Late differentiated CD4+ T cells can also mediate non-cytolytic functional mechanisms to limit CCR5-tropic HIV infection via autocrine production of β-chemokines CCL3 (MIP-1α), CCL4 (MIP-1β) and CCL5 (RANTES), through either blocking the interaction between gp120 and CCR5 or downregulating CCR5 from the cell surface [14]. This evidence concerns the gene CCL5 and HIV infectious disease.