Lack of Association between Tumor Necrosis Factor-α -308 and -238 Promoter Polymorphisms and Chronic Hepatitis B Virus Infection

The pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) is an important mediator of the immune response in hepatitis B virus (HBV) infection. Since the production of TNF-α is mostly regulated at the transcriptional level and polymorphisms in the TNF-α promoter alter its expression, TNF-α promoter polymorphisms could affect the pathogenesis of chronic HBV infection. In this study, we investigated the potential association of TNF-α promoter polymorphisms with chronic HBV infection. The study included 181 patients with chronic HBV infection, 201 persons who had been spontaneously recovered from hepatitis B, and 170 unrelated healthy controls. The -308G/A and -238G/A polymorphisms in the TNF-α promoter were analyzed by PCR-restriction fragment length polymorphism. The distribution of both the -308 and -238 genotypes in the patient group was not statistically different from that in the spontaneous recovery and control groups (p>0.05). There was also no significant difference in the allele frequency between the groups (p>0.05). The results suggest that the TNF-α -308 and -238 promoter polymorphisms are not associated with the development of chronic HBV infection in the Korean population.