Study says Covid-19 causes ‘unexpected’ cellular response in lungs

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<strong>Researchers have discovered a surprising response in lung cells infected with the SARS-CoV-2 virus, which might explain why the disease is so difficult to treat.</strong></p>
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The study, published in the journal Science Immunology, found that a biochemical pathway, known as the immune complement system, is triggered in lung cells by the virus.<br />
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"We observed that SARS-CoV2 infection of these lung cells causes expression of an activated complement system in an unprecedented way," said researcher Majid Kazemian from the Purdue University.<br />
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"This was completely unexpected to us because we were not thinking about activation of this system inside the cells, or at least not lung cells. We typically think of the complement source as the liver," Kazemian added.<br />
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The researchers propose that the pairing of antiviral drugs with drugs that inhibit this process may be more effective.<br />
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Using an in vitro model through human lung cells, they found that the antiviral drug Remdesivir, in combination with the drug Ruxolitinib, inhibited this complement response.<br />
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This is despite recent evidence that trials of using Ruxolitinib alone to treat Covid-19 have not been promising.<br />
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To identify possible drug targets, the research team examined more than 1,600 previously FDA-approved drugs with known targets, the researchers said.<br />
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"We looked at the genes that are up-regulated by Covid-19 but down-regulated by specific drugs, and Ruxolitinib was the top drug with that property," he said.<br />
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Within the last few years, scientists have discovered that the immune complement system — a complex system of small proteins produced by the liver that aids, or complements, the body's antibodies in the fight against blood-borne pathogens — can work inside cells and not just in the bloodstream.<br />
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Surprisingly, the study found that this response is triggered in cells of the small structures in the lungs known as alveoli, Kazemian said.</p>
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<em>(IANS)</em></p>