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SARS-CoV-2 Prevents Lung Tissue Repair and Regeneration-ScienceDaily

 


Lung autopsy and plasma samples of people who died of COVID-19 provide a clearer picture of how the SARS-CoV-2 virus spreads and damages lung tissue. National Institutes of Health scientists and their collaborators Scientific translation medicineIt may help predict severe and long-term cases of COVID-19, especially among high-risk people, and inform them of effective treatments.

Although the study was small (18 lung samples and 6 plasma samples), scientists have shown that their data tend to help develop new COVID-19 therapies, existing at various stages. It states that it will fine-tune when to use the treatment of the disease. The findings show how SARS-CoV-2, the virus that causes COVID-19, spreads to the lungs, manipulates the immune system, causes widespread thrombosis that cannot be resolved, and causes lung failure, fibrosis, and disorders. Tissue repair that includes details on how to target facilitating signaling pathways. Researchers say the data are particularly relevant for the care of patients with COVID-19 who are elderly, obese, or suffering from diabetes. All of these are considered high-risk populations of severe cases. The study sample was from at least one high-risk patient.

The study included patients who died between March and July 2020, with a death time of 3 to 47 days after the onset of symptoms. This various time frame allowed scientists to compare short-term, medium-term, and long-term cases. All cases showed findings consistent with diffuse alveolar injury. This impedes the proper flow of oxygen into the blood and ultimately thickens and hardens the lungs.

They also found that SARS-CoV-2 directly infects basal epithelial cells in the lungs, repairing damaged airways and lungs and interfering with their essential function of producing healthy tissue. This process is different from how the flu virus attacks lung cells. It provides scientists with additional information to use when evaluating or developing antiviral therapies.

Researchers at the National Institutes of Allergic Infectious Diseases at NIH led the project in collaboration with the National Institutes of Biomedical Imaging and Bioengineering and the US Food and Drug Administration. Other collaborators included the Seattle Institute for Systems Biology. University of Illinois at Champaign; St. John’s Cancer Institute in Santa Monica, California. USC Keck School of Medicine in Los Angeles. University of Washington Harbor View Medical Center, Seattle; University of Vermont Medical Center, Burlington; Memorial Sloan Kettering Cancer Center in New York City.

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