In addition to these classical apoptotic pathways, the innate immune response transcription factor, NF-kB, is activated following reovirus infection [8] . NF-kB activation by reovirus depends on the viral m1 protein and can be accomplished by genome-deficient reovirus particles [4, 7, 8] . Blockade of NF-kB signaling using chemical inhibitors or cell lines genetically deficient in NF-kB p50, NF-kB p65/RelA, IkB kinase (IKK)-a, or IKK adaptor IKKc/NEMO significantly diminishes reovirus-induced apoptosis [8, 28] . Consistent with these findings, activation of NF-kB occurs within the first few hours of reovirus infection and precedes the biochemical and morphological hallmarks of apoptotic cell death [8, 28] . These observations suggest that NF-kB couples m1-mediated events to the cellular apoptotic machinery. Although regulation and function of NF-kB has been extensively studied, the precise relationship between NF-kB and the cell-death machinery remains undefined.