Cyclophilin B is a functional regulator of hepatitis C virus RNA polymerase
Koichi Watashi, Naoto Ishii, Makoto Hijikata, Daisuke Inoue, Takayuki Murata, Yusuke Miyanari, Kunitada Shimotohno, Koichi Watashi, 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.
Source: PubMed