BACKGROUND: Mutants of the a determinant of hepatitis B surface antigen (HBsAg) can escape neutralization by vaccine-induced antibodies and prevail in an immunized population. METHODS: We evaluated the a mutants in a pediatric population surveyed in 2004 and compared these findings with the data of previous surveys. RESULTS: There were 38 children and 74 adolescents who were HBsAg positive, and serum hepatitis B virus (HBV) DNA was obtained and tested from 31 and 34 of them, respectively. The a mutants were found in 7 (22.6%) of 31 HBV DNA-positive children and in 7 (0.10%) of 7234 children, the entire population that was surveyed in 2004. After the beginning of universal immunization, the very low prevalence of mutants has remained unchanged for 20 years. More a mutants were found in immunized than in nonimmunized HBV DNA-positive children aged 1-4 years old (31% vs 4%, P = .016) but not in those children aged 5-12 years old. Approximately 68% of immunized, mutant-infected children had carrier mothers. More a mutants emerged in children immunized with plasma-derived vaccines than in those immunized with recombinant vaccines (14 of 5166 vs 3 of 4970, respectively; P = .04). HBV DNA levels were significantly lower in hepatitis B e antigen-positive sera containing the G145R mutant than were levels in sera containing wild-type virus. HBsAg-negative sera containing a mutants had very low HBV DNA levels. CONCLUSIONS: Less infectivity of G145R, recombinant vaccine use, and mutant loss with older age seem to decrease the a mutant prevalence in an immunized population over time.
BACKGROUND: Mutants of the a determinant of hepatitis B surface antigen (HBsAg) can escape neutralization by vaccine-induced antibodies and prevail in an immunized population. METHODS: We evaluated the a mutants in a pediatric population surveyed in 2004 and compared these findings with the data of previous surveys. RESULTS: There were 38 children and 74 adolescents who were HBsAg positive, and serum hepatitis B virus (HBV) DNA was obtained and tested from 31 and 34 of them, respectively. The a mutants were found in 7 (22.6%) of 31 HBV DNA-positive children and in 7 (0.10%) of 7234 children, the entire population that was surveyed in 2004. After the beginning of universal immunization, the very low prevalence of mutants has remained unchanged for 20 years. More a mutants were found in immunized than in nonimmunized HBV DNA-positive children aged 1-4 years old (31% vs 4%, P = .016) but not in those children aged 5-12 years old. Approximately 68% of immunized, mutant-infected children had carrier mothers. More a mutants emerged in children immunized with plasma-derived vaccines than in those immunized with recombinant vaccines (14 of 5166 vs 3 of 4970, respectively; P = .04). HBV DNA levels were significantly lower in hepatitis B e antigen-positive sera containing the G145R mutant than were levels in sera containing wild-type virus. HBsAg-negative sera containing a mutants had very low HBV DNA levels. CONCLUSIONS: Less infectivity of G145R, recombinant vaccine use, and mutant loss with older age seem to decrease the a mutant prevalence in an immunized population over time.