Dilazep synergistically reactivates latent HIV-1 in latently infected cells
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- 作者：Hanxian Zeng (1)
Sijie Liu (1)
Pengfei Wang (1)
Xiying Qu (1)
Haiyan Ji (1)
Xiaohui Wang (1)
Xiaoli Zhu (1)
Zhishuo Song (1)
Xinyi Yang (1)
Zhongjun Ma (2)
Huanzhang Zhu (1) - 关键词：Dilazep ; HIV ; 1 latency ; Synergistic reactivation
- 刊名：Molecular Biology Reports
- 出版年：2014
- 出版时间：November 2014
- 年：2014
- 卷：41
- 期：11
- 页码：7697-7704
- 全文大小：865 KB
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Sijie Liu (1)
Pengfei Wang (1)
Xiying Qu (1)
Haiyan Ji (1)
Xiaohui Wang (1)
Xiaoli Zhu (1)
Zhishuo Song (1)
Xinyi Yang (1)
Zhongjun Ma (2)
Huanzhang Zhu (1)
1. School of Life Sciences, Institute of Genetics, Fudan University, Shanghai, 200433, China
2. Institute of Marine Biology & Natural Products, Ocean College, Zhejiang University, Hangzhou, 310058, China - ISSN：1573-4978
文摘
The long-lived latently infected cells persist in spite of prolonged highly active anti-retroviral therapy and present a major barrier to a cure of human immunodeficiency virus type 1 (HIV-1) infection. Elimination of this reservoir requires reactivation of the latent virus. None of the current agents can safely and effectively reactivate latent HIV-1 reservoirs. Dilazep, a nucleoside transport inhibitor, is used to treat ischemic dysfunction. However, little is known about the effect of dilazep in inducing HIV expression in latently infected cells. Using the Jurkat T cell model of HIV-1 latency, we found that dilazep effectively reactivates latent HIV-1 gene expression in a dose manner. We observed that dilazep synergistically reactivated latent HIV-1 transcription with valproic acid. We also found that dilazep activates viral latency without inducing cell surface activation markers CD25 and CD69 activation. In summary, dilazep, alone or in combination with VPA, could be useful in future eradication strategies.