Chronic HBV infection, with the attendant risk of cirrhosis and hepatocellular carcinoma, occurs in 1%-5% of adults and up to 90% of infants who are infected with HBV.3-5 Providing vaccinations during adolescence without offering vaccinations during infancy misses this critical period when the acquisition of a HBV infection can be the most harmful. Epidemiologic studies show that the age distribution of HBV varies by jurisdiction and suggest that roughly one-third of chronic infections are acquired during infancy and early childhood.6-9 An ideal vaccine schedule should protect against infection both in infancy, when the risk of becoming a chronic HBV carrier is highest, and in adolescence, when high-risk sexual and drugusing behaviours occur more frequently.Epidemiologic data are critical for informing decisions about vaccination. Estimating the age-specific incidence of acute infections is valuable for planning prevention measures. However, acute infections in infants and toddlers may be missed because HBV infection is often asymptomatic in young children. In many jurisdictions, the age-specific incidence of HBV infection is unknown.The controversy surrounding booster injections stems in part from the rapid drop in antibodies after completion of the primary series of injections. Serum levels of antibodies against hepatitis B surface antigen have been used to measure the initial response to vaccination (antibody levels ≥ 10 IU/L are considered protective). This marker measures response to the vaccine within the first few weeks but is not an appropriate indicator of long-term immunity. Serologic studies have shown that the titre of antibodies against hepatitis B surface antigen drops within the first few years after vaccination and that one-third to one-half of children vaccinated as infants will have titres below 10 IU/L by 10-15 years of age. [10][11][12] This has been misinterpreted to mean that population-level protection shows a similar dramatic drop.Long-term observational data show that vaccinated individuals -even those who have an undetectable titre of hepatitis B surface antigen -can mount an anamnestic response to contact with HBV.11,13 A recent booster trial performed 18 years after vaccination of infants in Gambia provides further evidence of persistent immunity.14 Although almost 70% of participants had no detectable antibodies at baseline, of the 181 participants who were tested 2 weeks after receiving a booster dose, 92.3% (95% CI 87.4-95.7) showed an early anamnestic response.14 The geometric mean concentration of antibodies against hepatitis B surface antigen in this group rose to 524 IU/L (95% CI 441-621), which suggests that most people who have been vaccinated can mount a protective immune response even 18 years after receiving a primary series of vaccinations in infancy.
Universal vaccination of infantsAs of 2007, 171 of the 193 member countries of the World Health Organization (WHO) had implemented the recommendations of the Expanded Programme on Immunization to offer universal hepatitis B ...