首页    期刊浏览 2024年11月28日 星期四
登录注册

文章基本信息

  • 标题:Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat
  • 作者:Manabu Taura ; Manabu Taura ; Eric Song
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2019
  • 卷号:116
  • 期号:6
  • 页码:2282-2289
  • DOI:10.1073/pnas.1819386116
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:HIV-1 integrates into the genome of target cells and establishes latency indefinitely. Understanding the molecular mechanism of HIV-1 latency maintenance is needed for therapeutic strategies to combat existing infection. In this study, we found an unexpected role for Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A, abbreviated “A3A”) in maintaining the latency state within HIV-1–infected cells. Overexpression of A3A in latently infected cell lines led to lower reactivation, while knockdown or knockout of A3A led to increased spontaneous and inducible HIV-1 reactivation. A3A maintains HIV-1 latency by associating with proviral DNA at the 5′ long terminal repeat region, recruiting KAP1 and HP1, and imposing repressive histone marks. We show that knockdown of A3A in latently infected human primary CD4 T cells enhanced HIV-1 reactivation. Collectively, we provide evidence and a mechanism by which A3A reinforces HIV-1 latency in infected CD4 T cells.
  • 关键词:epigenetic regulation ; TRIM28 ; reactivation ; viral latency ; T cells
Loading...
联系我们|关于我们|网站声明
国家哲学社会科学文献中心版权所有