These approaches are designed to either inhibit infection of CD4+ target cells (e.g., by transplantation of bone marrow stem cells from a CCR5Δ32 donor, knockout of the endogenous CCR5 locus, and/or expression of antagonists that prevent viral entry into potential target cells)6,48,49 or to reverse latency and increase transcription of HIV (e.g., by provision of latency reversal agents such as histone deacetylase inhibitors, Toll-like receptor agonists, or disulfiram),50 thereby effecting virus- or immune-mediated cytolysis of infected cells (“kick-and-kill”). Here, CCR5 is linked to infection.