The mainstream preoccupation with antibodies as a signal of protection from COVID-19, coupled with worries about their declining levels, often fails to acknowledge the crucial role played by T-cells in conferring longer lasting immunity.
A new study in Nature shows that not only do people infected with SARS-CoV-2 develop lasting T-cell immunity, but so too do their close contacts who never experience a detectable infection and have no detectable antibodies.
The authors write:
Close contacts, who are SARS-CoV-2-exposed, are often both NAT [PCR] negative and antibody negative, indicating that SARS-CoV-2 failed to establish a successful infection within these individuals, presumably due to their exposure to limited numbers of viral particles or a short time of exposure. However, our analysis of the samples from 69 of these close contacts showed the presence of SARS-CoV-2 specific memory T-cell immunity.
For those infected, the study found the level of T-cell immunity was similar regardless of whether the infection was severe, moderate or asymptomatic. It also found T-cell levels stabilised and did not diminish over the course of three months, implying lasting protection.
For close contacts who were not infected, there were some differences in the quality of their T-cell immunity compared to those infected. The authors write:
The size and quality of the memory T-cell pool of COVID-19 patients are larger and better than those of close contacts. … The results show that 57.97% and 14.49% of close contacts contained virus-specific memory CD4+ and CD8+ T-cells, respectively.
Disappointingly, the study found that in those never exposed to SARS-CoV-2 (because the samples came from before September 2019) there was no evidence of T-cell cross-immunity from other coronaviruses.
In order to investigate whether the observed expanded T-cells may have originated from pre-existing cross-reactive T-cells specific for common cold coronaviruses from previous infections, we tested blood samples of 63 healthy donors collected before September of 2019. Following a 10-day in vitro peptide expansion only 3.17% of the healthy donors contained detectable levels of virus-specific memory CD4+ and CD8+ T-cells, respectively, suggesting that cross-reactive T-cells derived from exposure to other human coronaviruses do exist but are at a significantly lower frequency than those observed in close contacts.
They acknowledged that this was contrary to other recent studies and suggested the issue needed further study.
In agreement with recent reports,17,25 our data also demonstrated the presence of cross-reactive memory CD4+ and CD8+ T-cells, which target various surface proteins of SARS-CoV-2, in unexposed healthy donors. However, the failure of these cross-reactive memory CD4+ and CD8+ to expand in vitro suggests they have limited potential to function as part of a protective immune response against SARS-CoV-2. It is noteworthy that the SARS-CoV-2-reactive T-cells detected in the unexposed healthy donors in our study were lower than those detected by Grifoni et al.17 and Braun et al.26, but were consistent with those reported by Peng et al.27 and Zhou et al.28 Assumably, due to the use of different methodologies in assessing SARS-CoV-2-specific T-cell responses, it is difficult to directly reconcile the cell-number data between different studies. Thus, a thorough investigation is needed to determine whether the cross-reactive T memory can provide any protective immunity and exert an influence on the outcomes of COVID-19 disease.
The fact that exposure to SARS-CoV-2 can result in the development of more robust immunity (perhaps because of an immune system part-primed from earlier viral infections), rather than infection, is a salutary reminder of how the circulation of viruses helps us to develop and maintain healthy immune systems capable of fighting off a variety of diseases. Trying to avoid infection by staying away from people, insofar as that is possible, can be counterproductive as it can weaken our immune system by leaving us unexposed to a whole variety of pathogens.
It’s also a reminder that antibody testing is a very limited way of determining who has been exposed to and developed immunity to COVID-19. If millions of people exposed to the virus are developing immunity without ever being infected or developing antibodies, what does that mean for reaching herd immunity? It must be closer than we think.
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Omg….yet another variable to add to the confusion. Deliberate?
Any potential good news WILL be quickly quashed and articles such as this deleted or censored from the MSM. The T Cell immunity was previously broached only to be dismissed along with any other anti Covid cult articles. In the same way that Handjob is now setting up a task force to make a pill that reduce Covid symptoms in those that have symptoms, any info that will stop crony money making schemes must be summarily dismissed. With regarding to pill making task force, please correct me if I am wrong, but are there not already various drugs etc that help reduce the symptoms, some of which ‘protect’ the NHS are not allowed to use? We could save a lot of wasted money if we just had one task force labelled Reinvent the Wheel.
So why is Doris spending billions on sending out tests to everyone, oh yes, the rinsing continues
He either owns the company who make the tests or he following the orders of his puppet master Covid overlords at WEF or B&MGates Foundation. Either way its £1.3 billion of OUR money up the nose and down the drain the perpetuate the lockdown Yellow Star Health Apartheid Scheme.
A lot of these studies have sample sizes too small to get significant results. T-cell immunity has always been assumed in natural herd immunity estimates. Governments don’t want to engage with known science when it doesn’t suit their real target, which is to enforce vaccines, boosters etc together with biosecurity IDs.
If I knew this from O-level biology, you can’t tell me that nobody on Sage knew this all along.
Yeah, it’s pretty basic stuff.
I saw this study posted up on twitter a few days ago and although I don’t have the skills to properly evaluate it, it stunned me.
Thanks for the article on this. The last two paragraphs above are a very important summary of the potential implications of this.
Asymptomatic transmission is not a major vector of transmission (the scientific evidence strongly suggests this). But this suggests asymptomatic transmission could potentially even be beneficial in enabling the virus to transmit within the population in a setting where the infected are unlikely to be badly affected but will acquire some immunity. This is clearly better than encountering the virus in hospital when unwell and when in the proximity of patients with major symptoms who may be major transmitters.
Testing asymptomatic people makes even less sense viewed in the light of this. And the above indicates another possible mechanism by which the vulnerable are harmed by the lockdown of less vulnerable people.
Yes but we cannot have less testing, less mask wearing, less complying, less money in the trough. The T cell immunity info has previously been aired and quashed. All articles that do not support the Government fed propaganda will be ignored, discredited or deleted.
And likewise, unless I have read you wrongly, you would be better acquiring your FULL immunity from contact with an asymptomatic person than from having the experimental vaccine. Please someone, do correct me if I am wrong in thinking this.
Protection from certain upper respiratory tract infections, notably coronaviruses, has always been about innate immunity first with a cellular immunity response second. Antibodies appear to come as an additional response when there viral load exceeds a certain point and the disease becomes more serious.
This appears to be related to the health of the innate immune system, which is presumably why children tend to not make antibodies to coronavirus infections while pensioners do (on average across ‘modern populations’ only about half of people have some antibody response to coronavirus infections, with those who have serious symptomatic disease making the most antibodies).
Now, it could just be considered as ‘one of those things’. Ie, the body doesn’t make antibodies if it doesn’t need to. But presumably those antibodies would be useful to stop future infections — that is, after all, the theory behind the vaccines. So why would the body not get round to doing it for some diseases?
One theory is that there’s something about coronavirus (and other) antibodies that results in additional risks to the individual — perhaps through the generation of protein-antibody complexes (eg, similar to what happens with heparin induced thrombocytopenia), or perhaps through more general autoimmune effects (eg, Rheumatoid arthritis).
So, perhaps the human immune system has evolved to avoid producing antibodies to certain diseases when it can get away with it, to reduce the chances of certain conditions developing in the future, but it does produce an antibody response when it has no choice, such as in older people who tend to have a weak and dysregulared innate immune system.
In which case it might end up being a problem that we’ve decided to solve the coronavirus nuisance by forcing our children’s immune system to behave like that of a pensioner’s.
I’ll admit right now that I don’t know the answer to the above — but neither does anyone else. Maybe we’ll find out by the end of the clinical trials into the covid vaccines — after all, that’s what they’re for.