Although titers of reovirus in the CNS were decreased in Bidnull mice following PO inoculation, it was not clear whether reduced reovirus titer in the CNS was a consequence of diminished reovirus dissemination to the CNS or diminished reovirus replication at that site. To distinguish between these possibilities, we inoculated wild-type and Bid-deficient mice intracranially with 100 PFU of T3SA+ and monitored infected animals for signs of CNS disease and mortality for 21 days (Figure 6A ). At this dose of T3SA+, most wild-type and Biddeficient mice displayed symptoms of neurological disease. Concordantly, both strains of mice succumbed to reovirus-induced disease with equivalent frequency and a median survival time of 13 days. Reovirus titers in the brains of wild-type and Bid-deficient mice also were comparable at 4, 8, and 10 d post-inoculation ( Figure 6B ). These results indicate that following a high-dose Whole cell lysates were prepared at the indicated times after infection or 12 h following TNFa/CHX treatment and resolved in 18% polyacrylamide gels and transferred to nitrocellulose membranes. The membranes were probed with polyclonal antisera specific for Bid or actin and appropriate HRP-conjugated secondary antibodies and visualized using chemiluminescence. doi:10.1371/journal.ppat.1000980.g003 inoculation, Bid is dispensable for reovirus growth in the murine CNS and attendant encephalitis.