Here, we used NTAmers on well-identified virus-specific TCRαβ clonotypes or at the polyclonal CD8 T cell population level and observed for the first time a differential impact of TCR-pMHC binding kinetics on the long-term TCR clonal evolution during CMV (i.e. pp65 and IE-1) versus EBV/BMFL1 latent infection. The gene discussed is CD8A; the disease is disease arising from reactivation of latent virus.