Interleukin-6 promotor gene polymorphisms and susceptibility to chronic hepatitis B virus in Egyptians

Abstract

AimTo investigate the association between IL-6 polymorphisms (−174G/C, −572G/C and −597G/A) and susceptibility to chronic hepatitis B virus (CHB) infection. MethodTotal 108 subjects with CHB infection and 102 healthy controls were enrolled in this study. IL-6 (−174G/C) was genotyped using Mutagenically separated Polymerase Chain Reaction (MS-PCR) while sequence specific primers-PCR (SSP-PCR) was used for studying −572G/C and −597G/A. IL-6 plasma level was measured using Enzyme-linked immunosorbent assay (ELISA). ResultsA significant increase (P < 0.01, P < 0.01, P < 0.001) in −174GG, −572GC and −597GA; respectively in the CHB group compared to control group, while −572GG genotype was significantly decreased (P < 0.01) in CHB patients. A significant increase (p < 0.01, p < 0.01) in −174 G and −597A alleles was observed in the CHB patient group; respectively. GGA haplotype is significantly increased (P < 0.05) while GCA haplotype is significantly decreased (P < 0.001) in the patient group. A moderate linkage disequilibrium (LD) (D′ = 0.719, r2 = 0.474; P < 0.001) between IL-6 (−572G/C and −597G/A) was observed. A significant reduction (P < 0.01) in IL-6 plasma level in CHB patients compared to healthy controls (22.28 ± 1.93 versus 32.08 ± 2.41), which was negatively correlated (r = −0.216; P < 0.01) with HBV infection. ConclusionsThis study pointed to the potential role of IL-6 (−174G/C, −572 G/C and −597G/A) gene polymorphisms in the susceptibility to HBV infection. Our results allow for only preliminary conclusions due to relatively small sample size. There is a need for further larger scale studies to fully examine the possible relationship between these cytokine gene polymorphisms and the development of CHB.