Enhancement of hepatitis B virus replication by its X protein in transgenic mice

Zhenming Xu; T. S.Benedict Yen; Lanying Wu; Charles R. Madden; Wenjie Tan; Betty L. Slagle; Jing Hsiung Ou

doi:10.1128/jvi.76.5.2579-2584.2002

Enhancement of hepatitis B virus replication by its X protein in transgenic mice

Zhenming Xu, T. S.Benedict Yen, Lanying Wu, Charles R. Madden, Wenjie Tan, Betty L. Slagle, Jing Hsiung Ou

Research output: Contribution to journal › Article › peer-review

124 Scopus citations

Abstract

Hepatitis B virus (HBV) X gene encodes a multifunctional protein that can regulate cellular signaling pathways, interact with cellular transcription factors, and induce hepatocellular oncogenesis. In spite of its diverse activities, the precise role of the X protein in the viral life cycle of HBV remains unclear. To investigate this question, we have produced transgenic mice that carry either the wild-type HBV genome or a mutated HBV genome incapable of expressing the 16.5-kDa X protein. Our results indicate that while the X protein is not absolutely essential for HBV replication or its maturation in transgenic mice, it can enhance viral replication, apparently by activating viral gene expression. These results demonstrate a transactivation role of the X protein in HBV replication in transgenic mice.

Original language	English (US)
Pages (from-to)	2579-2584
Number of pages	6
Journal	Journal of virology
Volume	76
Issue number	5
DOIs	https://doi.org/10.1128/jvi.76.5.2579-2584.2002
State	Published - 2002
Externally published	Yes

ASJC Scopus subject areas

Insect Science
Virology
Microbiology
Immunology

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title = "Enhancement of hepatitis B virus replication by its X protein in transgenic mice",

abstract = "Hepatitis B virus (HBV) X gene encodes a multifunctional protein that can regulate cellular signaling pathways, interact with cellular transcription factors, and induce hepatocellular oncogenesis. In spite of its diverse activities, the precise role of the X protein in the viral life cycle of HBV remains unclear. To investigate this question, we have produced transgenic mice that carry either the wild-type HBV genome or a mutated HBV genome incapable of expressing the 16.5-kDa X protein. Our results indicate that while the X protein is not absolutely essential for HBV replication or its maturation in transgenic mice, it can enhance viral replication, apparently by activating viral gene expression. These results demonstrate a transactivation role of the X protein in HBV replication in transgenic mice.",

author = "Zhenming Xu and Yen, {T. S.Benedict} and Lanying Wu and Madden, {Charles R.} and Wenjie Tan and Slagle, {Betty L.} and Ou, {Jing Hsiung}",

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T1 - Enhancement of hepatitis B virus replication by its X protein in transgenic mice

AU - Xu, Zhenming

AU - Yen, T. S.Benedict

AU - Wu, Lanying

AU - Madden, Charles R.

AU - Tan, Wenjie

AU - Slagle, Betty L.

AU - Ou, Jing Hsiung

PY - 2002

Y1 - 2002

N2 - Hepatitis B virus (HBV) X gene encodes a multifunctional protein that can regulate cellular signaling pathways, interact with cellular transcription factors, and induce hepatocellular oncogenesis. In spite of its diverse activities, the precise role of the X protein in the viral life cycle of HBV remains unclear. To investigate this question, we have produced transgenic mice that carry either the wild-type HBV genome or a mutated HBV genome incapable of expressing the 16.5-kDa X protein. Our results indicate that while the X protein is not absolutely essential for HBV replication or its maturation in transgenic mice, it can enhance viral replication, apparently by activating viral gene expression. These results demonstrate a transactivation role of the X protein in HBV replication in transgenic mice.

AB - Hepatitis B virus (HBV) X gene encodes a multifunctional protein that can regulate cellular signaling pathways, interact with cellular transcription factors, and induce hepatocellular oncogenesis. In spite of its diverse activities, the precise role of the X protein in the viral life cycle of HBV remains unclear. To investigate this question, we have produced transgenic mice that carry either the wild-type HBV genome or a mutated HBV genome incapable of expressing the 16.5-kDa X protein. Our results indicate that while the X protein is not absolutely essential for HBV replication or its maturation in transgenic mice, it can enhance viral replication, apparently by activating viral gene expression. These results demonstrate a transactivation role of the X protein in HBV replication in transgenic mice.

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Enhancement of hepatitis B virus replication by its X protein in transgenic mice

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