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The study found that the overactivity of genes that control inflammation and immunological responses causes lung fibrosis.
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- Long Covid cases can be very debilitating and resistant to therapy.
- Lung function can continue to decrease even in the absence of a new COVID-19 infection.
- The lungs of people who had symptoms after infection with SARS-CoV-2 looked like the lungs of people with end-stage pulmonary fibrosis.
Stanford University researchers discovered that patients are having breathing issues with COVID-19 owing to lung fibrosis, a disease in which the injured lungs build scar tissue, making it harder for the lungs to stretch and contract.
The study found that the overactivity of genes that control inflammation and immunological responses causes lung fibrosis. According to Gerlinde Wernig, Assistant Professor of Pathology at Stanford University, long Covid cases can be very debilitating and resistant to therapy.
Moreover, Wernig says, lung function can continue to decrease even in the absence of a new COVID-19 infection. The discovery, which was published in the Proceedings of the National Academy of Sciences, raises the prospect of tailored medications intervening to suppress the genes responsible for the harm one day.
In the study, the team started by looking at lung tissue samples from five COVID-19 patients who had symptoms of the disease, such as shortness of breath for one or more months. The lungs of people who had symptoms after infection with SARS-CoV-2 looked like the lungs of people with end-stage pulmonary fibrosis.
The investigators discovered parallels in the pattern of RNA synthesis, which might hint at a cell’s overall function – between tissue samples from long Covid patients and samples from patients with pulmonary fibrosis by analysing single cells from the patient’s tissue samples.
“We saw this same pattern across all human Covid lung samples,” Wernig said. The first Covid-19 virus in the lungs, like other lung infections, triggered an inflammatory response. In the case of long-Covid patients, however, the immunological dysfunction persists long after the virus has been eradicated, akin to chronic pulmonary fibrosis.
The first COVID-19 virus in the lungs, like other lung infections, triggered an inflammatory response. In the case of long-Covid patients, however, the immunological dysfunction persists long after the virus has been eradicated, akin to chronic pulmonary fibrosis. They examined lung fibrosis in mice infected with a SARS-CoV-2-like virus to see if it may be linked to Covid infections and discovered substantial increases in fibrosis and immunological dysfunction.
“After that infection, innate immune cells go berserk,” Wernig added, referring to the component of the immune system that serves as the first line of defence against infections. Scarring in lung tissues increased when animals caught SARS-CoV-2, as did levels of immune cells interleukin-6, CD47, and pJUN in a mouse model tailored to more accurately resemble human biology. There was also a positive aspect to these tests.
“We detected very minimal fibrosis when we ran the identical studies but inhibited CD47 and Il-6,” Wernig added. “This suggests that medications that carry out specific immune blockades might be used to treat extended Covid.”
