This accords with observations in HIV-infected subjects monitored by Ki67 expression and ex vivo BrdU incorporation.[29] Similarly, in patients with acute infectious mononucleosis, we previously observed a similar phenomenon: massive alterations in CD8+CD45R0+ memory T-cell kinetics were associated with only minor changes in CD45RA+ cell kinetics.[31] Slow turnover CXCR4+ naïve cells thus appear relatively protected from apoptosis. The gene discussed is CD8A; the disease is infectious mononucleosis.