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Signals regulating hepatitis B surface antigen transcription

Nature volume 305, pages 336–338 (1983)Cite this article

Abstract

About 200 million people are chronic carriers of hepatitis B surface antigen (HBsAg), but since hepatitis B virus (HBV) cannot be propagated in vitro, HBsAg transcription has been studied only in cell lines containing HBV DNA integrated into chromosomes, and HBsAg-related mRNAs 2.0 to 2.5 kilobases (kb) long have been described1–4. We have analysed the transcripts produced in an infected chimpanzee liver and in a rat cell line containing HBV DNA5. In contrast to previous suppositions1,2 we report here that the major S gene transcript initiates close to the S gene, that is, within the ‘pre-S’ region6 and is processed/polyadenylated at a site situated within the core gene. The efficiency of processing/polyadenylation at this site varies between the chimpanzee liver and the rat cell line studied. The S gene promoter does not contain a TATA box but instead has a sequence homologous to that which positions the 5′ ends of the major simian virus 40 (SV40) late transcript7.

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Authors and Affiliations

  1. Department of Microbiology, University of Heidelberg, Im Neuenheimer Feld 230, 6900, Heidelberg, FRG

    Roberto Cattaneo, Hans Will & Heinz Schaller

  2. Institute for Cell and Tumor Biology of the German Cancer Research Center, Im Neuenheimer Feld 280, 6900, Heidelberg, FRG

    Nouria Hernandez

Authors
  1. Roberto Cattaneo
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  2. Hans Will
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  3. Nouria Hernandez
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  4. Heinz Schaller
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Cattaneo, R., Will, H., Hernandez, N. et al. Signals regulating hepatitis B surface antigen transcription. Nature 305, 336–338 (1983). https://doi.org/10.1038/305336a0

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