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J Gen Virol. 2002 May;83(Pt 5):991-6.

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

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1
Central Laboratory Animal Facility of the Johannes Gutenberg-University of Mainz, Obere Zahlbacherstr. 67-Hochhaus am Augustusplatz, D-55101 Mainz, Germany. reifenbe@mail.uni-mainz.de

Abstract

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.

PMID:
11961252
DOI:
10.1099/0022-1317-83-5-991
[Indexed for MEDLINE]
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