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The mechanisms underlying the resolution of hepatitis B virus (HBV) infection remain undetermined. Tumor necrosis factor-α (TNF-α) plays a pivotal role in host immune response to HBV, and the capacity for cytokine production in individuals has a major genetic component. The aim of this study was to examine whetherTNF-α promotor polymorphisms are associated with the clearance of HBV infection. A total of 1400 Korean subjects were enrolled in two different groups: ‘chronic carrier group’ (CC;n=1109), who were repeatedly hepatitis B surface antigen (HBsAg)-positive, and ‘subjects who spontaneously recovered’ (SR;n=291), who were HBsAg-negative with antibodies to HBsAg and hepatitis B core antigen.TNF-α promoter polymorphisms at positions −1031T&gt;C, −863C&gt;A, −857C&gt;T, −376G&gt;A, −308G&gt;A, −238G&gt;Aand −163G&gt;Awere determined and the genotype distributions of the CC and SR groups were compared. TheTNF-α promoter alleles that were previously reported to be associated with higher plasma levels, i.e. the presence of the −308Aallele (TNF-α-308A/GorA/A) or the absence of the −863A(TNF-α-863C/C) variant, were strongly associated with the resolution of HBV infection in three alternative analyzing models, i.e.TNF-α-308G&gt;A(P=0.01) andTNF-α-863C&gt;A(P=0.003–0.14), respectively. Haplotype analysis also revealed thatTNF-αhaplotype 1[−1031T; −863C; −857C; −308G; −238G; −163G] andhaplotype 2[−1031C; −863A; −857C; −308G; −238G; −163G] were significantly associated with HBV clearance, showing protective antibody production and persistent HBV infection, respectively (P=0.003–0.02). Our findings imply that variations in the genes governing the levels of constitutive and inducible TNF-α might be an important factor, which might explain the variable outcome of HBV infection.

Association of TNF -α promoter polymorphisms with the clearance of hepatitis B virus infection