lunes, 28 de septiembre de 2020

Coronavirus [NEW TOPIC PAGE]

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Coronavirus

We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern TLR3- and IRF7-dependent type I interferon (IFN) immunity to influenza virus, in 659 patients with life-threatening COVID-19 pneumonia, relative to 534 subjects with asymptomatic or benign infection.
101 of 987 patients with life-threatening COVID-19 pneumonia had neutralizing IgG auto-Abs against IFN-? (13 patients), the 13 types of IFN-a (36), or both (52). These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1,227 healthy individuals.
From the first months of the COVID-19 pandemic, scientists baffled by the disease’s ferocity have wondered whether the body’s vanguard virus fighter, a molecular messenger called type I interferon, is missing in action in some severe cases. Two papers published this week confirm that suspicion. They reveal that in a significant minority of patients with serious COVID-19, the interferon response has been crippled by genetic flaws or by rogue antibodies that attack interferon itself.
The code: How genetic science helped expose a secret coronavirus outbreak
S Kaplan et al, Washington Post, September 25, 2020
The coronavirus mutates as it moves through its victims. Infectious particles swabbed from a patient’s nose carry small but distinctive differences in its genome that can be used, like a molecular bar code, to track where the virus came from and how it had been transmitted.

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