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

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360 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)111-122
Number of pages12
JournalMolecular Cell
Issue number1
Publication statusPublished - 01-07-2005


All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

Watashi, K., Ishii, N., Hijikata, M., Inoue, D., Murata, T., Miyanari, Y., & Shimotohno, K. (2005). Cyclophilin B is a functional regulator of hepatitis C virus RNA polymerase. Molecular Cell, 19(1), 111-122.