Maternal HBeAg positivity is the main reason for hepatitis B vaccination failure

  Hepatitis B virus (HBV) infection is a global health problem. There are currently 2 billion hepatitis B virus carriers worldwide, of which 360 million are chronic hepatitis B surface antibody (HBsAg) positive carriers. The progression of hepatitis B can lead to liver failure, cirrhosis and liver cancer, resulting in a range of socio-economic problems. The most effective way of preventing hepatitis B is currently hepatitis B virus vaccination in infancy, but its immune effectiveness after infancy is not 100%. It has been reported in the literature that chronic hepatitis B infection still occurs in children after vaccination, and the mechanism of failure after hepatitis B vaccination in infants is not yet fully understood. A related study was conducted by Tzu-Wei Wu (pro-swimming S) et al. from the Department of Internal Medicine, Ma Chai Medical College, New Taipei City, Taiwan, and the results of this study were published online in the latest issue (2013 Jan) of Hepatology.  The study included 8733 high school students born after July 1987, who were tested for hepatitis B surface antigen (HBsAg) and surface antibodies (anti-HBs). Their overall HBsAg and anti-HBS positivity rates were 1.9% and 48.3%, respectively. Among students who received hepatitis B immunoglobulin, the HBsAg positivity rate was 15% (adjusted risk ratio: 15.63; 95% confidence interval: 10.99-22.22). Among students who did not receive hepatitis B immunoglobulin (HBIG), there was a direct and significant negative correlation between their hepatitis B virus vaccine dose and the rate of hepatitis B surface antigen positivity. (p trend value of 0.011). The adjusted risk ratios were 1.00, 1.52 (95% confidence interval 0.91-2.53) and 2.85 (95% CI: 1.39-5.81) among students who had received 4, 3 and 1-2 doses of hepatitis B vaccine, respectively. Students who received HBIG had significantly higher rates of HBsAg positivity if they had maternal hepatitis B e antigen positivity and received HBIG insufficiently.  Seventy-four HBsAg- and anti-HBs-negative students underwent a booster of hepatitis B vaccine. Blood anti-HBs counts were compared before and after the booster. Postboost anti-HBs titers with potency <10 mIU/mL accounted for 27.9% of all vaccinations. Pre-vaccination anti-HBs in the range of 1.0-9.9 IU/mL had significantly more potency enhancement after booster than students with antibody titers <1.0 mIU/mL before booster. (p<0.0001) This study ultimately concluded that the most important determinant of HBsAg-positive youth found in infants 15 years after postnatal active immunization with hepatitis B vaccine is HBeAg positivity in the maternal line. A significant proportion of fully immunized recipients lose immune memory for HBsAg.