More than 10 percent of people who develop severe COVID-19 have misguided antibodies that attack not the virus, but the immune system itself, new research shows. Another 3.5 percent, at least, carry a specific kind of genetic mutation. In both groups, the upshot is basically the same: The patients lack type I interferons, a set of 17 proteins crucial for protecting cells and the body from viruses. Whether the proteins have been neutralized by so-called auto-antibodies, or were not produced in sufficient amounts in the first place due to a faulty gene, their missing-in-action appears to be a common theme among a subgroup of COVID-19 sufferers whose disease has thus far been a mystery. Published online on September 24, 2020 in two papers in Science, the findings help explain why some people develop a disease much more severe than others in their age group—including, for example, individuals who required admission to the ICU despite being in their 20s and free of underlying conditions. The findings may also provide the first molecular explanation for why more men than women die from the disease. The two open-access Science articles are “Auto-Antibodies Against Type I IFNs in Patients with Life-Threatening COVID-19” (https://science.sciencemag.org/content/early/2020/09/23/science.abd4585) and “Inborn Errors of Type I IFN Immunity in Patients with Life-Threatening COVID-19” (https://science.sciencemag.org/content/early/2020/09/29/science.abd4570). “These findings provide compelling evidence that the disruption of type I interferon is often the cause of life-threatening COVID-19,” says Jean-Laurent Casanova, MD, PhD, Head of the St.
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