According to researchers, post-Covid-19 breathing issues are caused by lung fibrosis, a condition in which damaged lungs produce scar tissue, making it difficult for lungs to expand and contract.
Stanford University researchers discovered that overactivity of genes that govern 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.
The researchers began by examining lung tissue samples from five Covid-19 patients who exhibited signs of the condition, such as shortness of breath, for one or more months. The lungs of persons who developed symptoms following SARS-CoV-2 infection resembled the lungs of people with end-stage pulmonary fibrosis.
The investigators discovered parallels in the pattern of RNA production – which can 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 patients’ tissue samples.
“We saw this same pattern across all human Covid lung samples,” Wernig said.
The first Covid-19 infection 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 could be linked to Covid infections and discovered significant increases in fibrosis and immunological dysfunction.
“Innate immune cells go crazy after that infection,” Wernig said, referring to the part of the immune system that forms the first line of defence against pathogens.
Scarring in lung tissues increased when animals contracted 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.
“When we did the same experiments but blocked CD47 and Il-6, we saw very little fibrosis,” Wernig said. “This hints at possible treatments for long Covid involving drugs that carry out targeted immune blockades.”