While global IFN null mouse models have been instrumental in defining a critical role of IFN signaling in the control of gammaherpesvirus infection, the profoundly altered pathogenesis of MHV68 infection in these models precludes understanding of the role of cell type-specific IFN signaling during latent infection of an immunocompetent natural host. Here, IFNA1 is linked to disease arising from reactivation of latent virus.