The innate antiviral response requires the induction of genes and proteins with activities that limit virus replication. Among these, the well-character-ized interferon b (IFNB) gene is regulated through the cooperation of AP-1, NF-jB and interferon regulatory factor 3 (IRF-3) transcription fac-tors. Using a constitutively active form of IRF-3, IRF-3 5D, we showed previously that IRF-3 also regulates an IFN-independent antiviral response through the direct induction of IFN-stimulated genes.
