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

Department of Biochemistry and Molecular Medicine, School of Medicine, Autonomous University of Nuevo León, Monterrey, NL, Mexico.
Revista de gastroenterologia de Mexico 01/2010; 75(1):7-11.
Source: PubMed


Background: Tumor necrosis factor alpha (TNF-á) has been involved in the pathogenesis of chronic hepatitis C virus (HCV) infection. Two polymorphisms at positions -308 and -238 in the TNF-á promoter region influence TNF-á expression and these have been linked to a number of infectious diseases. Aim: To analyze the prevalence of the -308 and -238 TNF-á 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. Twentyfive 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-á 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-á polymorphism was found to be 2% and 12% in patients and control subjects, respectively (P=0.061). The TNF-á genotypes were found to be in Hardy-Weinberg equilibrium. Conclusions: No association was found between -308 and -238 TNF-á 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. Key words: viral hepatitis, chronic hepatitis C, tumor necrosis factor alpha, genetic polymorphism, polymerase chain reaction.

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