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Business News/ Opinion / Columns/  The role of genes in our covid vulnerability could be of help
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The role of genes in our covid vulnerability could be of help

Better vaccines can spring from research on variations in illness

Our genes partly explain why covid infects people so differently. Premium
Our genes partly explain why covid infects people so differently.

Even as covid has faded into the background for most, our curiosity of the virus’s idiosyncrasies hasn’t waned. Why does one member of a household suffer a hacking cough but another not even a sniffle? Why does long covid afflict only some? A cluster of studies suggests some of the answers lie in our genes. Learnings like this could help develop better vaccines.

Mild cases or asymptomatic infections have been relatively unstudied. Scientists’ focus on the sickest wasn’t just because of the urgency to save lives, but because it’s simply easier to study people in settings like hospitals. Collecting DNA, sequencing it and tracking the healthy is a tall order.

A team led by University of California at San Francisco’s Jill Hollenbach found a clever way of getting around that problem by tapping people who had already given their DNA: bone marrow donors. The team recruited nearly 30,000 such volunteers to get an app and answer questions on it if and when they tested positive for covid. Although they’ve been collecting data from them for years, this study was limited to the time before people were vaccinated so the results could be cleanly interpreted. The aim was to spot differences in a group of genes called HLA (short for human leukocyte antigen) that carry recipes for proteins that help our immune cells distinguish between our own biological detritus and unwelcome invaders. The proteins show little pieces of viruses to our T-cells, which take this as an invitation to attack. Because human T-cells have a long memory, they swoop in again fast the next time a similar virus invades. The researchers found that people who carried one copy of a version of a gene called HLA-B*15:01 were more than twice as likely to remain asymptomatic after being infected with covid. And people who inherited two copies of the gene (one from each parent) were eight times more likely to never suffer symptoms.

Hollenbach’s team found that this particular flavour of HLA is good at recognizing garden variety coronaviruses, and the T-cells exposed to those were later very good at detecting important bits of Sars-CoV-2. In other words, people with this variant who also had, say, a common cold “have this kind of superpower" of fighting their covid infection to the point where they don’t have symptoms, she explains.

“I think their findings are very exciting," says Jean-Laurent Casanova, a Rockefeller University scientist who studies the relationship between our genes and susceptibility to infectious diseases. “It suggests that T-cells are involved in the early phase of Sars-CoV-2 infection, and that a strong T-cell response can blunt infection and prevent clinical manifestations."

Another study, yet to be peer reviewed, offers genetic ties to the other end of the spectrum: when people suffer lingering symptoms. Researchers compared about 6,500 people with a long covid diagnosis to nearly one million people without. People were 1.6 times more likely to develop long covid if they had a variant in a gene called FoxP4. That same gene is also known to be a culprit in lung cancer and severe covid.

While these studies help explain the wide range of responses to the virus, many questions remain unanswered. For example, why were some people not just asymptomatically infected, but never infected? Casanova is interested in, say, that “health care worker without a mask in 2020 that has repeatedly tested negative, negative, negative. They’re seemingly resistant to infection and we think there’s a genetic basis for that." His lab is currently busy analysing some 2,000 genomes among that group to try to fish out the gene responsible.

Scientists would also like to understand if there are genes involved in other, rarer situations, like the people whose infections cause brain swelling, or others that get a form of heart inflammation called myocarditis after getting mRNA vaccines.

Like all science, understanding the genetic link to susceptibility is just pulling on the first thread. So much other work needs to be done to unravel the rest. Hollenbach’s findings about asymptomatic covid, for example, should prompt more exploration into alternate approaches to vaccination. The existing vaccines all try to prevent infection altogether, but there could be merit in focusing on vaccines designed to take advantage of that memory T-cell response that seems to work so well for people with the right genetics. “Maybe you get infected, but manage it so quickly and effectively that you don’t experience illness," she says.

It is important to keep unraveling these mysteries well past the pandemic. They teach us about better ways to address this virus, Sars-CoV-2, which we know is here to stay, and also contribute to the broader understanding of how genes shape our immune response.

Lisa Jarvis is a Bloomberg Opinion columnist covering biotech, health care and the pharmaceutical industry.

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Published: 24 Jul 2023, 09:34 PM IST
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