Virus infection results in the activation of a set of cellular genes involved in host antiviral defense. IRF-3 has been identifiedas a critical transcription factor in this process. The activationmechanismof IRF-3 is not fully elucidated,yet it involves a conformational change triggered by the virus-dependent phosphorylation of its C-terminus. This con-formational change leads to nuclear accumulation,DNA binding and transcriptional transactivation.