Modulation of hepatitis C virus release by the interferon-induced protein BST-2/tetherin

被引：49

作者：

Dafa-Berger, Avis ^{[1
,2
]}

Kuzmina, Alona ^{[1
]}

Fassler, Michael ^{[1
]}

Yitzhak-Asraf, Hila ^{[1
]}

Shemer-Avni, Yonat ^{[1
]}

Taube, Ran ^{[1
]}

机构：

[1] Ben Gurion Univ Negev, Fac Hlth Sci, Dept Virol & Dev Genet, Beer Sheva, Israel

[2] Ben Gurion Univ Negev, Natl Inst Biotechnol Negev, IL-84105 Beer Sheva, Israel

来源：

VIROLOGY | 2012年 / 428卷 / 02期

关键词：

Hepatitis C virus; Viral release; BST-2/Tetherin; IFN type I innate response; HIV vpu; RNA REPLICATION COMPLEX; MURINE LEUKEMIA-VIRUS; IMMUNODEFICIENCY-VIRUS; NONSTRUCTURAL PROTEINS; HIV-1; VPU; ENVELOPE GLYCOPROTEIN; CELLULAR COFACTORS; PARTICLE RELEASE; INHIBITS HIV-1; TETHERIN;

D O I：

10.1016/j.virol.2012.03.011

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Hepatitis C virus is a leading cause of chronic hepatitis and liver cancer. Little information exists on the interplay between innate defense mechanisms and viral antagonists that promote viral egress. Herein, the effects of Tetherin/BST-2 on HCV release were investigated. In Huh-7.5 hepatocytes, low expression levels of BST-2 were detected. Treatment of Huh-7.5 cells with IFN alpha, elevated BST-2 expression levels. However, HCV could not alter the expression of IFN alpha-induced BST-2, nor of stably over-expressed BST-2. Significantly, over expressed BST-2 moderately blocked HCV production and release from Huh-7.5 cells. Functional analysis of BST-2, confirmed its ability to inhibit the release of HIV delta-Vpu from Huh-7.5-BST-2 cells. HIV-Vpu antagonized BST-2 activity and rescued HIV delta-Vpu release from Huh-7.5-BST-2 cells. However, vpu slightly rescued HCV release and production from Huh-7.5-BST-2. We conclude that BST-2 moderately restricts HCV production and release from Huh-7.5 hepatocytes, while the virus lacks mechanisms to counteract this restriction. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：98 / 111

页数：14

共 84 条

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