Mitochondrial antiviral signaling adaptor mediated apoptosis in H3N2 swine influenza virus infection is inhibited by viral protein NS1 in vitro

We investigated the in vitro role of mitochondrial antiviral signaling adaptor (MAVS) in apoptosis induced by H3N2 swine influenza virus infection and the influence of viral NS1 (nonstructural protein 1) protein on this process. H3N2 swine influenza virus (SIV, A/Swine/Shandong/3/2005) was co-cultured with human lung epithelial A549 cells. The relationship of MAVS expression to SIV replication and apoptosis, and the influence of viral proteins on MAVS functions were studied. The data indicate that in response to SIV infection, MAVS was significantly upregulated at both the transcriptional and protein levels in the early stages of infection. Its expression and localization to mitochondria are necessary for apoptosis of epithelial cells induced by H3N2 swine influenza virus. Viral protein NS1 can antagonize MAVS-mediated apoptosis. These findings indicate that MAVS have a role in regulating innate mitochondrial responses to viral infection.