Upon recognition of RNA virus by retinoic acid inducible gene-I (RIG-I), MAVS functions as the adaptor to drive the phosphorylation of interferon regulatory factor 3 (IRF3), followed by IFN-β transcription.15,16 Intriguingly, stress has been reported to impact the mitochondria function and dynamics, which raised the possibility that stress-inhibited IFN-β response might stem from the deterioration of MAVS antivirus signaling.17,18 In this study, we utilized restraint stress mouse model to elucidate the potential mechanism responsible for stress-increased susceptibility to influenza. This evidence concerns the gene IRF3 and influenza.