Suppression of apoptotic cell death by hepatitis C virus core protein

Virology. 1996 Dec 15;226(2):176-82. doi: 10.1006/viro.1996.0644.

Abstract

We have previously demonstrated the role of hepatitis C virus (HCV) core protein in the transcriptional regulation of cellular and unrelated viral promoters. Furthermore, the core protein in cooperation with H-ras oncogene transforms primary rat embryo fibroblast cells to the tumorigenic phenotype. In the present study, the functional role of HCV core protein was investigated to determine its potential to inhibit the onset of apoptotic cell death. Expression of HCV core protein inhibited cisplatin mediated apoptosis in human cervical epithelial cells, and apoptosis induced by the overexpression of c-myc in Chinese hamster ovarian cells. Results from these studies suggest that the core protein may have a biological implication in the pathogenesis of HCV infection.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Apoptosis* / physiology
  • Apoptosis* / radiation effects
  • CHO Cells
  • Cell Line, Transformed
  • Cisplatin / antagonists & inhibitors
  • Cisplatin / pharmacology
  • Cricetinae
  • HeLa Cells
  • Hepacivirus / genetics
  • Hepacivirus / physiology*
  • Humans
  • Mice
  • Proto-Oncogene Proteins c-myc / antagonists & inhibitors
  • Proto-Oncogene Proteins c-myc / physiology
  • Rats
  • Recombinant Proteins / genetics
  • Recombinant Proteins / pharmacology
  • Tumor Suppressor Protein p53 / physiology
  • Ultraviolet Rays
  • Viral Core Proteins / genetics
  • Viral Core Proteins / physiology*

Substances

  • Proto-Oncogene Proteins c-myc
  • Recombinant Proteins
  • Tumor Suppressor Protein p53
  • Viral Core Proteins
  • nucleocapsid protein, Hepatitis C virus
  • Cisplatin