Posttransfusion Fulminant Hepatitis B Associated with Precore‐Defective HBV Mutants

Posttransfusion Fulminant Hepatitis B Associated with Precore‐Defective HBV Mutants Abstract. Fulminant hepatitis B developed in 8 recipients of blood units without detectable hepatitis B surface antigen on routine screening. All 124 hepatitis B virus (HBV) DNA clones propagated from their sera possessed defects in the precore region. A point mutation from guanine to adenine at nucleotide 83, converting codon 28 for tryptophan (TGG) to a stop codon (TAG), was the commonest, and it was found in all 113 clones from 7 cases. The remaining case displayed 1 clone with this point mutation and 10 clones with an insertion of 2 base pairs after nucleotide 26. Antibody to hepatitis B core antigen (anti‐HBc) was detected in a high titer in 1 of 10 pilot plasma samples of blood units transfused to this case. HBV DNA clones propagated from it exhibited the same precore‐region defects as those from the recipient. On the basis of these results HBV mutants, defective in the precore region, would appear to be responsible for posttransfusion fulminant hepatitis B, and the exclusion of blood units with high‐titered anti‐HBc would be efficacious in preventing it. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Vox Sanguinis Wiley

Posttransfusion Fulminant Hepatitis B Associated with Precore‐Defective HBV Mutants

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Publisher
Wiley
Copyright
© 1991 S. Karger AG, Basel
ISSN
0042-9007
eISSN
1423-0410
D.O.I.
10.1111/j.1423-0410.1991.tb00868.x
Publisher site
See Article on Publisher Site

Abstract

Abstract. Fulminant hepatitis B developed in 8 recipients of blood units without detectable hepatitis B surface antigen on routine screening. All 124 hepatitis B virus (HBV) DNA clones propagated from their sera possessed defects in the precore region. A point mutation from guanine to adenine at nucleotide 83, converting codon 28 for tryptophan (TGG) to a stop codon (TAG), was the commonest, and it was found in all 113 clones from 7 cases. The remaining case displayed 1 clone with this point mutation and 10 clones with an insertion of 2 base pairs after nucleotide 26. Antibody to hepatitis B core antigen (anti‐HBc) was detected in a high titer in 1 of 10 pilot plasma samples of blood units transfused to this case. HBV DNA clones propagated from it exhibited the same precore‐region defects as those from the recipient. On the basis of these results HBV mutants, defective in the precore region, would appear to be responsible for posttransfusion fulminant hepatitis B, and the exclusion of blood units with high‐titered anti‐HBc would be efficacious in preventing it.

Journal

Vox SanguinisWiley

Published: Jan 1, 1991

References

  • Detection of hepatitis B virus in serum using amplification of viral DNA by means of the polymerase chain reaction
    Sumazaki, Sumazaki; Motz, Motz; Wolf, Wolf; Heinig, Heinig; Jilg, Jilg; Deinhardt, Deinhardt
  • Targeting of the hepatitis B virus precore protein to the endoplasmic reticulum membrane: After signal peptide cleavage translocation can be aborted and the product released into the cytoplasm
    Garcia, Garcia; Ou, Ou; Rutter, Rutter; Walter, Walter
  • Detection of hepatitis B virus DNA in serum by a simple spot hybridization technique: Comparison with results for other viral markers
    Scotto, Scotto; Hadchouel, Hadchouel; Hery, Hery; Yvart, Yvart; Tiollais, Tiollais; Brechot, Brechot
  • Hepatitis B e antigen and infectivity of hepatitis B virus
    Shikata, Shikata; Karasawa, Karasawa; Abe, Abe; Uzawa, Uzawa; Suzuki, Suzuki; Oda, Oda; Imai, Imai; Mayumi, Mayumi; Moritsugu, Moritsugu
  • Is fulminant B hepatitis more common among infants born to e antigen‐negative carrier mothers
    Okuda, Okuda
  • Anticore antibody screening of transfused blood
    Lander, Lander; Gitnick, Gitnick; Gelb, Gelb; Aach, Aach

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