Interferon Regulation Of Innate And Antioxidant Responses In Respiratory Syncytial Virus Infection

摘要: Introduction viral-induced lung inflammation and oxidative damage play a critical role in disease pathogenesis. Oxidative stress in the course of RSV infection is due to a reduction in levels of the transcription factor NF-E2-related factor 2 (NRF2), resulting in decreased expression of antioxidant and cytoprotective enzymes, and. RSV-induced NRF2 degradation occurs via the ubiquitin ligase RNF4, which is in vitro in vivo associated with promyelocytic leukemia protein nuclear bodies (PML-NBs). Expression and assembly of PML-NB component is interferon (IFN) inducible. The goal of this study was to determine whether IFN contributes to RSV-mediated disease pathogenesis by affecting innate/inflammatory and antioxidant responses in the lung.