By contrast, the predominant mechanism for the inhibition of the R5 HIV-1 infection by the A120 mAb is most likely due to the production of the CCR5-binding β-chemokines, especially MIP-1α, from activated T cells and monocytes leading to down-modulation of CCR5 expression on CD4+ T cells. The gene discussed is CCL3; the disease is HIV-1 infection.