Host genetic factors associated with hepatitis B virus infection and progression to chronic disease: A systematic review and Meta analysis
Abstract Abstract Back ground Contradicting results from many laboratories on the role of genetic factors in the susceptibility/resistance to hepatitis B infection have been reported. In this review we examined 27 published full research articles and assessed the role of Th1/Th2 cytokine promoter and vitamin D receptor gene polymorphisms. We summarized the available data on the relationship between the gene polymorphisms and susceptibility/resistance to hepatitis B virus infection together with likely disease evolution to come up with candidate single nucleotide polymorphisms implicated in the disease state with the population. Method The study was done in tandem with the PRISMA standards and the Cochran’s Q test, I2 statistics for heterogeneity and the Odds ratio were calculated using a commercially available soft ware called MedCalcs (http://www.medcalc.org). A random effects model was used to pool the odds ratio for heterogeneities ≥50% or else a fixed effects model was used. All analyses were done at 95% Confidence Interval and a P<0.05 was considered statistically significant. Results We found that IL-10-592C/A genotype AA (P=0.017, OR=0.752, 95%CI=0.595 to 0.950) and TNF-α-238G/A genotype AA+ AG (P<0.001, OR=0.407, 95%CI=0.005 to 30.1) were significantly associated with reduced risk of hepatitis B infection by the random effects model. TNF-α-238G/A genotype GG had the risk of chronic infection (OR=3.587, 95% CI= 0.127 to 101.176) under the random effect model. Most of the other SNPs had borderline risk of HBV infection (OR 0.6 to 1.12) with a few cases of high risk, IL-10-1082A/G genotype AA (OR=1.608, 95%CI=0.861 to 3.003) and reduced risk, IL-10-1082A/G genotype AG (OR=0.485, 95% CI=0.232 to 1.014) Conclusion We found that IL-10-592C/A genotype AA and TNF-α-238G/A genotype AA+ AG were significantly associated with reduced risk of hepatitis B infection.