| Literature DB >> 15989969 |
Koichi Watashi1, Naoto Ishii, Makoto Hijikata, Daisuke Inoue, Takayuki Murata, Yusuke Miyanari, Kunitada Shimotohno.
Abstract
Viruses depend on host-derived factors for their efficient genome replication. Here, we demonstrate that a cellular peptidyl-prolyl cis-trans isomerase (PPIase), cyclophilin B (CyPB), is critical for the efficient replication of the hepatitis C virus (HCV) genome. CyPB interacted with the HCV RNA polymerase NS5B to directly stimulate its RNA binding activity. Both the RNA interference (RNAi)-mediated reduction of endogenous CyPB expression and the induced loss of NS5B binding to CyPB decreased the levels of HCV replication. Thus, CyPB functions as a stimulatory regulator of NS5B in HCV replication machinery. This regulation mechanism for viral replication identifies CyPB as a target for antiviral therapeutic strategies.Entities:
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Year: 2005 PMID： 15989969 DOI： 10.1016/j.molcel.2005.05.014
Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970