IRF-7 is a member of the interferon regulatory transcription factor family that plays key regulatory roles in innate immunity. Upon virus infection, IRF-7 forms a complex with MyD88 and TRAF6 when stimulated by toll-like receptors TLR7, TLR8, and TLR9, which in turn results in nuclear translocation and induction of interferon gene expression. IRF-7 gene expression is upregulated by the stimulation of interferon through the Jak-STAT signaling pathway, which forms a positive feedback loop. The protein level of IRF-7 after activation is then downregulated by the ubiquitin-proteasome system to avoid excessive production of interferons that may cause damage to the host. Virus induced type I interferon expression was completely abrogated in IRF-7 knockout mice, suggesting that IRF-7 is critical for interferon mediated host defense during virus infection.