期刊
JOURNAL OF VIROLOGY
卷 80, 期 4, 页码 2051-2054出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.80.4.2051-2054.2006
关键词
-
类别
资金
- NIAID NIH HHS [T32 AI007161, R01AI36199, R01 AI036199, T32AI007161] Funding Source: Medline
Arsenic trioxide (As2O3) increased human immunodeficiency virus type I (HIV-1) infectivity when particular Homo sapiens and Cercopithecus aethiops cell lines were used as targets. Knockdown of human TRIM5 alpha by RNA interference eliminated the As2O3 effect, demonstrating that the drug acts by modulating the activity of this retroviral restriction factor. In contrast, HIV-1 infectivity in target cell lines from other primate species (Cercopithecus tantalus, Macaca mulatta, and Aotus trivirgatus) was not increased by AS(2)O(3), despite the potent TRIM5-dependent HIV-1 restriction activity that these cells exhibit. To determine if As2O3 responsiveness is characteristic of particular TRIM5 orthologues and not others, TRIM5 cDNAs from these five primate species were transduced into cat fibroblasts, which lack endogenous HIV-1 restriction activity and, therefore, responsiveness to AS(2)O(3). In this context, the HIV-1 restriction activity conferred by all TRIM5 orthologues was largely eliminated by AS(2)O(3). The effect of As2O3 on HIV-1 restriction is thus shared by different TRIM5 orthologues but dependent on factors specific to the cell line in which TRIM5 is expressed.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据