Abstract Viral infection can activate cytokine expression and trigger cell death. Programmed necrosis, like apoptosis, eliminates pathogen-infected cells as a component of host defense while also regulating the function and survival of professional immune cells, including T cells. Receptor-interacting protein kinase (RIPK3) has been shown to mediate programmed necrosis induced by certain viral infections. Deficiency of RIPK3 results in compromised elimination of pathogen-infected cells and increased viral burdens. We present evidence for this effect in mice acutely infected with influenza A virus (IAV). RIPK3-deficient (RKO) mice have significantly increased body weight loss after both mild IAV x31 infection and severe IAV PR8 infections, with decreased survival in the latter case and significantly increased viral loads in the lungs compared to littermate controls. However these effects were primarily observed after day 7 post infection, indicating that regulation of death in the virally-targeted epithelial cell was not the cause of the observed pathogenic phenotype. Indeed, ex-vivo tetramer and ICCS assays showed significantly diminished virus-specific CD8 T cell responses with a reduced frequency of bifunctional IFNγ+ and TNFα+ cells and a lower MFI of IFNγ production by RKO CD8 T cells suggesting that the increased viral loads and weight loss in RKO animals may be a result of reduced T cell activity. Current studies are addressing the role of RIPK3 in regulating T cell function.