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Journal of Virology, February 2009, p. 1682-1688, Vol. 83, No. 4
0022-538X/09/$08.00+0 doi:10.1128/JVI.02208-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, 909 South Wolcott Avenue, Chicago, Illinois 60612,1 Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 191042
Received 18 October 2008/ Accepted 26 November 2008
Nuclear receptors have a unique role in governing hepatitis B virus (HBV) transcription and replication. Hepatocyte nuclear factor 4
(HNF4
) and retinoid X receptor
(RXR
) plus peroxisome proliferator-activated receptor
(PPAR
) have been shown to support viral biosynthesis in nonhepatoma cells in the absence of additional liver-enriched transcription factors. However, the in vivo importance of these nuclear receptors in HBV biosynthesis has been investigated only to a limited extent. Fasting has been shown to activate gluconeogenesis, in part, by activating PPAR
coactivator 1
, which in turn leads to activation of HNF4
- and RXR
/PPAR
-mediated transcription. As HBV pregenomic RNA synthesis is primarily believed to be regulated by HNF4
under normal physiological conditions, it was of interest to determine the effect of fasting on the levels of HBV RNA and DNA synthesis. Fasting was shown to rather modestly increase the levels of viral proteins, transcripts, and replication intermediates in the HBV transgenic mouse model of chronic viral infection, suggesting that caloric restriction may modulate viremia to some extent during natural infection.
Published ahead of print on 10 December 2008.
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