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All issues > Volume 42(10); 1999

Original Article
J Korean Pediatr Soc. 1999;42(10):1392-1402. Published online October 15, 1999.
Hepatitis B Virus Precore and Core Promotor Mutations in Children with Chronic Hepatitis B Infection
Woo Yeong WY Chung1, Jin Kuk JK Kim2, Yeong Hoon YH Kim3, Yeong Hong YH Park3, Chul Ho CH Kim1
1Department of Pediatrics, College of Medicine, Pusan Paik Hospital, Inje University, Pusan, Korea
2Department of Pediatrics, Kwang Hwae General Hospital, Pusan, Korea
3Department of Biochemistry, College of Medicine, Pusan Paik Hospital, Inje University, Pusan, Korea
Correspondence Woo Yeong WY Chung ,Email: 1
Abstract
Purpose
: The aims of this study were to investigate the frequencies and role of hepatitis B virus(HBV) precore and core promotor mutations in children with chronic hepatitis B infection.
Methods
: Sera from 31 children with chronic HBV infection were analyzed by direct sequencing of polymerase chain reaction amplification of HBV DNA.
Results
: Twenty-nine adr type were analyzed. The mutations in HBV precore region were observed in 8(27.6%) of 29 cases. The G→A mutation of nucleotide 1896(A1896; stop codon) were observed in 4 cases(13.8%). The mutations in HBV core promotor region were observed in 27 (93.1%) of 29 cases. The G(1764)→A mutation(A1764) was observed in 14 cases(48.3%), and among these 12 cases combined with a A to T change at nucleotide 1762(T1762). The mutations in HBV precore region were obsereved in 4(21%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. A1896 mutation was observed in 2 cases in both HBeAg positive and negative group, respectively. The mutations in HBV core promotor region were observed in 18(94.7%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. T1762 mutation were observed in 6(31.6%) of 19 cases of HBeAg positive group and 6(60%) of 10 cases of HBeAg negative group(P=0.14). A1764 mutation was obsereved in 7 (36.8%) of 19 cases of HBeAg positive group and 7(70%) of 10 cases of HBeAg negative group (P=0.089). A1896 mutation was observed in 2(18.2%) of 11 cases in increased AST/ALT group and 2(11.1%) of 18 cases in normal AST/ALT group. A1764 and T1762 mutations were higher (61.1%) in AST/ALT increased group than those(27.3%) in AST/ALT normal group, but there was no statistical significance(P=0.077).
Conclusion
: Mutations in the precore and core promotor regions can be frequently detected in children with chronic HBV infection. T1762 and A1764 mutations were observed more frequently in HBeAg negative group and in AST/ALT increased group but there was no statistical significance.

Keywords :Hepatitis B virus, Precore/Core promotor mutations, Chronic hepatitis B infection

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