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了解HIV-1潜伏状态为根除长期病毒储存库提供了线索。

Understanding HIV-1 latency provides clues for the eradication of long-term reservoirs.

作者信息

Coiras Mayte, López-Huertas María Rosa, Pérez-Olmeda Mayte, Alcamí José

机构信息

AIDS Immunopathology Unit, National Centre of Microbiology, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.

出版信息

Nat Rev Microbiol. 2009 Nov;7(11):798-812. doi: 10.1038/nrmicro2223.

DOI:10.1038/nrmicro2223
PMID:19834480
Abstract

HIV-1 can infect both activated and resting, non-dividing cells, following which the viral genome can be permanently integrated into a host cell chromosome. Latent HIV-1 reservoirs are established early during primary infection and constitute a major barrier to eradication, even in the presence of highly active antiretroviral therapy. This Review analyses the molecular mechanisms that are necessary for the establishment of HIV-1 latency and their relationships with different cellular and anatomical reservoirs, and discusses the current treatment strategies for targeting viral persistence in reservoirs, their main limitations and future perspectives.

摘要

HIV-1 能够感染活化的和静止的、非分裂细胞,之后病毒基因组可永久整合到宿主细胞染色体中。潜伏性HIV-1储存库在初次感染早期就已建立,即使在高效抗逆转录病毒治疗的情况下,它也是根除病毒的主要障碍。本综述分析了HIV-1潜伏建立所必需的分子机制及其与不同细胞和解剖学储存库的关系,并讨论了针对储存库中病毒持续性的当前治疗策略、其主要局限性和未来前景。

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本文引用的文献

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HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation.HIV储存库的大小和持久性由T细胞存活和稳态增殖驱动。
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Analysis of human immunodeficiency virus type 1 viremia and provirus in resting CD4+ T cells reveals a novel source of residual viremia in patients on antiretroviral therapy.对1型人类免疫缺陷病毒血症和静息CD4+ T细胞中前病毒的分析揭示了接受抗逆转录病毒治疗患者残余病毒血症的新来源。
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Treatment intensification does not reduce residual HIV-1 viremia in patients on highly active antiretroviral therapy.
High concentrations of Maraviroc do not alter immunological and metabolic parameters of CD4 T cells.
高浓度马拉维若不会改变 CD4 T 细胞的免疫和代谢参数。
Sci Rep. 2024 Jun 17;14(1):13980. doi: 10.1038/s41598-024-64902-y.
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Friends and Foes: The Ambivalent Role of Autophagy in HIV-1 Infection.朋友与敌人:自噬在HIV-1感染中的矛盾作用
Viruses. 2024 Mar 25;16(4):500. doi: 10.3390/v16040500.
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AP-1/c-Fos supports SIV and HIV-1 latency in CD4 T cells infected .AP-1/c-Fos维持感染的CD4 T细胞中的SIV和HIV-1潜伏状态。
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Metformin Treatment Leads to Increased HIV Transcription and Gene Expression through Increased CREB Phosphorylation and Recruitment to the HIV LTR Promoter.二甲双胍治疗通过增加 CREB 磷酸化和募集到 HIV LTR 启动子来增加 HIV 转录和基因表达。
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Viruses. 2022 Nov 23;14(12):2608. doi: 10.3390/v14122608.
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Viruses. 2022 Sep 7;14(9):1980. doi: 10.3390/v14091980.
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Front Immunol. 2022 Sep 5;13:1001068. doi: 10.3389/fimmu.2022.1001068. eCollection 2022.
对于接受高效抗逆转录病毒治疗的患者,强化治疗并不能降低残留的HIV-1病毒血症。
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Evidence that productive human immunodeficiency virus type 1 assembly can occur in an intracellular compartment.有证据表明,有生产性的1型人类免疫缺陷病毒组装可在细胞内区室中发生。
J Virol. 2009 Jun;83(11):5375-87. doi: 10.1128/JVI.00109-09. Epub 2009 Mar 18.
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MLL histone methylases in gene expression, hormone signaling and cell cycle.MLL组蛋白甲基化酶在基因表达、激素信号传导和细胞周期中的作用
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