PRECORE STOP CODON MUTANT IN CHRONIC HEPATITIS-B VIRUS-INFECTION IN CHILDREN - ITS RELATION TO HEPATITIS-B E-SEROCONVERSION AND MATERNAL HEPATITIS-B SURFACE-ANTIGEN

Citation
Mh. Chang et al., PRECORE STOP CODON MUTANT IN CHRONIC HEPATITIS-B VIRUS-INFECTION IN CHILDREN - ITS RELATION TO HEPATITIS-B E-SEROCONVERSION AND MATERNAL HEPATITIS-B SURFACE-ANTIGEN, Journal of hepatology, 28(6), 1998, pp. 915-922
Citations number
32
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
28
Issue
6
Year of publication
1998
Pages
915 - 922
Database
ISI
SICI code
0168-8278(1998)28:6<915:PSCMIC>2.0.ZU;2-8
Abstract
Background/Aims: The aims of this study were to investigate the signif icance of the precore stop codon mutant in the natural course of hepat itis B virus infection in children, and the influence of maternal tran smission. Methods: Sequential sera from 80 hepatitis B virus carrier c hildren both before and after e seroconversion during long-term follow -up were studied using the polymerase chain reaction-amplification cre ated restriction site method. Direct sequencing of the precore region was performed in 89 sera from 32 of the 80 children. Results: The prec ore stop codon mutant coexisting with wild strain was found in 10% of children initially, and later in 25% of children before e seroconversi on, After e seroconversion, wild type was still present in 75% and mut ant in 39% of children at the end of follow-up. The mutant alone was p resent in 15% of anti-HBe positive children without concomitant aminot ransferase elevation. Children with earlier emergence of this mutant t ended to have higher peak aminotransferase levels. This mutant emerged less frequently in children of hepatitis B virus carrier mothers (37. 5%) than in those of non-carrier mothers (65%) (p<0.05). Conclusions: These observations suggest that this mutant is selected by host immune pressure, but is not an initiator in the loss of immune tolerance dur ing childhood chronic hepatitis B virus infection.