Gladstone Institute of Virology and Immunology, University of California, San Francisco, San Francisco, California, USA.
Curr Opin HIV AIDS. 2011 Jan;6(1):19-24. doi: 10.1097/COH.0b013e3283412384.
A reservoir of latently infected cells remains in HIV-infected patients treated with highly active antiretroviral therapy treatment. Persistence of HIV in this latent reservoir has prevented full viral eradication. In order to understand and develop rational therapeutics to flush out HIV latency, the molecular mechanisms governing the phenomena of HIV latency need to be understood. Several mechanisms have been proposed to explain HIV latency.
Epigenetic regulation of the HIV promoter in the 5' long terminal repeat of HIV-1 via histone protein modifications and the presence of inhibitory nucleosomes play a critical role in the establishment, maintenance, and reactivation of HIV latency. Recent reports have shed further light on how HIV latency might be epigenetically regulated. In this review, we discuss how these recent reports broaden our understanding of how HIV latency is regulated. Here, we review how histone modifications and chromatin remodeling affect the transcriptional activity of the HIV promoter in the context of HIV latency.
These new epigenetic regulators of HIV latency pose as potential interesting candidates for therapeutics against HIV latency.
在接受高效抗逆转录病毒疗法治疗的 HIV 感染患者中,存在潜伏感染细胞的储存库。HIV 在这种潜伏储库中的持续存在阻止了病毒的完全清除。为了理解和开发合理的治疗方法以清除 HIV 潜伏,需要了解控制 HIV 潜伏现象的分子机制。已经提出了几种机制来解释 HIV 潜伏。
HIV-1 5'长末端重复序列中 HIV 启动子的表观遗传调控通过组蛋白蛋白修饰和抑制性核小体的存在,在 HIV 潜伏的建立、维持和激活中发挥着关键作用。最近的报道进一步阐明了 HIV 潜伏可能如何受到表观遗传调控。在这篇综述中,我们讨论了这些最新报道如何拓宽我们对 HIV 潜伏调控的理解。在这里,我们回顾了组蛋白修饰和染色质重塑如何在 HIV 潜伏的背景下影响 HIV 启动子的转录活性。
这些 HIV 潜伏的新的表观遗传调节剂为针对 HIV 潜伏的治疗提供了潜在的有趣候选物。