These data are supported by published studies demonstrating that either CD8 deficiency or β2-microglobulin (β2-m) deficiency is associated with increased latency and persistent replication [25,40–42], and by studies showing that antibody-mediated depletion of CD8 T cells from wild-type mice results in increased latent infection [20,43]. This evidence concerns the gene CD8A and disease arising from reactivation of latent virus.