Polymorphisms of interleukin-1B and interleukin-1 receptor antagonist genes in patients with chronic hepatitis B

AIM: To investigate the relationships between polymorphisms of interleukin-1B (IL-1B) promoter region -511C/T and interleukin-1 receptor antagonist gene (IL-1RN) and susceptibility to chronic hepatitis B in Chinese population.METHODS: Genomic DNA was extracted from the peripheral blood of 190 patients with chronic hepatitis B and 249 normal controls and then subjected to polymerase chain reaction (PCR) amplification. The PCR products were digested by restriction endonuclease AvaI. The products of digestion were subjected to 20 g/L gel electrophoresis and ethidium bromide staining.RESULTS: The frequencies of IL-1B (-511) genotypes CC,CT and TT in patients with chronic hepatitis B were 23.7%,49.5% and 26.8%, while 26.1%, 47.4% and 26.5%respectively in controls. The results showed that there was no significant difference in the frequencies of alleles or genotypes in IL-1B between patients with chronic hepatitis B and controls. The distributions of IL-1B (-511) genotype CC were significantly different between the two subgroups (HBV-DNA ≤1×103 copies/mL as subgroup I, HBV-DNA ＞ 1×103 copies/mL as subgroup Ⅱ) of chronic hepatitis B (P=0.029). Only four of the five kinds of polymorphism (1/1,1/2, 2/2 and 1/4) were found in this study. The frequencies of IL-1RN genotypes 1/1, 1/2, 2/2 and 1/4 were 88.9%, 9.0%,0.5% and 1.6% in patients with chronic hepatitis B respectively,while were 81.1%, 16.9%, 0.4% and 1.6% respectively in controls. The frequencies of genotype1/2 and IL-1RN allele 2 in patients with chronic hepatitis B were lower than those in controls (P=0.016 and P=0.029, respectively).CONCLUSION: There is an association between polymorphisms of the promoter region -511C/T of IL-1B and IL-1RN intron 2and chronic hepatitis B virus infection. Subjects with IL-1RN 2 may be resistant to HBV infection, and IL-1B(-511)genotype CC is closely related with HBV-DNA replication,which gives some new clues to the study of pathogenesis of chronic hepatitis B.