Genetic variants that are linked to immune signalling, mucus production and other functions increase the risk of critical COVID-19.
, defined by lung inflammation that leads to respiratory failure. To suss out more variants, Baillie and his co-authors analysed the genomes of nearly 7,500 people who had been treated for severe COVID-19 in UK intensive-care units. The researchers then compared these genomes with those of more than 48,000 people in the general population; the team’s data suggest that people in this group did not develop severe disease.
Baillie says that the functions of the genes implicated by the new analysis suggest two potential pathways for developing severe COVID-19. Five of the connected variants have roles in an immune-messaging system that relies on signalling molecules called interferons, which cells secrete in response to infection. This suggests that some people become critically ill after their immune systems initially fail to curb the virus’s reproduction.
The team also linked severe COVID-19 to genetic variants involved in blood clotting and mucus production. The variants in this category might predispose people to lung inflammation or clotting, meaning that even relatively low levels of the virus in the body could still lead to dangerous illness.
Similar associations have already borne fruit. In 2020, Baillie and his colleagues cited a variant uncovered in their previous research
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