| OBJECTIVE: Hepatitis B virus (HBV) is the major causal agent of hepatitis and the leading indication for liver transplantation worldwide. The field of immunogenetics has confirmed the significant role of heritability in host immune responses to infectious pathogens. Both the major and non-major histocompatibility complex genes are increasingly identified as candidate genes hypothesized to influence the susceptibility to, or the course of a particular disease. We hypothesized that polymorphisms with tumor necrosis factors (TNF)-alpha , TNF-beta and interleukin-10 (IL-10) might be predictive of response to interferon therapy in patients with chronic Hepatitis B. METHODS: A total of 43 HBV-seropositive individuals undergoing interferon therapy were studied. Including 26 responsers and 17 nonresponders. Genomic DNA was extracted, followed by Taqman sequencing for two promoter TNF-alpha variants (at positions -238 and -308), as well as within the TNF-beta(LTA) gene (+723)and IL-10(-592). RESULTS: There were no significant differences in the distribution of the genotypic polymorphisms of TNFα-238,TNFα-308 and LTA+723 between responders and nonresponders. IL-10 -592 A allele is more frequent in the responders than in the nonresponders.CONCLUSIONS: Although previous work has suggested potential roles for TNF in the pathogenesis of HBV infection, we were unable to identify any link between TNF genetic polymorphisms to intereron therapy. IL-10 -592 A allele is likely to play a role in the IFN treatment of HBV infection.
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