Signals regulating hepatitis B surface antigen transcription

Roberto Cattaneo, Hans Will, Nouria Hernandez, Heinz Schaller

Research output: Contribution to journalArticle

118 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)336-338
Number of pages3
JournalNature
Volume305
Issue number5932
DOIs
StatePublished - Dec 1 1983

ASJC Scopus subject areas

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    Cattaneo, R., Will, H., Hernandez, N., & Schaller, H. (1983). Signals regulating hepatitis B surface antigen transcription. Nature, 305(5932), 336-338. https://doi.org/10.1038/305336a0