T cells from the common cold cross-protect against SARS-CoV-2

T cells from the common cold cross-protect against SARS-CoV-2
© iStock/LaylaBird

New research provides the first evidence of a protective role for T cells from the common cold at the time of SARS-CoV-2 exposure and how that influences whether someone becomes infected.

Previous studies have highlighted that T cells induced by other coronaviruses, such as a common cold, can recognise SARS-CoV-2. The researchers also believe their findings provide a blueprint for a second-generation, universal vaccine that prevents infection from current and future SARS-CoV-2 variants, including Omicron.

The study was published in Nature Communications and led by Imperial College London researchers.  

How the common cold can have protective benefits 

Dr Rhia Kundu, the 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.”

The study conducted by researchers from Imperial College London began in September 2020 when most people in the UK had neither been infected nor vaccinated against SARS-CoV-2. It included 52 people who lived with someone with PCR-confirmed SARS-CoV-2 infection and who therefore had exposure to the virus. The participants did PCR tests at the outset and four and seven days later to determine if they developed an infection.

Blood samples from the 52 participants were taken within one to six days of exposure to the virus. This process enabled the researchers to analyse the levels of pre-existing T cells induced by previous common cold coronavirus infections that also cross-recognise proteins of the SARS-CoV-2 virus.

The researchers found significantly higher levels of these cross-reactive T cells in the 26 people who did not become infected, compared to the 26 people who did become infected. 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 infections.

The current vaccine offering 

Current vaccines do not induce an immune response to these internal proteins. The researchers said that alongside the existing effective spike protein-targeting vaccines, these internal proteins offer a new vaccine target. Therefore, this could provide long-lasting protection due to T cell responses persisting longer than antibody responses which wane within a few months of vaccination.

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 protect by attacking proteins within the virus, rather than the spike protein on its surface.

“The spike protein is under intense immune pressure from a vaccine-induced antibody which drives the 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.”

However, the researchers addressed that there are limitations to their study, including that because it is small and 88% of participants were of white European ethnicity, they cannot model demographic factors.


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