Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6143332 | Virus Research | 2012 | 5 Pages |
Abstract
Hepatitis C virus (HCV) elevated expression of the translocase of outer mitochondrial membrane 70 (Tom70). Interestingly, overexpression of Tom70 induces interferon (IFN) synthesis in hepatocytes, and it was impaired by HCV. Here, we addressed the mechanism of this impairment. The HCV NS3/4A protein induced Tom70 expression. The HCV NS3 protein interacted in cells, and cleaved the adapter protein mitochondrial anti-viral signaling (MAVS). Ectopic overexpression of Tom70 could not inhibit this cleavage. As a result, IRF-3 phosphorylation was impaired and IFN-β induction was suppressed. These results indicate that MAVS works upstream of Tom70 and the cleavage of MAVS by HCV NS3 protease suppresses signaling of IFN induction.
Related Topics
Life Sciences
Immunology and Microbiology
Virology
Authors
Yuri Kasama, Makoto Saito, Takashi Takano, Tomohiro Nishimura, Masaaki Satoh, Zhongzhi Wang, Salem Nagla Elwy Salem Ali, Shinji Harada, Michinori Kohara, Kyoko Tsukiyama-Kohara,