Because chronic immune responses against herpes virus can shape the CD8 repertoire [8], [20] and that HLA-B8 individuals have been shown to develop public anti-EBV responses [21] that can be studied by HLA-B*0801/EBNA-3A tetramers, we tested whether the observed TCR Vβ repertoire alteration could be explained by EBV infection. The gene discussed is CD8A; the disease is Epstein-Barr virus infection.