title: The prevalence of hepatitis B virus preS deletions occurring naturally in Korean patients infected chronically with genotype C.
abstract: Although Korea is one of the endemic areas for hepatitis B virus infection (HBV), the prevalence of deletions in HBV preS region occurring naturally have not been determined. In the present study, the prevalence of preS deletions was determined in terms of clinical state and HBeAg serostatus in 120 patients with different clinical features [59 HBeAg positive, 61 HBeAg negative; 38 asymptomatic carriers, 21 patients with chronic hepatitis, 21 patients with liver cirrhosis, 40 patients with hepatocellular carcinoma (HCC)]. A total of 37 strains (30.8%) harbored deletions in the preS region. Overall, the frequencies of preS deletions tended to increase gradually according to the degree of the clinical severity of liver disease. The prevalence of preS1 deletions in HCC patients tended to be higher than in patients with liver cirrhosis (32.5% vs. 19%). The prevalence of preS2 deletions in HBeAg negative patients was significantly higher than in HBeAg positive patients (23% vs. 6.8%). The type of deletion encountered most frequently was one disrupting the preS1 start codon [14/37 strains (37.8%)], which showed a very high prevalence in HCC patients (9/40, 22.5%; HCC vs. asymptomatic carriers, P=0.048). These results suggest that there might be the discrepancy between preS1 and preS2 mutations in the mechanism of enhancing the progression of chronic liver disease, especially the development of HCC and to maintain tolerance during the stage of immune tolerance. Specific deletion of the type disrupting preS1 start codon may play important roles in hepatocarcinogenesis, at least in Korean patients with chronic HBV infection.
authors.affiliation: Department of Microbiology and Immunology, Liver Research Institute and Cancer Research Institute, College of Medicine, Seoul National University, Seoul, South Korea.
authors.forename: Ho-Suk
authors.initials: HS
authors.lastname: Mun
authors.forename: Seoung-Ae
authors.initials: SA
authors.lastname: Lee
authors.forename: Youngmee
authors.initials: Y
authors.lastname: Jee
authors.forename: Hong
authors.initials: H
authors.lastname: Kim
authors.forename: Joo-Hee
authors.initials: JH
authors.lastname: Park
authors.forename: Byung-Cheol
authors.initials: BC
authors.lastname: Song
authors.forename: Jung-Hwan
authors.initials: JH
authors.lastname: Yoon
authors.forename: Yoon Jun
authors.initials: YJ
authors.lastname: Kim
authors.forename: Hyo-Suk
authors.initials: HS
authors.lastname: Lee
authors.forename: Jin-won
authors.initials: JW
authors.lastname: Hyun
authors.forename: Eung-Soo
authors.initials: ES
authors.lastname: Hwang
authors.forename: Yoon-Hoh
authors.initials: YH
authors.lastname: Kook
authors.forename: Bum-Joon
authors.initials: BJ
authors.lastname: Kim
mesh_terms: D000328:Adult; D000595:Amino Acid Sequence; D005260:Female; D005838:Genotype; D006514:Hepatitis B Surface Antigens / Q000737:chemistry / Q000235:genetics*; D006515:Hepatitis B virus / Q000145:classification / Q000235:genetics* / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000453:epidemiology / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011498:Protein Precursors / Q000737:chemistry / Q000235:genetics*; D017384:Sequence Deletion
chemical_list: D006514:Hepatitis B Surface Antigens; D011498:Protein Precursors; C050806:presurface protein 1, hepatitis B surface antigen; C050807:presurface protein 2, hepatitis B surface antigen