APOBEC3G restricts early HIV-1 replication in the cytoplasm of target cells
APOBEC3G restricts early HIV-1 replication in the cytoplasm of target cells
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DOI：
10.1016/j.virol.2008.01.042
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发表时间：
2008-05-25
期刊：
影响因子：
3.7
通讯作者：
Hope, Thomas J.
中科院分区：
文献类型：
--
作者：
Anderson, Jenny L.;Hope, Thomas J.
细胞APOBEC 3G（A3 G）蛋白在生产细胞中包装入人类免疫缺陷病毒1型（HIV-1）病毒粒子，但限制靶细胞中的病毒复制。为了表征靶细胞中的这种限制，通过定量实时PCR测量A3 G对产生各种HIV-1 cDNA产物的影响。A3 G减少了来自Vif缺陷型HIV-1的cDNA产物，对早期逆转录的影响较小，而对晚期逆转录的影响较大。然而，通常在核2-LTR环中观察到最大的下降。此外，这些下降的幅度随A3 G剂量而变化。加入整合抑制剂并不能阻止A3 G介导的2-LTR环丢失。此外，使用水泡性口炎病毒基质蛋白阻止HIV-1核进入并不能阻止A3 G介导的晚期逆转录的下降。总的来说，这些数据表明，A3 G在细胞质中具有重要的限制活性，并且在限制期间随着幅度的增加而逐渐减少病毒的细胞质和核cDNA形式。(c)2008年爱思唯尔公司All rights reserved.
Cellular APOBEC3G (A3G) protein is packaged into human immunodeficiency virus type 1 (HIV-1) virions in producer cells yet restricts viral replication in target cells. To characterize this restriction in target cells, the effect of A3G on generating various HIV-1 cDNA products was measured by quantitative real-time PCR. A3G decreased cDNA products from Vif-deficient HIV-1, with minor effects on early reverse transcripts and larger declines in late reverse transcripts. However, the greatest decline was typically observed in nuclear 2-LTR circles. Moreover, the magnitude of these declines varied with A3G dose. Adding integration inhibitor did not stop the A3G-mediated loss in 2-LTR circles. Moreover, obstructing HIV-1 nuclear entry using vesicular stomatitis virus matrix protein did not stop the A3G-mediated decline in late reverse transcripts. Collectively, these data suggest that A3G has important restriction activity in the cytoplasm and progressively diminishes viral cytoplasmic and nuclear cDNA forms with increasing magnitude during restriction. (c) 2008 Elsevier Inc. All rights reserved.