During latent infection expression of viral UL111A (vIL-10) results in down regulation of MHC class II and diminished CD4+ T cell recognition [49] and latent infection of CD34+ bone marrow progenitor cells induces release of cIL-10 and TGFβ which decreases CD4+ T cell IFNγ production and cytotoxicity [14]. This evidence concerns the gene IFNG and disease arising from reactivation of latent virus.