Story at a glance
- Two studies examining interferon genes found patients with a severe COVID-19 infection lacked in these crucial genes.
- A disproportionate amount of people with this condition were male patients.
One of the earliest challenges in fighting COVID-19 was confronting the plethora of manifestations and outcomes of an infection. The virus initially appeared to focus its attack on the body’s respiratory system, but cases have varied from asymptomatic to fatal as the pandemic continues.
A team of researchers set out to explain why infection outcomes varied so dramatically and found that the answer may lie in genes within the immune system.
Published in Science, two studies conducted by the same team focus on genes called interferons (IFNs), which are proteins that help the body defend itself against a foreign pathogen or virus.
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A lack in these crucial genes can make certain individuals more susceptible to infectious disease like COVID-19, which may help explain why some COVID-19 patients have more severe infections than others.
Results from an initial study appear to support this theory: Researchers found that 10.2 percent of 987 examined patients who experience a severe COVID-19 infection had an inborn genetic error where autoantibodies — cells that erroneously attack the body — interfere with IFNs meant to help stimulate an immune reaction to fight an infection.
Other patients with less severe or asymptomatic COVID-19 illnesses did not present the same autoantibody counts, meaning their IFNs could fight the virus properly.
The autoantibodies were found in patients prior to a COVID-19 infection, implying that people with this genetic trait may be predisposed to a deadly COVID-19 case.
Notably, 94 percent of patients with a severe COVID-19 infection linked to high autoantibody counts were male.
“These findings provide a first explanation for the excess of men among patients with life-threatening COVID-19 and the increase in risk with age,” the report concluded. “They also provide a means of identifying individuals at risk of developing life-threatening COVID-19 and ensuring their enrolment [sic] in vaccine trials.”
The second study worked to support this literature by examining the genome structure of 659 patients with a life-threatening coronavirus infection. They found that mutations in certain gene loci that also communicate immune responses to IFNs correspond to a high-risk COVID-19 infection.
Researchers can gauge from this data that genetic mutation in cells meant to help fight infectious diseases could lead to a more severe COVID-19 infection. It also suggests that therapies aimed at supporting IFNs “may be of therapeutic benefit in selected patients, at least early in the course of SARS-CoV-2 infection.”
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