Speaker
Description
It has been shown that infection with a mild respiratory virus prior to infection with a lethal respiratory infection can prevent mortality and morbidity, with influenza A and SARS-CoV-2 being two such viruses where this has been seen. In this study, we investigate the resulting cytokine storm arising from nonlethal single infection of SARS-CoV-2 and nonlethal coinfection of influenza A and SARS-CoV-2 in mice. Through statistical modeling, we identify regulatory cytokines key to inflammation, viral clearance, and lung damage, as measured by serum albumin. Our analysis indicates single infection with SARS-CoV-2 results in a lower accumulation rate of TNFα compared to coinfection with influenza A, a higher accumulation rate of IFNα, and lower rate of damage, as measured by serum albumin. This highlights key cytokines that, when taken together with serum albumin, can be used to form a holistic mathematical model of the cytokine storm resulting from the innate immune response to viral respiratory infection.
