title: [Interruption failure of heptitis B virus vaccination in mother-to-infant transmission and heptitis B virus genotypes and preC/BCP mutations].
abstract: OBJECTIVE
  To investigate the association of heptitis B virus (HBV) genotypes and precore(PreC)/basal core promoter(BCP) mutation with interruption failure of HBV vaccination in mother-to-infant transmission.
  
  
  METHODS
  A total number of 208 serum samples were collected from infants and mothers,including 16 infants who had become HBsAg-positive despite a complete and timely course of immunization and another 88 infants successfully protected from mother-to infant HBV transmission. HBV genotypes were determined by type-specific primers PCR method. PreC/BCP mutations were detected by direct sequencing of PCR products, and Clustal W 1.8 software was applied to analyzing the sequences.
  
  
  RESULTS
  Of 16 mothers who were having vaccine failure infants, 15 (93.8%) were HBeAg positive and infected with genotype C (15/15, 100%). Among 88 mothers of having children being protected by vaccine, 51 (58.0%) were HBeAg positive, with 45.1% (23/51) of genotype C. The proportion of genotype C in HBeAg mothers of infants with vaccine failure, was significantly higher than that of mothers with vaccine protected infants (chi2 = 14.3, P = 0.003). However, the frequencies of T1762/A1764 mutations had no significant differences between genotype C HBeAg positive mothers with vaccine failure or protected infants (33.3% and 13.3%, respectively, P = 0.4). No A1896 mutation was found in these two groups.
  
  
  CONCLUSIONS
  HBV genotype C might contribute to the immune failure of HBV vaccination in mother-to-infant transmission, while PreC/BCP mutation might not have correlation with it.
authors.affiliation: Department of Microbiology, Peking University Health Science Center, Beijing 100083, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Wang
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Hui
authors.initials: H
authors.lastname: Zhuang
authors.forename: She-lan
authors.initials: SL
authors.lastname: Liu
authors.forename: Rong-cheng
authors.initials: RC
authors.lastname: Li
authors.forename: Yan-ping
authors.initials: YP
authors.lastname: Li
authors.forename: Zheng-lun
authors.initials: ZL
authors.lastname: Liang
mesh_terms: D000328:Adult; D005260:Female; D005814:Genes, Viral; D005838:Genotype; D006509:Hepatitis B / Q000276:immunology / Q000517:prevention & control* / Q000635:transmission; D017325:Hepatitis B Vaccines / Q000276:immunology*; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007231:Infant, Newborn; D018445:Infectious Disease Transmission, Vertical / Q000517:prevention & control*; D009154:Mutation; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology / Q000821:virology; D011401:Promoter Regions, Genetic
chemical_list: D017325:Hepatitis B Vaccines