Is interleukin-10 gene polymorphism a predictive marker in HCV infection?

Cytokine Growth Factor Rev. 2012 Feb-Apr;23(1-2):47-59. doi: 10.1016/j.cytogfr.2012.01.005. Epub 2012 Mar 4.

Abstract

The clinical outcome of hepatitis C virus (HCV) infection varies between individuals - from spontaneous viral clearance and persistence without complication, to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Also patterns of response to interferon-based anti-HCV therapy are different from person to person. This diversity may be affected by host genetic factors, including alterations in genes encoding cytokines. Interleukin-10, as an anti-inflammatory cytokine and immune response modulator, may influence on HCV infection susceptibility as well as spontaneous and treatment-induced HCV eradication. Moreover, it is stated that IL-10 has antifibrotic properties and play a role in progression of liver disease. This review summarized studies on interleukin-10 gene polymorphisms (mainly promoter SNPs at positions -1082(G/A), -819(C/T) and -592(C/A)), which may determine IL-10 production, regarding susceptibility to HCV infection, course of HCV-related liver disease (fibrosis, cirrhosis, hepatocellular carcinoma, ALT abnormalities), spontaneous viral elimination as well as hepatitis C treatment outcomes. Analysis of hereby summarized studies shows that it is difficult to unambiguously determine the importance of IL-10 polymorphism as a predictor of clinical outcome of hepatitis C and response to anti-HCV therapy before its beginning. Thus, future larger studies need to address these issues. Continuation of studies on interleukin-10 polymorphisms as well as identification of other candidate predictive markers in HCV infection has important practical implications and there is a chance that may contribute to reduce the scale of hepatitis C problem.

Publication types

  • Evaluation Study
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Biomarkers / metabolism
  • Hepacivirus / physiology
  • Hepatitis C / diagnosis*
  • Hepatitis C / genetics
  • Hepatitis C / metabolism
  • Hepatitis C / therapy
  • Humans
  • Interleukin-10 / genetics*
  • Interleukin-10 / metabolism
  • Interleukin-10 / physiology
  • Models, Biological
  • Polymorphism, Genetic* / physiology
  • Prognosis
  • Viral Load / genetics

Substances

  • Biomarkers
  • Interleukin-10