Severe COVID-19 is identified as a viral response path

Severe COVID-19 is identified as a viral response path ...

Researchers at Yale have identified a specific immune response technique that can result in severe illness and fatalities among people infected with the SARS-CoV-2 virus.

The study was published in the journal Nature on April 28.

Researchers have discovered that once the COVID-19 virus infects the lungs it can trigger something called a cytokine storm or an overactive immune response that leads to deadly inflammation in the lungs. For the first time, a Yale team led by Esen Sefik, senior author ofRichard Flavell, examined the effects of SARS-CoV-2 infection in mice that were engineered to have a human immune system.

Inflammasomes, a component of the immune systems early warning system, produce and release cytokines which cause these immune cells to commit suicide in an attempt to avoid infection. However, these cytokines also recruit more inflammatory cells to the lungs from the blood, which results in a fatal cycle.

The broadcast system works like a broadcast system, but in this case, the message is lethal, according to Flavell, Sterling''s Professor of Immunobiology and investigator at the Howard Hughes Medical Institute.

Researchers used COVID-19''s mouse model to help rescue infected mice from pneumonia by blocking the NLPR3 inflammasome pathway. However, immune systems cells were still infected. However, they were no longer inflammatory and therefore could not lead to harmful levels of inflammation.

One of the benefits of this treatment is that the cells no longer die and thus further release the virus. Nonetheless, blockade of the inflammasome pathway along with antiviral therapy might provide a path to treat COVID-19 pneumonia and prevent severe COVID-19 cases, according to researchers.

Although there are no approved medications that block the NLPR3 pathway, several pharmaceutical and biotech companies are developing them, according to Flavell.

The Howard Hughes Medical Institute has funded the research.

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