Transfection of HeLa cells with HIV-1-VpuD52/56 proviral DNA or infection of activated primary human CD4+ T cells with HIV-1-VpuD52/56 revealed that the β-TrCP-binding mutant was strongly attenuated in its ability to promote HIV-1 particle release and down regulate surface BST2, yet was able to down regulate CD4 at the cell surface to levels comparable to Vpu-deficient or proficient viruses. The gene discussed is BST2; the disease is infection.