4%); and mixed genotypes, 2 (0.9%). The prevalence of genotype C was significantly higher in immunized cases with HBV breakthrough infection versus age-matched, unimmunized carriers (42.1% versus 16.4%, P< 0.001). Among unimmunized children, those born to HBsAg-positive mothers (n = 141) and those born to HBsAg-negative mothers (n = 73) had similar HBV genotype distributions (P = 0.93). Figure 2 depicts the HBV genotype distributions in HBsAg-carrier children stratified by immunization and maternal HBsAg status. All the mothers of immunized cases with HBV breakthrough

infection were HBsAg-positive (Table 1). As for the 214 unimmunized carriers, Palbociclib cost maternal HBsAg-seropositive rates were comparable among children with different HBV genotypes, and the rates were 65.5% for genotype B infection, 68.6% for genotype C infection, and 50% for infection with mixed genotypes (B and C; P = 0.93). Maternal blood samples for HBV genotyping were available for 82 of 107 immunized cases with HBV breakthrough infection and for 91 of 141 unimmunized HBsAg carriers whose mothers were HBsAg-positive. Those mothers with HBV viral loads lower than 103 copies/mL were excluded because of the limitations of the genotyping method.28 Table 2 shows the correlation of HBV genotypes in children and their HBsAg-positive mothers. A high degree of agreement

was found between mothers’ and children’s HBV genotypes in both the unimmunized group Fer-1 mouse (κ = 0.97, 95% CI = 0.90-1.00) and the immunized group (κ = 0.97, 95% CI = 0.92-1.00). Because

the hepatitis B immunization program launched on July 1, 1984 was a national program, most immunized cases with HBV breakthrough infection and unimmunized HBsAg carriers were in different birth cohorts (Table 1). Figure 3 shows the HBV genotype distributions in consecutive birth cohorts in unimmunized and immunized HBsAg-carrier children. For unimmunized children, HBV genotype distributions were comparable among different birth cohort groups (P = 0.391). Similarly, the genotype distributions in immunized HBsAg-carrier CHIR-99021 solubility dmso children of different birth cohorts were also comparable (P = 0.250). With respect to the maternal HBV genotype distribution in the general population in the postimmunization era, among the 136 HBsAg-positive mothers delivering babies in 2007-2009, 95 had a viral load higher than 103 copies/mL, and the HBV genotype B-infected. Among the 95 mothers, 81.1% (77/95) were genotype B–infected, and 18.9% (18/95) were genotype C–infected; the genotype distribution was comparable to that in the unimmunized HBsAg-carrier children (P = 0.558). Because of the high concordance between mothers’ and children’s HBV genotypes, we assumed that all children born to HBsAg-positive mothers acquired the virus from their mothers. Table 3 lists the clinical characteristics of HBsAg-carrier children born to HBsAg-positive mothers and stratified by their HBV genotypes.