title: Clinical significance of pre-S mutations in patients with genotype C hepatitis B virus infection.
abstract: We investigated the overall and site-specific prevalence of pre-S mutations and its clinical significance in patients with genotype C hepatitis B virus (HBV) infection. Three hundred subjects were included: 50 asymptomatic carriers (AC), 87 chronic hepatitis (CH), 91 liver cirrhosis (LC) and 72 hepatocellular carcinoma (HCC). Pre-S mutations were determined by nucleotide sequence analysis. Possible correlations between pre-S mutations and clinical/virological parameters were examined. Pre-S mutations were detected in 82 cases (27.3%); it was more frequently found in HCC (43.1%) and LC (35.2%) group than in the CH (20.7%) and AC (2.0%) group. Pre-S2 deletion was the most commonly found mutation (10.7%), followed by pre-S2 start codon mutation (9.7%), pre-S1-S2 deletion (3.0%) and both pre-S2 deletion and start codon mutation (2.7%). Pre-S2 deletion and pre-S2 start codon mutation were more frequently detected in advanced diseases (LC and HCC). Pre-S mutations were associated with older age and higher rates of positive HBV DNA (>/=0.5 pg/mL). Advanced disease and positive HBV DNA were shown to be independent predictors of pre-S mutations by logistic regression analysis. These findings suggest that pre-S mutations, especially pre-S2 deletions and pre-S2 start codon mutations, are common in patients with genotype C HBV infection and are associated with advanced liver disease and active viral replication.
authors.affiliation: Department of Medicine and Digestive Disease Research Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
authors.forename: M S
authors.initials: MS
authors.lastname: Choi
authors.forename: D Y
authors.initials: DY
authors.lastname: Kim
authors.forename: D H
authors.initials: DH
authors.lastname: Lee
authors.forename: J H
authors.initials: JH
authors.lastname: Lee
authors.forename: K C
authors.initials: KC
authors.lastname: Koh
authors.forename: S W
authors.initials: SW
authors.lastname: Paik
authors.forename: J C
authors.initials: JC
authors.lastname: Rhee
authors.forename: B C
authors.initials: BC
authors.lastname: Yoo
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000821:virology; D002353:Carrier State / Q000821:virology; D002648:Child; D002675:Child, Preschool; D018387:Codon, Initiator / Q000235:genetics; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005838:Genotype; D006514:Hepatitis B Surface Antigens / Q000235:genetics*; D006515:Hepatitis B virus / Q000235:genetics*; D019694:Hepatitis B, Chronic / Q000150:complications / Q000473:pathology* / Q000821:virology*; D006801:Humans; D008103:Liver Cirrhosis / Q000821:virology; D016015:Logistic Models; D008297:Male; D009154:Mutation; D011498:Protein Precursors / Q000235:genetics*; D012367:RNA, Viral / Q000235:genetics*; D017384:Sequence Deletion
chemical_list: D018387:Codon, Initiator; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D011498:Protein Precursors; D012367:RNA, Viral; C050806:presurface protein 1, hepatitis B surface antigen; C050807:presurface protein 2, hepatitis B surface antigen