Interferons specifically suppress the translation from the internal ribosome entry site of hepatitis C virus through a double-stranded RNA-activated protein kinase-independent pathway

J Infect Dis. 2002 Jul 15;186(2):155-63. doi: 10.1086/341467. Epub 2002 Jul 3.

Abstract

Interferon (IFN) therapy is used worldwide as the best available treatment for hepatitis C virus (HCV) infection; however, little is known about how IFN or other drugs work against liver diseases. The effect of 6 drugs (glycyrrhizin, ursodeoxycholic acid, ribavirin, methylprednisolone, IFN-alpha, and IFN-beta) on HCV RNA translation from the HCV internal ribosome entry site (IRES) was investigated, using a bicistronic reporter containing the HCV IRES. IFNs suppressed both cap-dependent and HCV IRES-dependent translation, with HCV IRES-dependent translation being more significantly suppressed. In contrast to HCV IRES, IFN did not suppress either foot-and-mouth disease virus IRES-dependent or encephalomyocarditis virus IRES-dependent translation more than it suppressed cap-dependent translation. Moreover, dominant inhibition of HCV IRES-dependent over cap-dependent translation depended neither on the double-stranded RNA-activated protein kinase activation nor on La protein function. These results indicate a novel antiviral effect of IFNs against HCV.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Infective Agents / pharmacology*
  • Antiviral Agents / pharmacology
  • Autoantigens / biosynthesis
  • Blotting, Western
  • Cholagogues and Choleretics / pharmacology
  • Encephalomyocarditis virus / metabolism
  • Foot-and-Mouth Disease Virus / metabolism
  • Glucocorticoids / pharmacology
  • Glycyrrhizic Acid / pharmacology
  • Hepacivirus / drug effects*
  • Hepacivirus / genetics
  • Hepacivirus / metabolism
  • Humans
  • Interferons / metabolism
  • Interferons / pharmacology*
  • Methylprednisolone / pharmacology
  • Protein Biosynthesis / drug effects
  • Protein Biosynthesis / physiology
  • RNA, Double-Stranded / genetics
  • RNA, Double-Stranded / metabolism
  • RNA, Viral / genetics
  • RNA, Viral / metabolism
  • Ribavirin / pharmacology
  • Ribonucleoproteins / biosynthesis
  • Ribosomes / drug effects*
  • Ribosomes / genetics
  • Ribosomes / metabolism
  • SS-B Antigen
  • Tumor Cells, Cultured
  • Ursodeoxycholic Acid / pharmacology

Substances

  • Anti-Infective Agents
  • Antiviral Agents
  • Autoantigens
  • Cholagogues and Choleretics
  • Glucocorticoids
  • RNA, Double-Stranded
  • RNA, Viral
  • Ribonucleoproteins
  • Ribavirin
  • Glycyrrhizic Acid
  • Ursodeoxycholic Acid
  • Interferons
  • Methylprednisolone