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

Virology. 2012 Jul 5;428(2):98-111. doi: 10.1016/j.virol.2012.03.011.

Avis Dafa-Berger ¹, Alona Kuzmina, Michael Fassler, Hila Yitzhak-Asraf, Yonat Shemer-Avni, Ran Taube

Affiliations

Affiliation

1 Department of Virology and Developmental Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer-Sheva, Israel.

PMID: 22520941 DOI: 10.1016/j.virol.2012.03.011

Abstract

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 IFNα, elevated BST-2 expression levels. However, HCV could not alter the expression of IFNα-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.

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