Association of TNF-alpha -308 polymorphism with the outcome of hepatitis B virus infection in Turkey.

BACKGROUND AND AIM

Cytokines play important roles in the regulation of immune response. The aim of the study was to investigate the association of the cytokine gene polymorphisms with persistence of hepatitis B virus (HBV) infection and the development of end-stage liver disease (ESLD) due to HBV infection.

METHODS

The study involved 27 patients with end-stage liver disease due to HBV infection, 23 HBV carriers and 60 healthy controls. All genotyping (TNF-alpha, TGF-beta, IL-10, IFN-gamma) experiments were performed using sequence specific primers (PCR-SSP) by using commercial kit according to manufacturers' instructions.

RESULTS

The frequencies of TNF-alpha -308 G/G and TGF-beta1 codon 10-25 T/C-G/G polymorphisms were significantly higher in HBV-infected individuals (patients+carriers) when compared with those of healthy controls (p: 0.02 and p: 0.004, respectively). The frequency of TNF-alpha -308 G/G polymorphism was significantly higher in the patients than those of the healthy controls (p: 0.02), whereas the frequency of TGF-beta1 codon 10-25 T/T-G/G polymorphism was lower (p: 0.028). On the other hand, TNF-alpha -308 G/G and TGF-beta codon 10-25 T/C-G/G polymorphisms were significantly more common in HBV carriers than the control group (p: 0.017 and p: 0.018, respectively). In addition, TNF-alpha -308 G allele frequency was significantly more common in HBV-infected individuals (patients+carriers) than those of healthy controls (p: 0.0007). TNF-alpha -308 G allele frequency was also found to be higher in patients or carriers when compared with those of healthy controls (p: 0.01 and p: 0.01, respectively). Statistically significant differences were still kept after Bonferroni correction of the p-values for only TNF-alpha -308 G allele frequency in patients or carriers (Pc).

CONCLUSION

Our study suggests that TNF-alpha gene polymorphism in patients infected with HBV would result in relatively inefficient inhibition of HBV and development of ESLD, and therefore, may be valuable predictor determinants for the development of ESLD in patients with chronic HBV infection.