Precore and Core Promoter Mutations of the Hepatitis B Virus Gene in Chronic Genotype C -Infected Children.
10.3346/jkms.2011.26.4.546
- Author:
Hyun Sik KANG
1
;
Ki Soo KANG
;
Byung Cheol SONG
Author Information
1. Department of Pediatrics, Jeju National University School of Medicine, Jeju, Korea. kskang@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Hepatitis B Virus;
Mutation;
Child
- MeSH:
Adolescent;
Alanine Transaminase/blood;
Aspartate Aminotransferases/blood;
Child;
Child, Preschool;
Cohort Studies;
DNA, Viral/blood;
Female;
Genotype;
Hepatitis B Core Antigens/*genetics;
Hepatitis B virus/*genetics;
Hepatitis B, Chronic/immunology/*virology;
Humans;
Infant;
Male;
Mutation;
Promoter Regions, Genetic;
Sequence Analysis, DNA
- From:Journal of Korean Medical Science
2011;26(4):546-550
- CountryRepublic of Korea
- Language:English
-
Abstract:
The precore (G1896A) and core promoter (A1762T, G1764A) mutations of the hepatitis B virus gene are known to be associated with changes in immunologic phase or the progression to complicated liver disease in adults. We analyzed these mutations in chronically HBV-infected children. Serum was collected from 37 children with chronic HBV infection from March 2005 to September 2008. HBV DNA extraction and nested PCR were followed by sequencing of the PCR products. The children were 6.7 +/- 4.6 yr old. All of 37 children had HBV genotype C. Of the cohort, 31 (83.8%) were HBeAg-positive and 6 (16.2%) were HBeAg-negative; the former group comprised 18 (48.6%) who were in the immune-tolerance phase (ITP) and 13 (35.2%) in the immune-clearance phase (ICP). Most of the patients had HBV DNA levels of > 1.0 x 10(8) copies/mL. In the ITP group, only 1 (5.5%) had core promoter mutations, and none had the precore mutation. In the ICP group, only 2 (15.4%) had core promoter mutations; the remaining 6 patients had HBV DNA levels of < 2.0 x 10(3) copies/mL and no core promoter/precore mutations. The very low incidence of the precore/core promoter gene mutation, in children, suggests that these mutations may be the result of life-long chronic HBV infection.
