A human TRIM5α B30.2/SPRY domain mutant gains the ability to restrict and prematurely uncoat B-tropic murine leukemia virus

被引：55

作者：

Diaz-Griffero, Felipe ^{[1
]}

Perron, Michel ^{[1
]}

McGee-Estrada, Kathleen ^{[1
]}

Hanna, Robert ^{[1
]}

Maillard, Pierre V. ^{[2
]}

Trono, Didier ^{[2
]}

Sodroski, Joseph ^{[1
,3
]}

机构：

[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol,Div AIDS, Boston, MA 02115 USA

[2] Ecole Polytech Fed Lausanne, Global Hlth Inst, Sch Life Sci, Frontiers Genet Natl Ctr Competence Res, CH-1015 Lausanne, Switzerland

[3] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

来源：

VIROLOGY | 2008年 / 378卷 / 02期

基金：

美国国家卫生研究院; 瑞士国家科学基金会;

关键词：

retrovirus; restriction factor; uncoating; tripartite motif; mechanism; capsid; reverse transcription;

D O I：

10.1016/j.virol.2008.05.008

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Human TRIM5 alpha restricts N-tropic murine leukemia virus (N-MLV) but not B-tropic MLV (B-MLV) infection. Here we study B30.2/SPRY domain mutants of human TRIM5 alpha that acquire the ability to inhibit B-MLV infection prior to reverse transcription Without losing the ability to restrict N-MLV infection. Remarkably, these Mutants gain the ability to decrease the amount of particulate B-MIV capsids in the cytosol of infected cells. In addition, these mutants gain the ability to restrict SIVmac and HIV-2 infection. B-MLV and SIVmac infections were blocked by the mutant TRIM5 alpha proteins prior to reverse transcription. Thus, the range of retroviruses restricted by human TRIM5a can be increased by changes in the B30.2/SPRY domain, which also result in the ability to cause premature uncoating of the restricted retroviral capsid. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：233 / 242

页数：10

共 32 条

[1] Proteasome inhibition reveals that a functional preintegration complex intermediate can be generated during restriction by diverse TRIM5 proteins [J].