After infection with influenza A virus (IAV), the viral protein PB1-F2 transfers to the IMM via the translocase of the outer mitochondrial membrane 40 (TOM40), activates OMA1 located in the inner membrane, and then shears L-OPA1, resulting in fragmentation of mitochondria (Yoshizumi et al., 2004); PB1-F2 has also been proved to bind to MAVS, thus inhibiting RLR-dependent antiviral immune response (Varga et al., 2012), but it is still unclear whether there is a functional relationship between mitochondrial fragmentation mediated by PB1-F2 and innate immune impairment. Here, F2 is linked to infection.