Heterogeneous HBV mutants coexist in Korean hepatitis B patients.
- Author:
Won Kyoung KEUM
1
;
Jee Youn KIM
;
Ja Young KIM
;
Sung Gil CHI
;
Jung Woo HONG
;
Sung Soo KIM
;
Joo Hun HA
;
In Sug KANG
Author Information
1. Department of Molecular Biology, School of Medicine, Kyung Hee University, Seoul, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
HBV DNA;
HBV mutant;
PCR-SSCP
- MeSH:
Adult;
Base Sequence;
Conserved Sequence;
Female;
Genetic Heterogeneity;
Hepatitis B Surface Antigens/genetics;
Hepatitis B Virus/genetics*;
Hepatitis B, Chronic/virology*;
Human;
Male;
Middle Age;
Molecular Sequence Data;
Mutation*;
Polymerase Chain Reaction;
Polymorphism, Single-Stranded Conformational;
Sequence Analysis, DNA
- From:Experimental & Molecular Medicine
1998;30(2):115-122
- CountryRepublic of Korea
- Language:English
-
Abstract:
Although many hepatitis B virus (HBV) mutants have been found in all open reading frames since the precore defective mutant was initially reported, systematic investigations of diverse HBV mutant populations in hepatitis B patients have not been performed. Therefore, we examined whether heterogeneous mutant populations simultaneously exist in Korean hepatitis B patients. In order to detect hepatitis B virus mutants, we amplified a conserved core region and a surface antigen region of HBV DNA by PCR from sera of 27 Korean chronic hepatitis B patients, and then performed single strand conformational polymorphism analysis followed by DNA sequencing analysis. The results showed that heterogeneous HBV mutants in both regions were present in a single as well as in various hepatitis B patients. Sequence analysis revealed a defective interfering particle with missense mutation in the core region. We also found that two subtypes of adr and adw coexisted in a single patient. In addition, a point mutation causing a stop codon in the surface antigen region was observed. We are further analyzing the clinical implications of HBV mutants to identify their roles in the pathogenesis of chronic hepatic disorders induced by HBV.
