Classical death-receptor-mediated extrinsic apoptotic pathways stimulated by reovirus infection execute the death response [16] . Treatment of cells with soluble TRAIL receptors or expression of a dominant-negative form of Fas-associated death domain (FADD) protein blocks apoptosis, demonstrating that signaling via death receptors is required for execution of the apoptotic program [17] . In keeping with the function of extrinsic apoptotic signaling in reovirus infection, caspase-8 activation [18] and Bid cleavage [19] are observed in cells infected with reovirus [16] . Reovirus infection also stimulates intrinsic apoptotic pathways, as evidenced by release of cytochrome c and Smac/DIABLO from the mitochondria and activation of caspase-9 [16, 20, 21, 22, 23] . Concordantly, reovirus-induced apoptosis is dampened by over-expression of Bcl-2 [24] , which inhibits mitochondrial apoptotic pathway activation [25] .