Mutations in the Pre-C and Core Region of Hepatitis B Virus DNA in Chronic HBV Carriers.
- Author:
Su Yul AHN
1
;
Jong Wook PARK
;
Su Jeong YUN
;
Min Ho SUH
;
Byung Kil CHOI
Author Information
1. Department of Internal Medicine, Kosin University School of Medicine, Pusan, Korea.
- Publication Type:Original Article
- Keywords:
Chronic Hepatitis B;
HBV pre core/core DNA mutation
- MeSH:
Amino Acid Substitution;
DNA;
DNA, Viral;
Epitopes, T-Lymphocyte;
Hepatitis B virus*;
Hepatitis B*;
Hepatitis B, Chronic;
Hepatitis*;
Hepatitis, Chronic;
Humans;
Nucleotides;
Point Mutation;
Polymerase Chain Reaction;
Sequence Deletion
- From:Korean Journal of Medicine
1999;56(1):1-8
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Causes of diverse clinical sourses of patients with chronic hepatitis B virus(HBV) infection are not fully-known. The host immune response to HBV antigen and the appearance of mutant viruses are believed to be important factors. To determine whether appearance of precore and core mutant viruses are related to the clinical course of the patients, we analysed the entire core region of viral DNA in 7 HBV chronic carriers. METHODS: Serum was obtained from 7 patients(3 chronic active hepatitis, 4 CAH with cirrhosis) and pre-C and core region of HBV were amplified by polymerase chain reaction, then directly sequenced. RESULT: In all 7 HBV DNA there was a point mutation from T to C at nucleotide 2104 of core region, and each DNA also contained 6 to 17 variable point mutations at different nucleotides yielding various amino acid substitution. One of DNA had a point mutation from A to G at nucleotide 1898, converting tryptophan(TGG) to a stop codon(TAG). Two cases of deletion mutations covered C-region segment ranging from nucleotide 2142 to 2306 and one case of deletion covered pre-C region ranging from nucleotide 1815 to 1843. CONCLUSION: Three out of seven DNA contained mutational sites coincided with known immunodominant T cell epitopes and rest of the mutational sites could also affect the antigenecity of the HBV. Therefore, mutant HBV could after the host immune response, and may modulate the clinical course of infection.
