title: Precore wild-type hepatitis B virus with G1896 in the resolution of persistent hepatitis B virus infection.
abstract: OBJECTIVE
  Factors influencing the resolution of persistent hepatitis B virus (HBV) infection were sought for.
  
  
  METHODS
  The loss of hepatitis B surface antigen (HBsAg) from serum was correlated with mutations in HBV DNA for a hepatitis B e antigen (HBeAg)-minus phenotype in patients infected with HBV genotype C and positive for HBeAg at presentation.
  
  
  RESULTS
  HBeAg turned negative in all the 22 patients in whom HBV infection resolved, but only in 11 of the 25 patients with severe liver diseases (100 vs. 44%, p = 0.0001). The precore wild type (G1896) persisted significantly more frequently in the 22 patients in whom HBV infection resolved than in the 11 patients who developed decompensated liver cirrhosis or hepatocellular carcinoma (15/22 or 68% vs. 1/11 or 9%, p = 0.005). The double mutation in the core promoter (T1762/A1764) was comparably frequent in the two groups of patients at presentation (14/22 or 64% vs. 7/11 or 64%) and >15 years thereafter (18/22 or 82% vs. 10/11 or 91%).
  
  
  CONCLUSIONS
  The precore wild type (G1896) would seem to facilitate the resolution of HBV infection, while the precore mutant (A1896) may induce severe liver diseases in patients with HBeAg-positive chronic hepatitis who have lost HBeAg from serum.
authors.affiliation: Research Institute for Hepatology, Toranomon Hospital, Tokyo, Japan. vj7m-kbys@asahi-net.or.jp
authors.forename: Mariko
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Yasuji
authors.initials: Y
authors.lastname: Arase
authors.forename: Kenji
authors.initials: K
authors.lastname: Ikeda
authors.forename: Akihito
authors.initials: A
authors.lastname: Tsubota
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Saitoh
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Suzuki
authors.forename: Norio
authors.initials: N
authors.lastname: Akuta
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hosaka
authors.forename: Takashi
authors.initials: T
authors.lastname: Someya
authors.forename: Marie
authors.initials: M
authors.lastname: Matsuda
authors.forename: Junko
authors.initials: J
authors.lastname: Sato
authors.forename: Kimiko
authors.initials: K
authors.lastname: Takagi
authors.forename: Yuzo
authors.initials: Y
authors.lastname: Miyakawa
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Kumada
mesh_terms: D000328:Adult; D004279:DNA, Viral / Q000097:blood / Q000235:genetics; D018450:Disease Progression; D005260:Female; D006510:Hepatitis B Antibodies / Q000097:blood; D006512:Hepatitis B Core Antigens / Q000235:genetics*; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006513:Hepatitis B e Antigens / Q000097:blood* / Q000235:genetics / Q000276:immunology; D006515:Hepatitis B virus / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000276:immunology / Q000503:physiopathology* / Q000821:virology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D011401:Promoter Regions, Genetic; D011498:Protein Precursors / Q000235:genetics*
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D011498:Protein Precursors