Although our finding suggests that B7-H1 plays a role in promoting CNS-TRM after virus infection, the absolute number of total CD8+ T-cells that remain in the CNS of mice infected for 98 days was increased in B7-H1KO mice compared to B7-H1WT (Figure 3C), suggesting that non-specified CD8+ T-cell populations fail to contract or are maintained in the CNS at this extended time point post-infection. This evidence concerns the gene CD8A and viral infectious disease.