Prevalence of the -308 and -238 tumor necrosis factor alpha (TNF-α) promoter polymorphisms in Mexican chronic hepatitis C patients

Rev Gastroenterol Mex. 2010;75(1):7-11.

Abstract

Background: Tumor necrosis factor alpha (TNF-α) has been involved in the pathogenesis of chronic hepatitis C virus (HCV) infection. Two polymorphisms at positions -308 and -238 in the TNF-α promoter region influence TNF-α expression and these have been linked to a number of infectious diseases.

Aim: To analyze the prevalence of the -308 and -238 TNF-α polymorphisms in a group of Mexican HCV-infected patients and in healthy control subjects not related to the patients.

Material and methods: Both polymorphisms were determined in peripheral blood samples from 48 patients with positive anti-HCV antibodies and discernible HCV-RNA levels. Twenty five patients were women and 23 were men. The control group included 100 healthy subjects. Forty-four were women and 56 were men. The polymorphisms were evaluated by polymerase chain reaction amplification (PCR), followed by the Restriction Fragment Length Polymorphism (RFLP) method.

Results: The prevalence of the -308 TNF-α polymorphism was found to be 12% in patients with chronic hepatitis C and 20% in control subjects, (P=0.2616); whereas that of the -238 TNF-α polymorphism was found to be 2% and 12% in patients and control subjects, respectively (P=0.061). The TNF-α genotypes were found to be in Hardy-Weinberg equilibrium.

Conclusions: No association was found between -308 and -238 TNF-α polymorphisms and chronic hepatitis C in the Mexican group studied. Our data suggest that additional studies increasing the sample size and a control group which has been exposed to an equal risk of infection are required to investigate whether these polymorphisms represent genetic susceptibility for chronic HCV infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Female
  • Hepatitis C, Chronic / genetics*
  • Humans
  • Male
  • Mexico
  • Middle Aged
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic / genetics*
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • Tumor Necrosis Factor-alpha