Brians356
Gold $$ Contributor
You could be right. But some experts are thinking outside the box on this virus.By mid-July fewer than 20% of Swedes showed serological evidence of past SARS-CoV-2 infection. Sweden is nowhere near herd immunity for a virus with an R0 of 2.5 or more.
From BBC on 1 July (excerpts):
People testing negative for coronavirus antibodies may still have some immunity, a study has suggested. For every person testing positive for antibodies, two were found to have specific T-cells which identify and destroy infected cells. This was seen even in people who had mild or symptomless cases of Covid-19. But it's not yet clear whether this just protects that individual, or if it might also stop them from passing on the infection to others.
Researchers at the Karolinksa Institute in Sweden tested 200 people for both antibodies and T-cells. Some were blood donors while others were tracked down from the group of people first infected in Sweden, mainly returning from earlier affected areas like northern Italy. This could mean a wider group have some level of immunity to Covid-19 than antibody testing figures, like those published as part of the UK Office for National Statistics Infection Survey, suggest. It's likely those people did mount an antibody response, but either it had faded or was not detectable by the current tests. And these people should be protected if they are exposed to the virus for a second time.
Prof Danny Altmann at Imperial College London described the study as "robust, impressive and thorough" and said it added to a growing body of evidence that "antibody testing alone underestimates immunity".
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More analysis needs to be done to understand whether these T-cells provide "sterilising immunity", meaning they completely block the virus, or whether they might protect an individual from getting sick but not stop them from carrying the virus and transmitting it.
Much of the discussion around Covid-19 immunity has focused on antibodies - Y-shaped proteins which act like "missiles shooting down a target", assistant Prof Buggert explained. They bind to the virus before it can enter your cells, and neutralise it. If antibodies fail to neutralise the virus, it can enter your cells and turn them into virus-making factories.
T-cells, on the other hand, target already-infected cells and completely destroy them, stopping them from spreading to other, healthy cells.
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Like antibodies, T-cells are part of the bit of your immune system that has a memory. Once it recognises a particular virus, it can quickly target cells infected with it and kill them.
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T-cells are very complex and much harder to identify than antibodies, requiring specialist labs and small batches of samples being tested by hand over the course of days.
This means mass testing for T-cells is not a very likely prospect at the moment.
https://www.bbc.com/news/health-53248660
Here's excerpts from an article in Science Magazine by Derek Lowe (15 July):
Here’s a post from May on a paper in Cell that looked at T cell responses in recovering SARS CoV-2 patients and compared them to reports of people who had been infected with “original SARS” back in 2003, and to people who had never encountered either. It also has some background on T cells in general, which might be useful if you don’t have that info right at the top of your brain’s queue. That’s the paper that showed that the T-cell response to this virus is less “Spike-o-centric” than it was to SARS. It also showed that there are, in fact, people who have both CD4+ and CD8+ T cells that recognize protein antigens from the new coronavirus even though they have never been exposed to SARS, MERS, or the new virus. The paper speculated that this might be due to cross-reactivity with proteins from the “common cold” coronaviruses”, and raised the possibility that there might be a part of the population that has at least some existing protection against the current pandemic.
Now comes a new paper in press at Nature. It confirms that convalescent patients from the current epidemic show T-cell responses (mostly CD4+ but some CD8+ as well) to various epitopes of the N (nucleocapsid) protein, which the earlier paper had identified as one of the main antigens as well (along with the Spike and M proteins, among others, with differences between the CD4+ and CD8+ responses as well). Turning to patients who had caught SARS back in 2003 and recovered, it is already known (and worried about) that their antibody responses faded within two or three years. But this paper shows that these patients still have (17 years later!) a robust T-cell response to the original SARS coronavirus’s N protein, which extends an earlier report of such responses going out to 11 years. This new work finds that these cross-react with the new SARS CoV-2 N protein as well. This makes one think, as many have been wondering, that T-cell driven immunity is perhaps the way to reconcile the apparent paradox between (1) antibody responses that seem to be dropping week by week in convalescent patients but (2) few (if any) reliable reports of actual re-infection. That would be good news indeed.
And turning to patients who have never been exposed to either SARS or the latest SARS CoV-2, this new work confirms that there are people who nonetheless have T cells that are reactive to protein antigens from the new virus. As in the earlier paper, these cells have a different pattern of reactivity compared to people who have recovered from the current pandemic (which also serves to confirm that they truly have not been infected this time around). Recognition of the nsp7 and nsp13 proteins is prominent, as well as the N protein. And when they looked at that nsp7 response, it turns out that the T cells are recognizing particular protein regions that have low homology to those found in the “common cold” coronaviruses – but do have very high homology to various animal coronaviruses.
https://blogs.sciencemag.org/pipeline/archives/2020/07/15/new-data-on-t-cells-and-the-coronavirus
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