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). Overall design: 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