## Abstract The incidence of perinatal transmission of hepatitis B virus (HBV) depends on the HBeAg/anti‐HBe status of the mother. While children of HBeAg‐positive mothers have a 90% probability of acquiring a chronic hepatitis B virus carrier state, babies of anti‐HBe‐positive mothers are more lik
Selective transmission of variant genomes from mother to infant in neonatal fulminant hepatitis B
✍ Scribed by Fritz Von Weizsäcker; Irmgard Pult; Katja Geiss; Stefan Wirth; Hubert E. Blum
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 649 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
Hepatitis B virus (HBV) nucleotide sequences isolated from motherkhild pairs were analyzed in three cases of neonatal fulminant hepatitis B (FHB). Heterogeneous HBV sequences consistent with both adw2 and ayw subtype were found in all three mothers. In one case, in which the child survived, both subtypes were transmitted. By contrast, only the ayw subtype was present in the two other children with a fatal course of FHB. In one fatal case, studied in greater detail, multiple HBV variants (viral quasi-species) were identified in both mother and child. A direct sequence comparison showed that only a subfraction of the virus pool from the mother was transmitted and that multiple new mutations emerged in the child. These data suggest that a minor HBV subpopulation from the mother may prevail as the dominant species in the child and that neonatal FHB is associated with the selection of mutant strains. (HEPA-TOLOGY 1995; 2 1 :8-13.)
Neonatal fulminant hepatitis B (FHB) is a rare but serious form of perinatal hepatitis B virus (HBV) infection that often takes a fatal course. Infection by hepatitis B e antigen (HBeAg)-positive carrier mothers usually results in a chronic carrier status of infected babies, possibly by induction of immunologic tolerance to HBeAg in utero." On the other hand, babies born to HBeAg-negative mothers are more likely to clear the virus' and more frequently present with a severe clinical course of HBV infection, including FHB.3 Little is known about the pathogenesis of neonatal FHB. Several lines of evidence suggest that HBV variants may be involved in the development of severe liver disease4x5 and that multiple genotypes may be present in the serum of individuals with chronic liver d i ~e a s e . ~, ~ However, it has not been established whether the predomi-
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