Hepatitis B vaccination in children: The Taiwan experienceVaccination des enfants contre l’hépatite B : l’expérience taïwanaise
Section snippets
Natural history of hepatitis B virus infection
Hepatitis B virus (HBV) infection is a major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) in many parts of the world. In endemic areas, the majority of chronic HBV carriers were infected in early life. The age at infection is an important factor affecting the outcome of HBV infection. The earlier the infection, the higher the chronicity rate. Perinatal transmission results in a very high rate of chronicity (> 90%) if left un-immunized. The rate of chronicity declines
Universal infant immunization program
The world's first nationwide HBV universal vaccination program for infants was launched in Taiwan in July, 1984 [4]. Before July 1992, four doses of plasma-derived vaccine (Hevac B; Pasteur-Mérieux, Lyon, France, or its local equivalent, Lifeguard hepatitis B vaccine; Hsin-Chu, Taiwan) were given at zero, one, two, and 12 months of age. After July 1992, three doses of recombinant vaccine H-B-Vax II (5 μg/0.5 mL; Merck Sharp & Dohme, Rahway, NJ) or Engerix-B (20 μg/1 mL; SmithKline Beecham,
Impact of the universal vaccination program
We performed serial sero-epidemiologic surveys to evaluate the long-term protection afforded by HBV vaccination and to rationalize further prevention strategies. These studies were done every five years since 1984, just before the launch of our universal HBV vaccination program [9], [10], [11], [12], [13]. HBsAg seroprevalence declined from 10 to 0.6% in children under 15 years old in Taipei city during the past two decades [13]. The seropositive rates for HBsAg, antibody to HBsAg (anti-HBs),
Vaccine failure
A positive maternal HBsAg status was found in 89% of the HBsAg seropositive subjects born after the vaccination program [13]. Maternal HBsAg was found to be positive in 97% of the infants with HBV-positive FHF [14]. In spite of the success of hepatitis B immunization, childhood HCC still failed to be completely prevented by the universal vaccination program [17]. Mother-to-child transmitted HBV infection is an important risk factor of HCC development. This is evidenced by the very high HBsAg
A universal boost dose is not required
To address whether a boost dose is needed 15 years after primary infant immunization with plasma-derived hepatitis B vaccines, we measured anti-HBc, HBsAg, and pre- and post-booster titers of anti-HBs 15 years after primary infant immunization with plasma-derived HBV vaccines in two cohorts of 15-year-old children in Taiwan [32]. Group A consisted of 78 children who were born to HBeAg-positive carrier mothers and had developed protective levels of anti-HBs antibodies (≥ 10 mIU/mL). Group B
Development of new vaccines
In addition to the plasma-derived vaccines and the yeast-derived recombinant vaccines available in the markets, several new vaccines are in development, including the followings:
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yeast-derived or CHO cell-derived Pre-S/S vaccines [39], [40], the preliminary results were promising, especially for the hyporesponders and non-responders to current vaccines;
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DNA vaccine: this may be developed not only for the augmentation of immunogenecity, but also for therapeutic application [41];
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oral vaccine: such
Conclusions
Universal HBV vaccination provides long-term protection for at least 20 years, and a universal booster is not indicated for the primary HBV vaccinees before adulthood. Mother-to-child transmission is the primary reason for vaccine failure and needs to be tackled in future control programs. This may include an appropriate antiviral strategy for the carrier pregnant mothers and adequate protection for the high-risk infants and involve efforts to minimize noncompliance. The emergence of
Conflict of interest statement
The authors have not declared any conflict of interest.
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