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本文引用的文献

1
HIV persistence in macrophages.HIV在巨噬细胞中的持续存在。
Nat Med. 2017 May 5;23(5):538-539. doi: 10.1038/nm.4337.
2
The effect of Ingenol-B on the suppressive capacity of elite suppressor HIV-specific CD8+ T cells.Ingenol-B对精英抑制性HIV特异性CD8+ T细胞抑制能力的影响。
PLoS One. 2017 May 3;12(5):e0174516. doi: 10.1371/journal.pone.0174516. eCollection 2017.
3
Benzotriazoles Reactivate Latent HIV-1 through Inactivation of STAT5 SUMOylation.苯并三唑通过使信号转导和转录激活因子5(STAT5)的SUMO化失活来重新激活潜伏的HIV-1。
Cell Rep. 2017 Jan 31;18(5):1324-1334. doi: 10.1016/j.celrep.2017.01.022.
4
Rapamycin-mediated mTOR inhibition uncouples HIV-1 latency reversal from cytokine-associated toxicity.雷帕霉素介导的mTOR抑制作用将HIV-1潜伏激活与细胞因子相关毒性分离开来。
J Clin Invest. 2017 Feb 1;127(2):651-656. doi: 10.1172/JCI89552. Epub 2017 Jan 17.
5
Janus kinase inhibition suppresses PKC-induced cytokine release without affecting HIV-1 latency reversal ex vivo.Janus激酶抑制可抑制蛋白激酶C诱导的细胞因子释放,而不影响离体条件下HIV-1潜伏状态的逆转。
Retrovirology. 2016 Dec 20;13(1):88. doi: 10.1186/s12977-016-0319-0.
6
HIV-1 Latency-Reversing Agents Prostratin and Bryostatin-1 Induce Blood-Brain Barrier Disruption/Inflammation and Modulate Leukocyte Adhesion/Transmigration.HIV-1潜伏逆转剂原锥虫素和苔藓抑素-1可导致血脑屏障破坏/炎症,并调节白细胞黏附/迁移。
J Immunol. 2017 Feb 1;198(3):1229-1241. doi: 10.4049/jimmunol.1600742. Epub 2016 Dec 19.
7
The mTOR Complex Controls HIV Latency.mTOR复合物控制HIV潜伏。
Cell Host Microbe. 2016 Dec 14;20(6):785-797. doi: 10.1016/j.chom.2016.11.001.
8
Euphorbia Kansui Reactivates Latent HIV.甘遂可重新激活潜伏的艾滋病毒。
PLoS One. 2016 Dec 15;11(12):e0168027. doi: 10.1371/journal.pone.0168027. eCollection 2016.
9
In vitro effects of the small-molecule protein kinase C agonists on HIV latency reactivation.小分子蛋白激酶 C 激动剂对 HIV 潜伏期再激活的体外作用。
Sci Rep. 2016 Dec 12;6:39032. doi: 10.1038/srep39032.
10
Promising Role of Toll-Like Receptor 8 Agonist in Concert with Prostratin for Activation of Silent HIV.Toll样受体8激动剂与原苏木素协同激活潜伏HIV的潜在作用。
J Virol. 2017 Jan 31;91(4). doi: 10.1128/JVI.02084-16. Print 2017 Feb 15.

新型 HIV-1 治愈潜伏逆转剂

Novel Latency Reversal Agents for HIV-1 Cure.

机构信息

Department of Medicine, University of Utah School of Medicine, Salt Lake City, Utah 84112.

Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84112; email:

出版信息

Annu Rev Med. 2018 Jan 29;69:421-436. doi: 10.1146/annurev-med-052716-031710. Epub 2017 Nov 3.

DOI:10.1146/annurev-med-052716-031710
PMID:29099677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5892446/
Abstract

Antiretroviral therapy (ART) has rendered HIV-1 infection a treatable illness; however, ART is not curative owing to the persistence of replication-competent, latent proviruses in long-lived resting T cells. Strategies that target these latently infected cells and allow immune recognition and clearance of this reservoir will be necessary to eradicate HIV-1 in infected individuals. This review describes current pharmacologic approaches to reactivate the latent reservoir so that infected cells can be recognized and targeted, with the ultimate goal of achieving an HIV-1 cure.

摘要

抗逆转录病毒疗法(ART)使 HIV-1 感染成为一种可治疗的疾病;然而,由于复制能力强的潜伏前病毒在长寿静止 T 细胞中持续存在,ART 并不能治愈。为了在感染个体中根除 HIV-1,需要针对这些潜伏感染的细胞的策略,以允许免疫识别和清除这个储库。这篇综述描述了目前药理学方法来重新激活潜伏储库,以便可以识别和靶向受感染的细胞,最终目标是实现 HIV-1 的治愈。