title: A Quasi species of the pre-S/S gene and mutations of enhancer II/core promoter/pre-C in mothers and their children infected with hepatitis B virus via mother-to-infant transmission.
abstract: BACKGROUND
  Hepatitis B virus (HBV) infection has a tendency to be chronic. The quasi species of HBV in the pre-S/S gene and mutations in enhancer II (EnhII)/core promoter (CP)/pre-C of HBV were studied in asymptomatic carrier (AsC) mothers and their children with different virus loads, to gain a better understanding of the pathogenic mechanisms of HBV.
  
  
  METHODS
  Quasi species were analyzed using an established phylogenetic tree based on the sequences of the pre-S/S gene from 3 mother-child pairs. The mutations of EnhII/CP/pre-C were studied in 15 mother-child pairs.
  
  
  RESULTS
  Substitution was the main mutation model. The phylogenetic tree indicated that the pre-S/S gene in every mother-child pair had the same root. The sequences of the pre-S/S gene of each patient were somewhat different from one another, but there was limited evolutionary distance between them. The evolutionary distances between the pre-S/S gene and the base of the tree in patients with low virus loads were greater than those in patients with high virus loads. The mutations in patients with low virus loads were much more frequent than those in patients with high virus loads and were not related to age, irrespective of whether the pre-S/S gene or EnhII/CP/pre-C was considered.
  
  
  CONCLUSIONS
  There are HBV quasi species in the sera of AsCs, and the mutations are related to virus load and hepatitis B e antigen seroconversion, irrespective of age.
authors.affiliation: Institute of Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, People's Republic of China.
authors.forename: Hongmei
authors.initials: H
authors.lastname: Xu
authors.forename: Mingli
authors.initials: M
authors.lastname: Peng
authors.forename: Yuling
authors.initials: Y
authors.lastname: Qing
authors.forename: Ning
authors.initials: N
authors.lastname: Ling
authors.forename: Yinghua
authors.initials: Y
authors.lastname: Lan
authors.forename: Zengwei
authors.initials: Z
authors.lastname: Liang
authors.forename: Dachuan
authors.initials: D
authors.lastname: Cai
authors.forename: Yongguo
authors.initials: Y
authors.lastname: Li
authors.forename: Hong
authors.initials: H
authors.lastname: Ren
mesh_terms: D000328:Adult; D001483:Base Sequence; D002353:Carrier State / Q000821:virology; D002648:Child; D004742:Enhancer Elements, Genetic / Q000235:genetics; D005260:Female; D006509:Hepatitis B / Q000635:transmission / Q000821:virology; D006512:Hepatitis B Core Antigens / Q000235:genetics*; D006514:Hepatitis B Surface Antigens / Q000235:genetics*; D006515:Hepatitis B virus / Q000145:classification / Q000235:genetics*; D006801:Humans; D018445:Infectious Disease Transmission, Vertical; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D011401:Promoter Regions, Genetic / Q000235:genetics; D011498:Protein Precursors / Q000235:genetics*; D017422:Sequence Analysis, DNA
chemical_list: D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D011498:Protein Precursors