title: Comparison of complete sequences of hepatitis B virus genotype C between inactive carriers and hepatocellular carcinoma patients before and after seroconversion.
abstract: BACKGROUND
  Most patients who acquire chronic hepatitis B virus (HBV) infection by perinatal transmission become inactive carriers (IC) after hepatitis B e (HBe) antigen seroconversion, whereas some patients have persistent abnormal serum transaminase levels and develop hepatocellular carcinoma (HCC) in the anti-HBe-positive phase. The aim of this study was to investigate the HCC-related mutations of HBV.
  
  
  METHODS
  Complete sequences of HBV were examined among eight IC and eight HCC patients infected with HBV genotype C before and after seroconversion.
  
  
  RESULTS
  The frequency of the T1653 mutation tended to be higher among HCC patients after seroconversion (16.7% vs. 62.5%; P = 0.086). The prevalence of a basal core promoter double mutation (T1762/A1764) was high among both IC and HCC patients after seroconversion (83.3% vs. 87.5%; P = 0.825). Among the HCC patients, a pre-S deletion mutant was detected in 62.5% patients before seroconversion, and in 37.5% patients after seroconversion. The core deletion mutant was also detected in 50% of HCC patients only before seroconversion. Deletion mutants of the pre-S or core region before seroconversion were significantly associated with HCC patients (0% vs. 62.5%; P = 0.007, 0% vs. 50%; P = 0.021, respectively).
  
  
  CONCLUSIONS
  Our data showed a significant association of pre-S and core deletion mutants before seroconversion with HCC development. The T1653 mutation after seroconversion was frequently found in HCC patients infected with HBV genotype C. These results suggest that mutations may be predictive factor for development of HCC.
authors.affiliation: Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho, Nagoya 467-8601, Japan.
authors.forename: Kiyoaki
authors.initials: K
authors.lastname: Ito
authors.forename: Yasuhito
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Michio
authors.initials: M
authors.lastname: Kato
authors.forename: Kei
authors.initials: K
authors.lastname: Fujiwara
authors.forename: Fuminaka
authors.initials: F
authors.lastname: Sugauchi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Noboru
authors.initials: N
authors.lastname: Shinkai
authors.forename: Etsuro
authors.initials: E
authors.lastname: Orito
authors.forename: Masashi
authors.initials: M
authors.lastname: Mizokami
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000209:etiology* / Q000235:genetics; D002353:Carrier State; D005260:Female; D005544:Forecasting; D005814:Genes, Viral / Q000276:immunology; D005838:Genotype; D006513:Hepatitis B e Antigens / Q000276:immunology*; D006515:Hepatitis B virus / Q000235:genetics* / Q000472:pathogenicity; D019694:Hepatitis B, Chronic / Q000150:complications* / Q000276:immunology; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009154:Mutation
chemical_list: D006513:Hepatitis B e Antigens