Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.
Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.
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DOI：
10.1155/2012/614120
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Henderson AJ
中科院分区：
文献类型：
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作者：
Schiralli Lester GM;Henderson AJ
长期潜伏的HIV感染细胞导致抗逆转录病毒治疗中断后病毒复制反弹，并成为消除HIV感染的主要障碍。这些潜伏的储库，包括静止的记忆T细胞和组织驻留的巨噬细胞，代表了前病毒转录减少或失活的细胞亚群。HIV前病毒转录在多个水平上受到调节，包括转录起始、聚合酶募集、转录延伸和染色质组织。这些生化过程是如何协调和他们的潜在作用，抑制艾滋病毒转录沿着建立和维持潜伏期。
Long-lived latent HIV-infected cells lead to the rebound of virus replication following antiretroviral treatment interruption and present a major barrier to eliminating HIV infection. These latent reservoirs, which include quiescent memory T cells and tissue-resident macrophages, represent a subset of cells with decreased or inactive proviral transcription. HIV proviral transcription is regulated at multiple levels including transcription initiation, polymerase recruitment, transcription elongation, and chromatin organization. How these biochemical processes are coordinated and their potential role in repressing HIV transcription along with establishing and maintaining latency are reviewed.