When a protein linked to persistent inflammation is inhibited, mice infected with COVID-19 have healthier lungs.
According to a research that examined lung samples from COVID patients, a signaling molecule that aids in kicking off lung inflammation may be crucial in exacerbating certain persistent symptoms of the illness.
The results, which were published on July 17 in Science Translational Medicine, may aid researchers in creating longer-lasting COVID therapies. Long-term COVID can cause symptoms like exhaustion, brain fog, dyspnea, and lung damage, and it can linger for months or even years following infection with the SARS-CoV-2 virus, which is the source of COVID-19.
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According to study co-author Jie Sun, an immunology researcher at the University of Virginia in Charlottesville, “we were able to dampen the chronic conditions after infection” by blocking the chemical known as interferon gamma (IFN-γ) in mice infected with COVID-19. “We may target this pathway in the future as a possible treatment for long COVID.”
Protein involved with inflammation
The body produces a variety of proteins to combat infections, one of which is IFN-γ. It propagates inflammation and transmits signals to other immune cells when it is released by T cells, a subset of white blood cells. While this helps the healing process in the short term by increasing blood flow to the affected region, long-term inflammation may harm tissues and cells.
Prior studies have shown that individuals with prolonged COVID have higher IFN-γ2 levels, and data also implies that the protein may be involved in damage to the alveoli3—the fragile lungs’ air sacs responsible for transferring gases into and out of the bloodstream. However, these investigations were unable to establish whether IFN-γ is only a sign of a different mechanism or the actual cause of lung damage linked to prolonged COVID.
Sun and his colleagues used a two-pronged method to look into this. In order to compare lung samples from individuals with prolonged COVID-19 with those from individuals who had recovered from COVID-19 a few weeks before to the study and a control group that had not been infected, the researchers first recruited individuals with lengthy COVID. They examined the composition of the lung-cell samples using a method known as single-cell RNA sequencing. Researchers found that samples from individuals with long-term COVID-19 infection had greater amounts of T cells that produce IFN-γ than those from individuals without COVID-19 or from those who had recovered from the infection.
Next, the scientists gave SARS-CoV-2 to mice. The mice exhibited, twenty-one days after infection, a cellular response in their lungs like that of individuals with prolonged COVID-19, including increased numbers of T cells that produce IFN-γ.
A substance that suppresses IFN-γ was given to some of the infected mice by the researchers. The animals’ total pulmonary inflammation was much reduced, as were the immune cells that fuel the inflammation and the deposits of collagen, a material that may harm and scar lung tissue. These observations indicated that the animals’ general health had greatly improved.
upcoming therapies
The group believes that individuals with lengthy COVID might benefit similarly by targeting IFN-γ. As an immunologist at the International Centre for Infectiology Research in Lyon, France, and a longtime COVID sufferer herself, Stéphanie Longet adds, “The next step would be to see if we can use a treatment which impacts this pathway to see if symptoms are improved in patients.” She continues by pointing out that there are existing medications on the market that block IFN-γ, such baricitinib, which is used to treat severe COVID-19 and lessen rheumatoid arthritis-related inflammation.
The significance of examining other plausible causes of extended COVID-19, which is estimated to impact millions of individuals globally, is underscored by the researchers. Sun states, “It’s likely that this is one component of a prolonged COVID condition.” “In order to help identify more targets in the future, we want to investigate a wider variety of mechanisms.”
