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Complete hepatitis B virus genome analysis in HBsAg positive mothers and their infants with fulminant hepatitis B.

Friedt M, Gerner P, Wintermeyer P, Wirth S - BMC Gastroenterol (2004)

Bottom Line: Nucleotide exchanges in the basic core promotor and precore region were identified in all cases.A heterogeneous virus population was detected in four mothers.HBeAg negative variants were the predominant population in all children, whereas these mutants could only be detected as subpopulations in four mothers.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatrics, University of Zurich, Steinwiesstr. 75, CH-8032 Zurich, Switzerland. mfriedt@web.de

ABSTRACT

Background: After perinatal transmission of hepatitis B virus, infants of anti-HBe positive HBsAg carrier mothers may develop fulminant hepatitis B. Previously it has been suggested, that fulminant hepatitis B in adults was associated with specific mutations in the HBV-genome. The aim of this study was to investigate, whether specific viral variants are associated with fulminant hepatitis B in young infants.

Methods: The complete HBV-genomes of five mothers and their infants with fulminant hepatitis were isolated from the sera, amplified and directly sequenced.

Results: Between 6 and 43 base pair exchanges between the HBV genomes of the infants and their mothers were identified. The mutations spread over the entire virus genome. Nucleotide exchanges in the basic core promotor and precore region were identified in all cases. A heterogeneous virus population was detected in four mothers.

Conclusions: Many new mutations were proved to emerge during fulminant hepatitis B in infants, who had been perinatally infected. HBeAg negative variants were the predominant population in all children, whereas these mutants could only be detected as subpopulations in four mothers. The data suggest that the selection of a specific HBeAg negative viral strain may be associated with the development of fulminant hepatitis B in children.

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Nucleotide Exchanges between mothers (M1–M5) and their infants (1–5) in comparison with the Reference Sequence. Nucleotide positions are according to the nomenclature of Galibert et al. 1979. Mutations occurring in the HBV genomes of both, mother and child-compared to the reference sequence, are not listed. Nucleotide positions with a heterogeneous HBV population are shown in italics.
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Figure 1: Nucleotide Exchanges between mothers (M1–M5) and their infants (1–5) in comparison with the Reference Sequence. Nucleotide positions are according to the nomenclature of Galibert et al. 1979. Mutations occurring in the HBV genomes of both, mother and child-compared to the reference sequence, are not listed. Nucleotide positions with a heterogeneous HBV population are shown in italics.

Mentions: Sequence alignments were performed using the Sequencher 3.0 software program. The HBV-DNA sequences were assigned to the appropriate genotype according to Li et al. [10]. Additionally, sequences were genotyped by alignment to published HBV sequences of genotypes A to E including the two strains HT and FH which were isolated from patients with FHB (Genbank/EMBL no. M57663, X02763, V00866, E00010, X65257-59, M32138, X02496, V01460, I08805, I27106; L08805 and L27106). The sequences were aligned according to Galibert [11]. The first base pair is the first T residue in the EcoRI recognition site. Nucleotide differences between mother and infant were defined as mutations. The reference genome [11] is depicted for better comparison (Figure 1).


Complete hepatitis B virus genome analysis in HBsAg positive mothers and their infants with fulminant hepatitis B.

Friedt M, Gerner P, Wintermeyer P, Wirth S - BMC Gastroenterol (2004)

Nucleotide Exchanges between mothers (M1–M5) and their infants (1–5) in comparison with the Reference Sequence. Nucleotide positions are according to the nomenclature of Galibert et al. 1979. Mutations occurring in the HBV genomes of both, mother and child-compared to the reference sequence, are not listed. Nucleotide positions with a heterogeneous HBV population are shown in italics.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC425580&req=5

Figure 1: Nucleotide Exchanges between mothers (M1–M5) and their infants (1–5) in comparison with the Reference Sequence. Nucleotide positions are according to the nomenclature of Galibert et al. 1979. Mutations occurring in the HBV genomes of both, mother and child-compared to the reference sequence, are not listed. Nucleotide positions with a heterogeneous HBV population are shown in italics.
Mentions: Sequence alignments were performed using the Sequencher 3.0 software program. The HBV-DNA sequences were assigned to the appropriate genotype according to Li et al. [10]. Additionally, sequences were genotyped by alignment to published HBV sequences of genotypes A to E including the two strains HT and FH which were isolated from patients with FHB (Genbank/EMBL no. M57663, X02763, V00866, E00010, X65257-59, M32138, X02496, V01460, I08805, I27106; L08805 and L27106). The sequences were aligned according to Galibert [11]. The first base pair is the first T residue in the EcoRI recognition site. Nucleotide differences between mother and infant were defined as mutations. The reference genome [11] is depicted for better comparison (Figure 1).

Bottom Line: Nucleotide exchanges in the basic core promotor and precore region were identified in all cases.A heterogeneous virus population was detected in four mothers.HBeAg negative variants were the predominant population in all children, whereas these mutants could only be detected as subpopulations in four mothers.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatrics, University of Zurich, Steinwiesstr. 75, CH-8032 Zurich, Switzerland. mfriedt@web.de

ABSTRACT

Background: After perinatal transmission of hepatitis B virus, infants of anti-HBe positive HBsAg carrier mothers may develop fulminant hepatitis B. Previously it has been suggested, that fulminant hepatitis B in adults was associated with specific mutations in the HBV-genome. The aim of this study was to investigate, whether specific viral variants are associated with fulminant hepatitis B in young infants.

Methods: The complete HBV-genomes of five mothers and their infants with fulminant hepatitis were isolated from the sera, amplified and directly sequenced.

Results: Between 6 and 43 base pair exchanges between the HBV genomes of the infants and their mothers were identified. The mutations spread over the entire virus genome. Nucleotide exchanges in the basic core promotor and precore region were identified in all cases. A heterogeneous virus population was detected in four mothers.

Conclusions: Many new mutations were proved to emerge during fulminant hepatitis B in infants, who had been perinatally infected. HBeAg negative variants were the predominant population in all children, whereas these mutants could only be detected as subpopulations in four mothers. The data suggest that the selection of a specific HBeAg negative viral strain may be associated with the development of fulminant hepatitis B in children.

Show MeSH
Related in: MedlinePlus