Fischer SF, Schmidt K, Fiedler N, Glebe D, Schüttler C, Sun J, Gerlich WH, Repp R, Schaefer S. Genotype-dependent activation or repression of HBV enhancer II by transcription factor COUP-TF1. World J Gastroenterol 2006; 12(37): 6054-6058 [PMID: 17009409 DOI: 10.3748/wjg.v12.i37.6054]
Corresponding Author of This Article
Stephan Schaefer, Abteilung für Virologie, Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universität Rostock, Schillingallee 70, Rostock D-18057, Germany. stephan.schaefer@med.uni-rostock.de
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Rapid Communication
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World J Gastroenterol. Oct 7, 2006; 12(37): 6054-6058 Published online Oct 7, 2006. doi: 10.3748/wjg.v12.i37.6054
Genotype-dependent activation or repression of HBV enhancer II by transcription factor COUP-TF1
Silke F Fischer, Katja Schmidt, Nicola Fiedler, Dieter Glebe, Christian Schüttler, Jianguang Sun, Wolfram H Gerlich, Reinald Repp, Stephan Schaefer
Silke F Fischer, Katja Schmidt, Nicola Fiedler, Dieter Glebe, Christian Schüttler, Wolfram H Gerlich, Institut für Medizinische Virologie, Justus-Liebig-Universität Giessen, Germany
Reinald Repp, Zentrum für Kinderheilkunde, Justus-Liebig-Universität Giessen; Klinik für Kinder-und Jugendmedizin, Klinikum Fulda, Germany
Silke F Fischer, Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Germany
Stephan Schaefer, Jianguang Sun, Abteilung für Virologie, Universität Rostock, Germany
Supported by grant 10-1854-Scha I from Deutsche Krebshilfe, grant Scha778/2-1 from DFG to S.S. and Graduiertenkolleg Nucleoprotein complexes to S.S. and W.H.G.
Correspondence to: Stephan Schaefer, Abteilung für Virologie, Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universität Rostock, Schillingallee 70, Rostock D-18057, Germany. stephan.schaefer@med.uni-rostock.de
Telephone: +49-381-4945920 Fax: +49-381-4945925
Received: May 5, 2006 Revised: May 28, 2006 Accepted: June 14, 2006 Published online: October 7, 2006
Abstract
AIM: To study the expression of HBV enhancer II by transcription factor COUP-TF1.
METHODS: In order to study the regulation of HBV variants in the vicinity of the NRRE we cloned luciferase constructs containing the HBV enhancer II from variants and from HBV genotypes A and D and cotransfected them together with expression vectors for COUP-TF1 into HepG2 cells.
RESULTS: Our findings show that enhancer II of HBV genotype A is also repressed by COUP-TF1. In contrast, two different enhancer II constructs of HBV genotype D were activated by COUP-TF1. The activation was independent of the NRRE because a natural variant with a deletion of nt 1763-1770 was still activated by COUP-TF1.
CONCLUSION: Regulation of transcription of the HBV genome seems to differ among HBV genomes derived from different genotypes. These differences in transcriptional control among HBV genotypes may be the molecular basis for differences in the clinical course among HBV genotypes.
