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Precore stop codon mutant in chronic hepatitis B virus infection in children: its relation to hepatitis B e
1Department of Pediatrics, College of Medicine, National Taiwan University, Taipei. mhchang@ha.mc.ntu.edu.tw
Insights
The precore stop codon mutant in hepatitis B virus infection is selected by immune pressure in children but does not initiate immune tolerance loss. Maternal transmission influences its emergence.
Area of Science:
- Hepatology
- Virology
- Pediatric Infectious Diseases
Background:
- Hepatitis B virus (HBV) infection in children can lead to chronic disease.
- The precore stop codon mutant is a variant of HBV.
- Understanding its role in disease progression and transmission is crucial.
Purpose of the Study:
- To investigate the significance of the precore stop codon mutant in childhood HBV infection.
- To determine the influence of maternal HBV transmission on the mutant's prevalence.
- To analyze the mutant's behavior during the natural course of infection, including seroconversion.
Main Methods:
- Longitudinal follow-up of 80 HBV carrier children.
- Analysis of sequential sera using polymerase chain reaction-amplification created restriction site (47) method.
- Direct sequencing of the precore region in selected samples.
Main Results:
- The precore stop codon mutant was detected in 10% of children initially, rising to 25% before e seroconversion.
- Post-seroconversion, wild type HBV was present in 75% and the mutant in 39% of children.
- Earlier emergence of the mutant correlated with higher peak aminotransferase levels.
- The mutant emerged less frequently in children of HBV carrier mothers (37.5%) compared to non-carrier mothers (65%).
Conclusions:
- The precore stop codon mutant appears to be selected by host immune responses.
- This mutant is not the primary cause of immune tolerance loss in childhood chronic HBV.
- Maternal transmission plays a role in the prevalence of this HBV mutant.
Background/Aims:
The aims of this study were to investigate the significance of the precore stop codon mutant in the natural course of hepatitis B virus infection in children, and the influence of maternal transmission.
Methods:
Sequential sera from 80 hepatitis B virus carrier children both before and after e seroconversion during long-term follow-up were studied using the polymerase chain reaction-amplification created restriction site method. Direct sequencing of the precore region was performed in 89 sera from 32 of the 80 children.
Results:
The precore stop codon mutant coexisting with wild strain was found in 10% of children initially, and later in 25% of children before e seroconversion. After e seroconversion, wild type was still present in 75% and mutant in 39% of children at the end of follow-up. The mutant alone was present in 15% of anti-HBe positive children without concomitant aminotransferase elevation. Children with earlier emergence of this mutant tended 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 during childhood chronic hepatitis B virus infection.