The pathogenesis of HIV infection is based on three interrelated events: (i) the ability to infect T-CD4+ lymphocytes and macrophages, which is determined by the expression of the HIV cell receptor CD4 [16,17], and a member of the chemokine receptor family acting as a co-receptor, namely, CCR5, CXCR4, or other alternative receptors [18,19]; (ii) the establishment of latently infected cells harbouring the HIV genome integrated into the chromosomal DNA of the cell [20]; and (iii) the induction of immune hyperactivation throughout infection, leading to accelerated immune senescence [21]. This evidence concerns the gene CXCR4 and HIV infectious disease.