Virus-induced heterodimer formation between IRF-5 and IRF-7 modulates assembly of the IFNA enhanceosome in vivo and transcriptional activity of IFNA genes.

Transcription factors of the interferon regulatory factor (IRF) family have been identified as critical mediators of early inflammatory gene transcription in infected cells. We have shown previously that IRF-5, like IRF-3 and IRF-7, is a direct transducer of virus-mediated signaling and plays a role in the expression of multiple cytokines/chemokines. The present study is focused on the molecular mechanisms underlying the formation and function of IRF-5/IRF-7 heterodimers in infected cells.