title: Connecting mitochondria and innate immunity.
abstract: Viral infection results in the activation of multiple signaling pathways, but how these pathways are coordinated remains a mystery. Two studies, one published in this issue of Cell (Seth et al., 2005) and the other in Molecular Cell (Xu et al., 2005), identify a new intracellular signaling protein that is required for activating type I interferon expression in response to viral infection. In addition,Seth et al. (2005) show that the function of this protein, which they call MAVS, requires that it be localized to the mitochondria. This observation establishes an unexpected link between innate immunity and an organelle with evolutionary origins in aerobic bacteria.
authors.affiliation: Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
authors.forename: Sarah M
authors.initials: SM
authors.lastname: McWhirter
authors.forename: Benjamin R
authors.initials: BR
authors.lastname: Tenoever
authors.forename: Tom
authors.initials: T
authors.lastname: Maniatis
mesh_terms: D000818:Animals; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000096:biosynthesis / Q000276:immunology; D008928:Mitochondria / Q000276:immunology*; D012330:RNA, Double-Stranded / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology*; D048029:TNF Receptor-Associated Factor 6 / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology*
chemical_list: D007370:Interferon Type I; D012330:RNA, Double-Stranded; D048029:TNF Receptor-Associated Factor 6