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While a new study shows that having caught a cold may give you additional protection against Covid-19, it does not mean we should all rush out and get as close as we can to someone who’s sneezing and sniffling.

But the results of the study may lead one day to a vaccine that provides protection against all coronaviruses, researchers hope.

The University College London study, published on Nov 10 in the journal Nature, examined data from dozens of healthcare workers in the UK, which showed that there are individuals who can clear an early SARS-CoV-2 infection in such a short time that they never even test positive for the virus, and neither do their bodies produce antibodies against it.

What’s intriguing is that this type of resistance is provided by a person’s memory T cells, which could happen after the person is exposed to coronaviruses that cause the common cold.

The authors of the study warn that it does not mean that anyone who catches a cold is protected against Covid-19, and add that it’s too soon to say for sure that infection can be stopped in its beginning stages.

What the study does show were the results in the samples from almost 60 health workers whose blood was examined early in the pandemic. 

All of the workers were at high risk of catching the infection since they work at hospitals. But none of them got Covid, and nor did they produce antibodies to the virus for four months after enrolling in the study.

And among the healthcare workers, designated as  ‘seronegative’ participants, were 20 in whom T cells had multiplied, which signifies that their immune systems were likely preparing to fight off an infection.

Interestingly, 19 of the 20 also had higher levels of IFI27, an immune-system protein that could be an early marker of SARS-CoV-2 infection.

According to the study’s authors, this is proof that the healthcare workers had “abortive infections”, which means that the virus tried to infect their bodies but did not succeed.

Dr Swadling said: “If you think of the continuum of disease outcomes that you can have after exposure to SARS-Cov-2 – from asymptomatic to mild infection and severe disease – what we’ve described is a new level on this spectrum called abortive infection.

This is where people have been exposed to the virus, inducing a T-cell response, but they control the virus before it becomes detectable by PCR,” said Dr Leo Swadling, the author of the study.

Dr Swadling said of the ‘seronegative’ healthcare workers: “Previous common cold exposure may have given these individuals a head start against the virus, tipping the balance in favour of their immune system eliminating the virus before it could start to replicate.”

“These pre-existing T-cells are poised ready to recognise Sars-CoV-2,” he added.

Researchers said that rather than having avoided infection completely, a subset of healthcare workers appear to have experienced a transient low-level infection, not detectable by routine tests.

“If you think of it as a race against time between the virus and the immune system, what we’ve described is that early pre-existing T-cells, particularly targeting the RTC, can give the immune system a headstart against the virus, leading to very early control blunting viral replication so it’s not detectable and doesn’t induce an antibody response,” the researchers added.

Additionally, more seronegative participants showed T cells that stop “SARS-CoV-2 by disabling a cluster of viral proteins called the replication transcription complex, which helps the virus to reproduce” than healthcare workers who were infected with Covid.

The study found that T cells from blood samples gathered prior to the pandemic could also recognize SARS-CoV-2 “and most strongly recognized the replication complex.”

These T cells are likely to have developed by coronaviruses that cause regular colds, although the researchers admitted that other triggers also could have caused the T cells to develop.

And while spike proteins differ among different coronaviruses, replication complexes do not.

Therefore, a vaccine that targets the replication complex could work against most coronavirus infections.

“T-cells recognising the virus’ replication machinery would provide an additional layer of protection to that provided by the spike-focused immunity that is generated by the already highly efficacious current vaccines,” said Prof Mala Maini, a co—author of the study.

“This dual-action vaccine would provide more flexibility against mutations, and because T-cells can be incredibly long-lived, could also provide longer-lasting immunity.

By expanding pre-existing T-cells, such vaccines could help to stop the virus in its tracks at a very early stage,” she added. /TISG

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