| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3424315 | Virology | 2012 | 14 Pages |
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.
► The regulation of HCV release by BST-2/Tetherin in Huh-7.5 hepatocytes was studied. ► BST-2 expression in cells is low and is induced following treatment with IFNα. ► BST-2 efficiently inhibits the release of HIV delta vpu from Huh-7.5 cells that express BST-2. ► HIV vpu partially overcomes BST-2 restriction and rescues HCV release. ► In vitro, BST-2 moderately restricts HCV production and release from infected cells.
