Summary
Project Summary Influenza infection in susceptible patients results in a higher viral load, cytokine storm, tissue damage, lung function decline, and mortality. It is well known that interferons control influenza burden and inflammatory responses. However, mechanistic understandings of IFN-mediated regulation of influenza burden in the lung epithelial cells is unclear. We have identified a novel association between Endoplasmic Reticulum (ER)-specific-autophagy response, termed ER- phagy, as regulators of the influenza burden in lung epithelial cells. Characterizing the epithelial ER-Phagy-IFN
