Mammalian reoviruses injure infected cells via apoptosis both in culture and in tissues of infected animals. As such, studies of these viruses have contributed to an understanding of how virus infection culminates in apoptotic cell death. Unlike other viruses in which virulence correlates with cell-death capacity, the identity of viral and cellular factors that regulate reovirus-induced apoptosis in cell culture are for the most part known [4, 5, 6, 7, 8, 9, 10] . Moreover, many of these intermediaries also modulate reovirus-induced apoptosis in vivo [4, 7, 11, 12] . Studies using reassortant reoviruses [5, 6] , ectopically expressed proteins [13] , and genetically engineered reovirus mutants [4, 7] highlight a critical role for reovirus outer-capsid protein m1 in apoptosis induction. Collectively, these studies indicate that prodeath signaling evoked by m1 occurs subsequent to membrane penetration but prior to synthesis of viral RNA or protein [4, 7, 14, 15] .