cell response?
Last edited by Oracle; 29-06-2020 at 08:49 PM.
