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Journal of General Virology (2002), 83, 991-996.
© 2002 Society for General Microbiology

Animal: DNA Viruses

Virus replication and virion export in X-deficient hepatitis B virus transgenic mice

Kurt Reifenberg1, Petra Nusser2, Jürgen Löhler3, Gabriele Spindler2, Christa Kuhn4, Fritz von Weizsäcker5 and Josef Köck5

Central Laboratory Animal Facility of the Johannes Gutenberg–University of Mainz, Obere Zahlbacherstr. 67 – Hochhaus am Augustusplatz, D-55101 Mainz, Germany1
Laboratory Animal Research Unit of the University of Ulm, Albert Einstein Allee 11, D-89081 Ulm, Germany2
Heinrich Pette Institute for Experimental Virology and Immunology, Martinistr. 52, D-20251 Hamburg, Germany3
Zentrum für Molekulare Biologie, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany4
Department of Medicine II, University of Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany5

Author for correspondence: Kurt Reifenberg. Fax +49 6131 39 30220. e-mail reifenbe{at}mail.uni-mainz.de

The function of the X protein (pX) in the replication cycle of mammalian hepadnaviruses is enigmatic. Using tissue culture experiments it has been shown that the X gene product is not central to hepatitis B virus (HBV) replication and virion export. However, at present it is still unclear whether this also applies to the in vivo situation. Using a terminally redundant X-deficient HBV DNA construct, transgenic mice were established that exhibited high-level expression of the viral core protein in liver and kidneys. Importantly, replicative DNA intermediates and mature viral genomes could be detected in the liver and serum of these mice, respectively. These findings indicate that, in the in vivo model of transgenic mice, the HBV X (HBx) gene product is not required for HBV replication and virion secretion.




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