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Journal of Virology, January 2001, p. 161-170, Vol. 75, No. 1
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.1.161-170.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Duck Hepatitis B Virus Expresses a Regulatory HBx-Like Protein from a Hidden Open Reading Frame

Shau-Feng Chang,1,2 Hans Jürgen Netter,1,3 Eberhard Hildt,4 Ralph Schuster,5 Stephan Schaefer,5 Yin-Chen Hsu,2 Andreas Rang,1 and Hans Will1,*

Heinrich-Pette-Institut für experimentelle Virologie und Immunologie an der Universität Hamburg, Hamburg,1 Institut für experimentelle Onkologie und Therapieforschung, Klinikum rechts der Isar, Munich,4 and Institut für Medizinische Virologie, Justus-Liebig-Universität, Giessen,5 Germany; Molecular Biomedical Technology Division, Biomedical Engineering Center, Industrial Technology Research Institute, Hsinchu, Taiwan2; and Sir Albert Sakzewski Virus Research Centre, Brisbane, Australia3

Received 31 March 2000/Accepted 2 October 2000

Duck hepatitis B viruses (DHBV), unlike mammalian hepadnaviruses, are thought to lack X genes, which encode transcription-regulatory proteins believed to contribute to the development of hepatocellular carcinoma. A lack of association of chronic DHBV infection with hepatocellular carcinoma development supports this belief. Here, we demonstrate that DHBV genomes have a hidden open reading frame from which a transcription-regulatory protein, designated DHBx, is expressed both in vitro and in vivo. We show that DHBx enhances neither viral protein expression, intracellular DNA synthesis, nor virion production when assayed in the full-length genome context in LMH cells. However, similar to mammalian hepadnavirus X proteins, DHBx activates cellular and viral promoters via the Raf-mitogen-activated protein kinase signaling pathway and localizes primarily in the cytoplasm. The functional similarities as well as the weak sequence homologies of DHBx and the X proteins of mammalian hepadnaviruses strongly suggest a common ancestry of ortho- and avihepadnavirus X genes. In addition, our data disclose similar intracellular localization and transcription regulatory functions of the corresponding proteins, raise new questions as to their presumed role in hepatocarcinogenesis, and imply unique opportunities for deciphering of their still-enigmatic in vivo functions.

* Corresponding author. Mailing address: Heinrich-Pette-Institut, Martinistrasse 52, 20251 Hamburg, Germany. Phone: 49-40-48051-221. Fax: 49-40-48051-222. E-mail: will{at}hpi.uni-hamburg.de.

Journal of Virology, January 2001, p. 161-170, Vol. 75, No. 1
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.1.161-170.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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