Sluis-Cremer Nicolas
Department of Medicine, Division of Infectious Diseases, University of Pittsburgh School of Medicine, S817 Scaife Hall, 3550 Terrace Street, Pittsburgh PA, 15261, USA.
Curr Top Med Chem. 2016;16(10):1191-7. doi: 10.2174/1568026615666150901114138.
While combination antiretroviral therapy (cART) can drive HIV-1 RNA levels to < 50 copies/mL in patient plasma, most infected individuals continue to harbor low-level persistent viremia. Latently infected resting CD4+ T cells are thought to constitute the major reservoir of HIV-1 persistence. In this reservoir, the integrated provirus remains transcriptionally silent as long as the host cell is in a resting state. On discontinuation of cART, these viruses can reactivate and lead to waves of de novo infection events. The prevailing hypothesis in the field is that molecules that reactivate latent HIV-1 infection will purge this reservoir by inducing transcription of the latent provirus, thereby causing cells to undergo apoptosis. This review article summarizes the results of all therapeutic approaches that have been clinically evaluated for their potential to reverse HIV latency.
虽然联合抗逆转录病毒疗法(cART)可使患者血浆中的HIV-1 RNA水平降至<50拷贝/毫升,但大多数受感染个体仍存在低水平的持续性病毒血症。潜伏感染的静息CD4+ T细胞被认为是HIV-1持续存在的主要储存库。在这个储存库中,只要宿主细胞处于静息状态,整合的前病毒就保持转录沉默。停止cART后,这些病毒可重新激活并导致一波又一波的从头感染事件。该领域的主流假说是,重新激活潜伏HIV-1感染的分子将通过诱导潜伏前病毒的转录来清除这个储存库,从而使细胞发生凋亡。这篇综述文章总结了所有已进行临床评估以逆转HIV潜伏可能性的治疗方法的结果。