Innate immune sensing of influenza virus through IFI16 promote pyroptosis.

We report that IFI16, which was previously identified as a cytosolic DNA sensor, is essential for the activation of programmed cell death pathways in IAV infected cells. We have identified IFI16 as an innate immune sensor of the influenza A virus. We find that IFI16 recognizes viral genomic RNA upon infection. The activation of IFI16, in turn, triggers the production of type I, III interferons, and also other pro-inflammatory cytokines via the STING-TBK1 and Pro-caspase-1 signalling axis, thereby promoting cell death (apoptosis and pyroptosis in IAV infected cells). To investigate the effects of IFI16 on cell death during influenza infecction, A549 cells were transfected with either scrambled shRNA (shSCR) or IFI16 specific shRNA (shIFI), cells were