‘Decisive discovery’ explains why some COVID-19 infections become serious


One of the earliest challenges in fighting COVID-19 was overcoming the manifestations and consequences of infection. The virus initially appeared to focus its attack on the body’s respiratory system, but varied from asymmetry to death in cases ranging from epidemics to death.]

A team of researchers set out to explain why the infection results 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 protect the body from a foreign pathogen or virus.


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Lack of these important genes may make some individuals more susceptible to infectious disease such as COVID-19, which may help explain why some COVID-19 patients have more severe infections than others.

Results from an early study appear to support this theory: Researchers found that 10.2 percent of 987 patients experienced a severe COVID-19 infection, with a congenital genetic error where autoantibodies — cells that were mislabeled. When invading the body – Interfering with IFNs means encouraging an immune response to fight an infection.

Other patients with less severe or asymptomatic COVID-19 diseases did not have the same autoantibody count, meaning that their IFNs could properly fight the virus.

Autoantibodies were found in patients prior to COVID-19 infection, meaning that people with this genetic trait could be notified of a fatal COVID-19 case.

Specifically, 94 percent of men with a severe COVID-19 infection associated with a high autoantibody count were.

The report concluded, “These findings provide the first explanation for the excess of men in patients with life-threatening COVID-19 and risk.” “They provide a means of identifying individuals at risk of developing life-threatening COVID-19 and ensuring their enrollment.” [sic] In vaccine trials. “

Second study Worked to support this literature by examining the structure of the genome of 659 patients with life-threatening coronovirus infection. They found that mutations at some gene loci that transmit the immune response to IFNs correspond to a high-risk COVID-19 infection.

Researchers can infer from this data that genetic mutations in cells can lead to more severe COVID-19 infections to help fight infectious diseases. This also suggests that treatment aimed at supporting IFNs “may be of therapeutic benefit in selected patients, at least early during SARS-CoV-2 infection.”


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