共 43 条
Complete hepatitis B virus genome analysis in HBsAg positive mothers and their infants with fulminant hepatitis B
被引:21
作者:

Friedt, M
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Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany

Gerner, P
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Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany

Wintermeyer, P
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Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany

Wirth, S
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Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany
机构:
[1] Univ Witten Herdecke, Childrens Hosp, Helios Klinikum Wuppertal, D-42349 Wuppertal, Germany
关键词:
D O I:
10.1186/1471-230X-4-11
中图分类号:
R57 [消化系及腹部疾病];
学科分类号:
摘要:
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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