Selective restriction of Nef-defective human immunodeficiency virus type 1 by a proteasome-dependent mechanism

被引：28

作者：

Qi, Mingli ^{[1
]}

Aiken, Christopher ^{[1
]}

机构：

[1] Vanderbilt Univ, Sch Med, Dept Microbiol & Immunol, Nashville, TN 37232 USA

来源：

JOURNAL OF VIROLOGY | 2007年 / 81卷 / 03期

关键词：

D O I：

10.1128/JVI.02099-06

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The Nef protein enhances human immunodeficiency virus type 1 (HIV-1) infectivity by facilitating an early postentry step in the virus life cycle. We report here that the addition of MG132 or lactacystin, each a specific inhibitor of cellular proteasome activity, preferentially enhances cellular permissiveness to infection by Nef-defective versus wild-type HIV-1. Pseudotyping by the glycoprotein of vesicular stomatitis virus rendered Nef-defective HIV-1 particles minimally responsive to the enhancing effects of proteasome inhibitors. These results suggest that Nef enhances the infectivity of HIV-1 particles by reducing their susceptibility to proteasomal degradation in target cells.

引用

页码：1534 / 1536

页数：3

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