This stuff adds fuel to COVID-19 inflammation, blood clots
In a recent study published in JCI Insight, researchers found another functional autoantibody in COVID-19 patients that contributes to the disease’s development and the “firestorm” of blood clots and inflammation it induces.
The study is from Michigan Medicine. One author is Yu (Ray) Zuo, M.D.
A growing body of studies suggests COVID-19 emulates many aspects of systemic autoimmune disorders, including the release of a flurry of overactive immune cells that produce toxic webs of proteins and DNA called neutrophil extracellular traps, or NETs.
In this study, the team analyzed serum from over 300 hospitalized COVID patients, searching for a novel autoantibody that shields the toxic NETs from being destroyed and produces a lasting noxious effect in a patient’s body.
The results showed strongly increased levels of the anti-NET antibodies in many of the participants. Those with higher levels of autoantibodies were more likely to develop severe COVID-19 symptoms.
Researchers generated NETs in the lab and incubated them with COVID patient serum. They found the serum from patients with higher levels of anti-NET antibodies struggled to degrade the toxic traps.
The team also spiked healthy serum with anti-NETs purified from the infected patients. While a healthy person’s serum should completely disintegrate the extracellular traps, the purified anti-NET antibodies strongly hindered the process.
The team says that people with severe forms of COVID have higher amounts of these neutrophil extracellular traps, which amplify inflammation and promote blood clot formation.
They have now found that this process is exacerbated by the anti-NET antibodies, which disrupt our body’s immune homeostasis during COVID-19 infection.
How COVID-19 manages to trigger the production of a variety of autoantibodies, including anti-NETs, remains unknown.
Further study of the virus’ autoimmune aspects, will not only lead to a better understanding of the disease but will also likely shed light on the origins of autoimmune diseases.
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