Abstract
The universal HBV vaccination programme in Taiwan has effectively led to the reduction of acute and chronic hepatitis B, and of hepatocellular carcinoma among vaccinated children. Seropositivity rates for hepatitis B surface antigen (HBsAg) decreased from 10-17% in those born before the start of the vaccination programme to the current 0.5-1.7%. Nonetheless, breakthrough infection continues to be observed. The main causes include high maternal viral load, intrauterine infection, emergence of S gene mutants and immunosuppression. Among vaccinated individuals with breakthrough HBV infection, sG145R & sT126A/S mutations (which account for 48% of the mutants detected) have become prominent. However, owing to the marked reduction in the HBsAg carrier rate, the prevalence rate of S gene mutants in the total vaccinated population has not increased. With limited evidence of spread, S gene mutants do not need to be incorporated into the HBV vaccine. Further studies are required to design better strategies to prevent breakthrough HBV infection of both wild-type and S gene mutants.
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