Association Of Ephrin Receptor A3Gene Polymorphism With Susceptibility To HBV-Related Acute On Chronic Liver Failure

Aim: Previous researches had suggested that Ephrin receptor A3(EphA3) played signalingroles in the processes of inflammation by regulating lymphocyte migration and proliferation.In this study, we investigated whether the EphA3gene polymorphism was associated withdisease progression of chronic hepatitis B virus (HBV) infection.Methods: A hospital-based, case-control study was performed and a total of1,245unrelated Han Chinese HBV carriers were recruited in Hubei province.800cases and445controls were included. We obtained the blood samples, collected their clinical history andlaboratory data. Genome DNA was extracted from peripheral whole blood and then usingthe genome DNA as templates, the EphA3variant rs9310117was genotyped in1245unrelated Han Chinese HBV carriers by TaqMan method according to the protocol ofTaqManâ—‹RSNP Genotyping Assays. Statistical analysis was performed using SPSS17.0software. Chi-square Test was used to examine the difference in allele frequencies andgenotype distributions between groups. The association between the polymorphism anddisease progression of HBV infection was conducted by unconditional logistic regressionanalysis.Results: Clinical data suggested that there were more men in the three active liver diseasethan those in the asymptomatic HBV carriers group (P<0.001). And individuals in theHBV-related acute on chronic liver failure (ACLF) group were younger than the controlgroup (P<0.001). However, no significant difference among the liver cirrhosis (LC) group,the hepatocellular carcinoma (HCC) group and the control group in age (P>0.05). Statisticalanalysis revealed that the genetic variant was significantly associated with the occurrence of acute on chronic liver failure after chronic HBV infection. On the basis of multivariablelogistic regression with adjustment for gender and age, we observed that subjects bearing atleast one T allele (C/T or T/T genotype) had a decreased susceptibility to HBV-relatedacute on chronic liver failure. Compared to those bearing C/C genotype (P=0.003, oddsratio=0.560;95%confidence interval,0.381-0.824, recessive model). Genotype C/T hadalso been confirmed to protect subjects from suffering HBV-related acute on chronic liverfailure (P=0.001, odds ratio=0.498;95%confidence interval,0.330-0.752, additivemodel).Conclusion: Our results suggest that the genetic alteration at EphA3locus plays a part rolein the occurrence of acute on chronic liver failure after HBV infection. Compared to Callele, the allele T has a protect role from people suffering acute on chronic liver failure.