To assess the capacity of T3SA+ to produce neurological injury in the presence and absence of Bid, we examined hematoxylin and eosin (H&E)-stained coronal brain sections prepared from wildtype and Bid-deficient mice euthanized 10 d following IC inoculation with 5 PFU of T3SA+ (Figure 7) . This time point was chosen to coincide with the presence of maximal viral titers following inoculation by this route. Since the inoculum used for these experiments was at least ,10-fold lower than that used for most other studies of reovirus CNS pathogenesis [4, 7, 11, 12, 43, 48, 51] , the extent of injury following infection of wild-type mice was not as extensive. Nonetheless, inoculation of wild-type mice with T3SA+ resulted in neuronal death in the cerebral cortex, hippocampus, thalamus, and hypothalamus, consistent with previous reports [4, 7, 11, 12, 43, 48, 51] . While the majority of infected wild-type mouse brains showed signs of injury, tissue damage was minimal in all of the brains examined from similarly infected Bid-deficient animals. Examination of the hippocampal region of a representative wild-type mouse brain at higher magnification showed damage to the CA3 region, with the pyramidal cells showing condensed nuclei characteristic of apoptosis ( Figure 7B ). In contrast, little damage was detected in an equivalent region of a Bid-deficient mouse brain ( Figure 7B ). These findings indicate that Bid is required for neurological injury produced by reovirus in mice.