This adaptive biology was confirmed by our analysis of patients following acute CMV infection, which highlighted a striking expansion of the Vγ9− Vδ2+ subset after infection, linked to the selection of dominant clonotypes, which occurred concomitantly with differentiation from a naive CD27hi to a CD27lo/neg phenotype, and acquisition of CX3CR1 and cytotoxic granzymes, similar to CMV-specific cytotoxic CD8+ T cells46,47. The gene discussed is CD8A; the disease is infection.