Archives of Virology

, Volume 153, Issue 11, pp 1991–1997

Hepatitis C virus (HCV) NS2 protein up-regulates HCV IRES-dependent translation and down-regulates NS5B RdRp activity

Authors

  • Yinglong She
    • State Key Laboratory of Virology, College of Life ScienceWuhan Univerisity
  • Qingjiao Liao
    • State Key Laboratory of VirologyWuhan Institute of Virology, Chinese Academic of Science
  • Xulin Chen
    • State Key Laboratory of VirologyWuhan Institute of Virology, Chinese Academic of Science
    • State Key Laboratory of Virology, College of Life ScienceWuhan Univerisity
  • Zhenghui Wu
    • State Key Laboratory of Virology, College of Life ScienceWuhan Univerisity
Original Article

DOI: 10.1007/s00705-008-0198-3

Cite this article as:
She, Y., Liao, Q., Chen, X. et al. Arch Virol (2008) 153: 1991. doi:10.1007/s00705-008-0198-3

Abstract

Chronic hepatitis C virus (HCV) infection often leads to liver cancer. The HCV NS2 protein is a hydrophobic transmembrane protein that associates with several cellular proteins in mammalian cells. In this report, we investigated the function of NS2 protein on HCV replication and translation by using a transient cell-based expression system. Cells co-transfected with pcDNA3.1 (−)-NS2 and the dual-luciferase reporter construct containing the HCV IRES were used to detect the effect of NS2 protein on HCV translation. Cells co-transfected with pcDNA3.1(−)-NS2, pcDNA-NS5B and a reporter plasmid were used to detect the effect of NS2 protein on HCV replication. The results showed that HCV NS2 protein up-regulated HCV IRES-dependent translation in a specific and dose-dependent manner in Huh7 cells but not in HeLa and HepG2 cells, and NS2 protein inhibited NS5B RdRp activity in a dose-independent manner in all three cell lines. These findings may suggest a novel mechanism by which HCV modulates its NS5B replication and IRES-dependent translation and facilitates virus persistence.

Copyright information

© Springer-Verlag 2008