title: Virological and clinical implication of core promoter C1752/V1753 and T1764/G1766 mutations in hepatitis B virus genotype D infection in Mongolia.
abstract: OBJECTIVE
  The aim of the present study was to reveal virological and clinical features of hepatitis B virus (HBV) genotype D infection.
  
  
  METHODS
  One hundred and twenty-two Mongolian chronic liver disease (CLD) patients infected with HBV were subjected for serological HBV-markers screening and HBV-enzyme immunoassay (EIA) genotyping. Nucleotide sequences were analyzed for 48 HBV/D strains (23 isolated from hepatocellular carcinoma (HCC) and 25 from CLD patients).
  
  
  RESULTS
  Prevalence of hepatitis B e antigen (HBeAg) positivity was low (25.9%) in young patients (< or =30 years old) indicating early HBeAg seroclearance in HBV/D carriers. The T1764/G1766 double mutation was the most common basal core promoter (BCP) mutation (29.2%) and was frequent in HBeAg-negative patients (39.3%). Patients harboring T1764/G1766 mutants exhibited lower HBV-DNA and HBV core antigen (HBcAg) levels than those with wild-type BCP strains (P = 0.024, 0.049, respectively). C1752 and/or V (not T) 1753 mutation was significantly prevalent in HCC patients (HCC vs CLD; 52.2% vs 20%, P = 0.033). T1762/A1764 mutation was detected in 75.0% of HCC patients with high viral load (> or =5 log copies/mL). Precore stop codon mutation A1896 was detected in (70.8%) of HBV/D-infected patients.
  
  
  CONCLUSIONS
  In Mongolians infected with HBV/D, C1752 and/or V1753 mutation was associated with HCC.
authors.affiliation: Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
authors.forename: Abeer
authors.initials: A
authors.lastname: Elkady
authors.forename: Yasuhito
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Fuat
authors.initials: F
authors.lastname: Kurbanov
authors.forename: Tsendsuren
authors.initials: T
authors.lastname: Oynsuren
authors.forename: Masashi
authors.initials: M
authors.lastname: Mizokami
mesh_terms: D000328:Adult; D006528:Carcinoma, Hepatocellular / Q000821:virology*; D018388:Codon, Terminator; D004279:DNA, Viral / Q000097:blood*; D005260:Female; D005838:Genotype; D006512:Hepatitis B Core Antigens / Q000097:blood; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000150:complications / Q000209:etiology / Q000235:genetics* / Q000276:immunology; D019698:Hepatitis C, Chronic / Q000150:complications / Q000209:etiology / Q000235:genetics; D019701:Hepatitis D, Chronic / Q000150:complications / Q000209:etiology / Q000235:genetics; D006801:Humans; D008113:Liver Neoplasms / Q000821:virology*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D008986:Mongolia; D009154:Mutation; D010641:Phenotype; D010802:Phylogeny; D011401:Promoter Regions, Genetic; D014758:Viral Core Proteins / Q000235:genetics*; D019562:Viral Load
chemical_list: D018388:Codon, Terminator; D004279:DNA, Viral; D006512:Hepatitis B Core Antigens; D006513:Hepatitis B e Antigens; D014758:Viral Core Proteins