Viral infection triggers the innate antiviral response in part through activation of RIG-I,a cytoplasmic sensor of 5'-triphosphorylated and uncapped single- or double-stranded RNA,which are not found among endogenous selfRNA.RIG-I signaling depends on the function of mitochondrial antiviral signaling (MAVS) protein,an adapter that links RIG-I,and the related RNA sensor MDA5,to events leading to transcriptional activation by NF-κB and IRF3.In contrast to the cytoplasmic localization of other innate immune signaling adapters,MAVS is positioned at mitochondrial membranes [ 1 ],and to a lesser extent at peroxisomal membranes [2],by virtue of a C-terminal transmembrane domain.