Some of the body’s defences generated after an infection of the common cold could help to ward off the virus that causes Covid-19, researchers have said.
A small study found that people with high levels of T cells – generated after infection with other coronaviruses such as the common cold – were less likely to catch Covid-19.
But the authors stressed that vaccination was the best way a person could protect themselves against Covid-19.
The new study, conducted by experts at Imperial College London set out to investigate why some people don’t get Covid-19, despite being in contact with the virus.
Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against Sars-CoV-2 infection.
Professor Ajit Lalvani
Dr Rhia Kundu, first author of the study, from Imperial’s National Heart & Lung Institute, said: “Being exposed to the Sars-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why.
“We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against Covid-19 infection.
“While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone. Instead, the best way to protect yourself against Covid-19 is to be fully vaccinated, including getting your booster dose.”
Previous work had suggested that T cells induced by other coronaviruses could recognise Sars-CoV-2 – the virus that causes Covid-19.
The new study, published in the journal Nature Communications, examined how the presence of these T cells at the time of exposure influences whether someone becomes infected.
Experts studied a group of people in September 2020 when fewer people in the UK had been infected and the vaccination campaign had not yet started.
Researchers studied 52 people who lived with someone with a confirmed case of Covid-19.
The participants did PCR tests at the onset of the study, and four and seven days later, to see if they developed an infection themselves.
Blood samples were taken in the first six days of exposure to enable the researchers to analyse the levels of pre-existing T cells induced by previous common cold coronavirus infections.
Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against Sars-CoV-2 infection
Professor Ajit Lalvani
The researchers found that there were significantly higher levels of these “cross-reactive” T cells in the 26 people who did not become infected, compared with the 26 people who did become infected.
The authors of the study said that these T cells targeted internal proteins within the Sars-CoV-2 virus, rather than the spike protein on the surface of the virus, to protect against infection.
Current Covid-19 vaccines target the spike protein of the virus, not these internal proteins.
This finding could lead to the development of new vaccines that target the internal proteins of the virus – which could potentially provide longer-lasting protection, as T cell responses can persist longer than antibody responses.
Professor Ajit Lalvani, senior author of the study and director of the NIHR Respiratory Infections Health Protection Research Unit at Imperial, said: “Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against Sars-CoV-2 infection.
“These T cells provide protection by attacking proteins within the virus, rather than the spike protein on its surface.
“The spike protein is under intense immune pressure from vaccine-induced antibody, which drives evolution of vaccine-escape mutants. In contrast, the internal proteins targeted by the protective T cells we identified mutate much less.
“Consequently, they are highly conserved between the various Sars-CoV-2 variants, including Omicron New vaccines that include these conserved, internal proteins would therefore induce broadly protective T cell responses that should protect against current and future Sars-CoV-2 variants.”