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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Cyclophilin B is a functional regulator of hepatitis C virus RNA polymerase.

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.[1]

References

  1. Cyclophilin B is a functional regulator of hepatitis C virus RNA polymerase. Watashi, K., Ishii, N., Hijikata, M., Inoue, D., Murata, T., Miyanari, Y., Shimotohno, K. Mol. Cell (2005) [Pubmed]
 
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