Abstract
The host cellular factors that promote persistent viral infections in vivo are, in general, poorly understood. Utilizing the hepatitis B virus (HBV) transgenic mouse model of chronic infection, we demonstrate that the nuclear receptor, hepatocyte nuclear factor 4alpha (HNF4alpha, NR2A1), is essential for viral biosynthesis in the liver. The dependency of HBV transcription on HNF4alpha links viral biosynthesis and persistence to a developmentally regulated transcription factor essential for host viability.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Animals, Newborn
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Blood Glucose / metabolism
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DNA, Viral / genetics
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Gene Expression Regulation, Viral
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Growth and Development*
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Hepatitis B virus / genetics
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Hepatitis B virus / physiology*
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Hepatocyte Nuclear Factor 4 / deficiency
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Hepatocyte Nuclear Factor 4 / metabolism*
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Liver / metabolism
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Liver / virology
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Mice
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Mice, Transgenic
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Organ Specificity
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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RNA, Viral / genetics
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Transcription, Genetic
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Virus Replication / physiology*
Substances
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Blood Glucose
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DNA, Viral
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Hepatocyte Nuclear Factor 4
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RNA, Messenger
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RNA, Viral