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接受抗逆转录病毒治疗的感染者潜伏感染、静止 CD4+T 细胞中 HIV DNA 甲基化不足。

Paucity of HIV DNA methylation in latently infected, resting CD4+ T cells from infected individuals receiving antiretroviral therapy.

机构信息

National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

J Virol. 2012 May;86(9):5390-2. doi: 10.1128/JVI.00040-12. Epub 2012 Feb 15.

DOI:10.1128/JVI.00040-12
PMID:22345448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3347337/
Abstract

Maintenance of HIV latency in vitro has been linked to methylation of HIV DNA. However, examinations of the degree of methylation of HIV DNA in the latently infected, resting CD4(+) T cells of infected individuals receiving antiretroviral therapy have been limited. Here, we show that methylation of the HIV 5' long terminal repeat (LTR) in the latent viral reservoir of HIV-infected aviremic individuals receiving therapy is rare, suggesting that other mechanisms are likely involved in the persistence of viral latency.

摘要

体外维持 HIV 潜伏期与 HIV DNA 的甲基化有关。然而,对接受抗逆转录病毒治疗的感染者潜伏感染、静止的 CD4(+)T 细胞中 HIV DNA 甲基化程度的检测受到限制。在这里,我们表明,接受治疗的 HIV 血症抑制个体潜伏病毒库中 HIV 5'长末端重复(LTR)的甲基化很少,这表明其他机制可能参与了病毒潜伏期的持续存在。

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CpG methylation suppresses transcriptional activity of human syncytin-1 in non-placental tissues.CpG甲基化抑制人内源性逆转录病毒包膜糖蛋白1在非胎盘组织中的转录活性。
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