Previous studies have demonstrated that both CD4 T cells and CD8 T cells can control acute replication and latent infection of MHV68 [37, 38], whereas CD4 T cell control of acute and latent infection of MHV68 requires IFN-γ that has also been shown to regulate MHV68 reactivation [39]. Here, IFNG is linked to disease arising from reactivation of latent virus.