Differences in the nature of these β-herpesviruses during latent infection could in part explain the gradual contraction of high avidity CMV/pp65- and CMV/IE-1-specific T cell clonotypes observed over time, contrasting with the striking stability of EBV/BMFL1-specific CD8 T cell clonal repertoires. This evidence concerns the gene CD8A and disease arising from reactivation of latent virus.