HIV cure is impeded by the persistence of a strenuous reservoir of latent but replication competent infected cells, which remain unsusceptible to c-ART and unrecognized by the immune system for elimination. Ongoing progress in understanding the molecular mechanisms that control HIV transcription and latency has led to the development of strategies to either permanently inactivate the latent HIV infected reservoir of cells or to stimulate the virus to emerge out of latency, coupled to either induction of death in the infected reactivated cell or its clearance by the immune system. This review focuses on the currently explored and non-exclusive pharmacological strategies and their molecular targets that 1. stimulate reversal of HIV latency in infected cells by targeting distinct steps in the HIV-1 gene expression cycle, 2. exploit mechanisms that promote cell death and apoptosis to render the infected cell harboring reactivated virus more susceptible to death and/or elimination by the immune system, and 3. permanently inactivate any remaining latently infected cells such that c-ART can be safely discontinued.

大量潜伏但具有复制能力的受感染细胞的持续存留，阻碍了HIV的治愈，这些细胞对c-ART仍然不敏感，免疫系统也无法消除。在了解控制HIV转录和潜伏期的分子机制方面的不断进步，导致了开发策略以永久性灭活被HIV感染的潜伏性细胞库或刺激病毒摆脱潜伏期，从而诱发死亡。被感染的活化细胞或其被免疫系统清除。这篇综述着重于当前探索的和非排他性的药理策略及其分子靶标，其1.通过靶向HIV-1基因表达周期的不同步骤，刺激感染细胞中HIV潜伏期的逆转，2。