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Interferon regulatory factor (IRF)-1 is an immunomodulatory transcription factor that functions downstream of pathogen recognition receptor signaling and has been implicated as a regulator of type I interferon (IFN)-αβ expression and the immune response to virus infections. However, this role for IRF-1 remains controversial because altered type I IFN responses have not been systemically observed in  IRF-1   -/-  mice. To evaluate the relationship of IRF-1 and immune regulation, we assessed West Nile virus (WNV) infectivity and the host response in  IRF-1   -/-  cells and mice.  IRF-1   -/-  mice were highly vulnerable to WNV infection with enhanced viral replication in peripheral tissues and rapid dissemination into the central nervous system. Ex vivo analysis revealed a cell-type specific antiviral role as  IRF-1   -/-  macrophages supported enhanced WNV replication but infection was unaltered in  IRF-1   -/-  fibroblasts. IRF-1 also had an independent and paradoxical effect on CD8 +  T cell expansion. Although markedly fewer CD8 +  T cells were observed in naïve animals as described previously, remarkably,  IRF-1   -/-  mice rapidly expanded their pool of WNV-specific cytolytic CD8 +  T cells. Adoptive transfer and in vitro proliferation experiments established both cell-intrinsic and cell-extrinsic effects of IRF-1 on the expansion of CD8 +  T cells. Thus, IRF-1 restricts WNV infection by modulating the expression of innate antiviral effector molecules while shaping the antigen-specific CD8 +  T cell response.

Interferon Regulatory Factor-1 (IRF-1) Shapes Both Innate and CD8+ T Cell Immune Responses against West Nile Virus Infection