Since the original demonstration that CMV seropositivity was associated with phenotypic and functional alterations of T-cell immunity similar to those found in ageing [27], and that CMV infection induces a strong decrease in T cell telomere length [60], cumulative evidences have extensively documented that CMV infection is characterized by the expansion of CD28/CD27 negative or CD57+ senescent T cells, with short telomeres and high production of pro-inflammatory cytokines [25,26,34,54,60,65,66,67,68,69,70,71,72]. This evidence concerns the gene CD28 and cytomegalovirus infection.