Immunity for common cold coronaviruses may ward off severe covid-19

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In a laboratory experiment, a strong T-cell response against the coronaviruses that cause common cold-like symptoms was linked to greater covid-19 immunity

Health 8 August 2022

By Jason Arunn Murugesu

Antibodies attacking SARS-CoV-2, the coronavirus that can cause covid-19

Antibodies attacking SARS-CoV-2, the coronavirus that can cause covid-19

Shutterstock/Kateryna Kon

People with a stronger immune response to the coronaviruses that cause common cold-like symptoms may be better protected against covid-19, raising hopes that a pan-coronavirus vaccine could be achieved.

Ricardo da Silva Antunes at La Jolla Institute for Immunology in California and his colleagues analysed blood samples collected from 32 people between 2016 and 2019, before covid-19 emerged.

Multiple samples were taken from each person over six months to three years. The team wanted to see how the immune cells in these samples responded to four coronaviruses that cause common cold-like symptoms as well as the original SARS-CoV-2 strain, which emerged in Wuhan, China, at the end of 2019.

Within the coronavirus class, seven strains are known to infect humans. Of these, four viruses cause common cold-like symptoms. There is also SARS-CoV, which causes severe acute respiratory syndrome (SARS); MERS-CoV, which causes Middle East respiratory syndrome (MERS); and SARS-CoV-2, the cause of the ongoing pandemic.

Antunes says it was important to use samples taken before the pandemic. “This means that when we’re looking at our results, we know that they are caused by pre-existing immune memory and that they’re not contaminated by people’s immune responses to SARS-CoV-2.”

SARS-CoV-2 has similar genetic sequences to the four common cold-like coronaviruses, says Antunes. Previous studies also suggest that stronger T-cell responses induced by prior coronaviruses may protect against SARS-CoV-2.

In the latest study, the researchers combined the participants’ blood with peptides – strings of amino acids – from the different coronaviruses. Immune responses are typically triggered by the body recognising the peptides of a virus. Next, they measured the T-cell and antibody responses in the blood when exposed to these viruses.

Looking at multiple samples from each participant, the researchers found the T-cell and antibody responses were stable and persistent for all four common cold-like coronaviruses.

By looking at the T-cells, some of which are more likely to be activated by recent re-infections, they determined these immune responses weren’t due to regular re-infections. Instead, this immune response may be relatively stable.

Antunes speculates that if these common cold-like coronaviruses elicit similar immune responses, it may generate a stable immune memory.

In the second part of the experiment, the researchers combined the participants’ blood with SARS-CoV-2. They found that those with the strongest T-cell immune response to the common cold-like coronaviruses had the strongest response to SARS-CoV-2. The same wasn’t found for antibody levels.

But the participants with stronger responses against common cold-like coronaviruses weren’t necessarily less likely to experience severe covid-19, says Antunes. “The link between [the common] cold response and SARS-CoV-2 response is still not clear,” he says. Assuming most people have been exposed to common cold-like coronaviruses throughout their life, it isn’t clear why some still become severely ill with covid-19.

Overall, similar findings are expected with newer SARS-CoV-2 variants, such as omicron, as the mutations that result in these variants haven’t been found to affect the T-cell response much, says Antunes.

According to Mala Maini at University College London, the study adds to the evidence that suggests T-cell immunity to common cold-like coronaviruses shapes our SARS-CoV-2 response.

Her team is working on a pan-coronavirus vaccine that targets a genetic sequence shared between SARS-CoV-2 and common cold-like coronaviruses.

Journal reference: Cell Host & Microbe, DOI: https://doi.org/10.1016/j.chom.2022.07.012

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