To determine whether decreased apoptosis in Bid-deficient cells is attributable to alterations in reovirus infection in the absence of Bid, we compared reovirus infectivity in wild-type and Biddeficient cells using an indirect immunofluorescence staining assay ( Figure 2C ). An equivalent proportion of reovirus antigen-positive cells was detected at 20 h post-adsorption of wild-type and Biddeficient cells. These data indicate that reovirus is capable of initiating infection in Bid-deficient cells. To determine whether reovirus completes a full infectious cycle in Bid-deficient cells, wild-type and Bid-deficient cells were adsorbed with T3D, and viral titers were determined by plaque assay at 0, 12, 24, and 48 h after infection ( Figure 2D ). Reovirus replicated with similar kinetics and produced equivalent yields in wild-type and Biddeficient cells. Thus, the failure of Bid-deficient cells to undergo apoptosis in response to reovirus is not a consequence of diminished reovirus infection of these cells. We conclude that Bid is a key regulator of reovirus-induced apoptotic cell death.