It is not known how activation of NF-kB by reovirus culminates in cell death. Three previous studies have attempted to identify proapoptotic host genes that serve as effectors of the death response following reovirus infection. In the first, gene-expression profiles following infection with reovirus strains type 1 Lang (T1L) and type 3 Abney (T3A), which differ in the capacity to induce apoptosis [58] , were compared by microarray analysis [59] . These experiments did not demonstrate differences in expression of death ligands or their respective receptors following infection by either strain. Thus, it was concluded that expression of these death mediators by reovirus is unlikely to contribute to apoptosis induction by reovirus. However, some differences were observed in expression of regulators of death-receptor signaling [59] . But since T1L and T3A display significant genetic diversity and vary in the modulation of multiple signaling pathways [9, 60] , the contribution of NF-kB to the expression of prodeath genes could not be established. In the second study, gene-expression profiles following T3D infection in the presence and absence of functional NF-kB were compared [61] . Although this study identified several NF-kB-dependent genes that coordinate the cellular antiviral immune response, including numerous interferon-stimulated genes (ISGs), no classical components of death receptor-mediated signaling pathways or proapoptotic Bcl-2 family members were significantly upregulated in response to reovirus infection. In the third study, gene-expression profiles of reovirus strains that differ in the capacity to elicit translational shutoff were compared [62] . This study also demonstrated an increase in ISG expression but did not identify obvious NF-kB-dependent candidates that could serve to activate death receptor signaling.