Investigating cellular redox modulation upon Influenza A virus infection

Abstract

The Influenza A virus (IAV) is a dangerous respiratory pathogen that infects millions of people worldwide every year, causing significant morbidity and mortality. Although IAV is a well-known virus, much remains unknown about the molecular mechanisms underlying its pathogenesis. One of the key aspects of IAV pathophysiology is its interference with redox homeostasis within cells. IAV causes acute infections leading to a sharp increase in oxidative stress at later stages of infection. However, only few studies attempt to decipher the molecular processes of Influenza A virus-induced redox perturbation. We exploited a genetically encoded redox biosensor to measure cellular redox potential following IAV infection with high sensitivity and temporal resolution. We explored the cell-type differences and IAV strain-to-strain differences in redox regulation, and sought to identify the viral proteins responsible for this regulation. Altogether, our research underscores the importance of careful investigation of the relationship between IAV pathogenesis and redox modulation, with a focus on viral components involved, to aid in the development of effective antiviral therapeutic avenues.