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Cyclophilin B Is a Functional Regulator of Hepatitis C Virus RNA Polymerase

2005; Elsevier BV; Volume: 19; Issue: 1 Linguagem: Inglês

10.1016/j.molcel.2005.05.014

1097-4164

Koichi Watashi, Naoto Ishii, Makoto Hijikata, Daisuke Inoue, Takayuki Murata, Yusuke Miyanari, Kunitada Shimotohno,

Hepatitis B Virus Studies

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.