The interferon-induced protein BST-2 restricts HIV-1 release and is downregulated from the cell surface by the viral Vpu protein

被引：883

作者：

Van Damme, Nanette ^{[2
]}

Goff, Daniel ^{[1
]}

Katsura, Chris ^{[1
]}

Jorgenson, Rebecca L. ^{[3
]}

Mitchell, Richard ^{[1
]}

Johnson, Marc C. ^{[3
]}

Stephens, Edward B. ^{[4
]}

Guatelli, John ^{[1
,2
]}

机构：

[1] Univ Calif San Diego, Dept Med, San Diego, CA 92093 USA

[2] San Diego Dept Vet Affais Healthcare Syst, San Diego, CA 92161 USA

[3] Univ Missouri, Dept Mol Microbiol & Immunol, Columbia, MO 65212 USA

[4] Univ Kansas, Med Ctr, Dept Anat & Cell Biol, Kansas City, KS 66160 USA

来源：

CELL HOST & MICROBE | 2008年 / 3卷 / 04期

关键词：

D O I：

10.1016/j.chom.2008.03.001

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The HIV-1 accessory protein Vpu counteracts a host factor that restricts virion release from infected cells. Here we show that the interferon-induced cellular protein BST-2/HM1.24/CD317 is such a factor. BST-2 is downregulated from the cell surface by Vpu, and BST-2 is specifically expressed in cells that support the vpu phenotype. Exogenous expression of BST-2 inhibits HIV-1 virion release, while suppression of BST-2 relieves the requirement for Vpu. Downregulation of BST-2 requires both the transmembrane/ion channel domain and conserved serines in the cytoplasmic domain of Vpu. Endogenous BST-2 colocalizes with the HIV-1 structural protein Gag in endosomes and at the plasma membrane, suggesting that BST-2 traps virions within and on infected cells. The unusual structure of BST-2, which includes a transmembrane domain and a lumenal GPI anchor, may allow it to retain nascent enveloped virions on cellular membranes, providing a mechanism of viral restriction counteracted by a specific viral accessory protein.

引用

页码：245 / 252

页数：8

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