Morphine inhibits intrahepatic interferon- alpha expression and enhances complete hepatitis C virus replication

J Infect Dis. 2007 Sep 1;196(5):719-30. doi: 10.1086/520093. Epub 2007 Jul 18.

Abstract

Heroin addicts are a high-risk group for hepatitis C virus (HCV) infection and the development of chronic HCV disease. We thus examined whether morphine, the active metabolite of heroin, has the ability to inhibit intrahepatic interferon (IFN)- alpha expression, facilitating HCV replication in human hepatocytes. Morphine inhibited intrahepatic IFN- alpha expression, which was associated with an increase in HCV replication in hepatocytes. Moreover, morphine compromised the anti-HCV effect of recombinant IFN- alpha . Investigation of the mechanism responsible for the morphine action revealed that morphine inhibited expression of IFN regulatory factor 5 in the hepatocytes. In addition, morphine suppressed the expression of p38, an important signal-transducing molecule involved in IFN- alpha -mediated anti-HCV activity. These findings indicate that morphine plays a cofactor role in facilitating HCV persistence in human hepatocytes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Down-Regulation
  • Gene Expression Regulation / drug effects*
  • Hepacivirus / drug effects*
  • Hepacivirus / physiology
  • Hepatocytes / drug effects*
  • Hepatocytes / metabolism
  • Hepatocytes / virology*
  • Humans
  • Interferon Regulatory Factors / biosynthesis
  • Interferon-alpha / biosynthesis*
  • Morphine / pharmacology*
  • Naltrexone / analogs & derivatives
  • Naltrexone / pharmacology
  • Narcotic Antagonists / pharmacology
  • Narcotics / pharmacology
  • Virus Replication / drug effects*

Substances

  • IRF5 protein, human
  • Interferon Regulatory Factors
  • Interferon-alpha
  • Narcotic Antagonists
  • Narcotics
  • Naltrexone
  • beta-funaltrexamine
  • Morphine