Multiple nuclear receptors may regulate hepatitis B virus biosynthesis during development. Int J Biochem Cell Biol 2011 Feb;43(2):230-7
Date
11/28/2009Pubmed ID
19941970Pubmed Central ID
PMC3773232DOI
10.1016/j.biocel.2009.11.016Scopus ID
2-s2.0-78651423014 (requires institutional sign-in at Scopus site) 32 CitationsAbstract
Hepatitis B virus (HBV) replicates by the reverse transcription of the viral 3.5 kb pregenomic RNA. Therefore the level of expression of this transcript in the liver is a primary determinant of HBV biosynthesis. In vivo neonatal transcription of the HBV 3.5 kb pregenomic RNA is developmental regulated by hepatocyte nuclear factor 4α (HNF4α). In addition, viral biosynthesis in non-hepatoma cells can be supported directly by this nuclear receptor. However HBV transcription and replication can be supported by additional nuclear receptors including the retinoid X receptor α/peroxisome proliferator-activated receptor α (RXRα/PPARα), retinoid X receptor α/farnesoid X receptor α (RXRα/FXRα), liver receptor homolog 1 (LRH1) and estrogen-related receptors (ERR) in non-hepatoma cells. Therefore during neonatal liver development, HNF4α may progressively activate viral transcription and replication by binding directly to the proximal HNF4α recognition sequence within the nucleocapsid promoter. Alternatively, HNF4α may support viral biosynthesis in vivo indirectly by activating a network of liver-enriched nuclear receptors that, in combination, direct HBV 3.5 kb pregenomic RNA transcription and replication.
Author List
Reese V, Ondracek C, Rushing C, Li L, Oropeza CE, McLachlan AAuthor
Vanessa Mcfadden MD Associate Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Base SequenceHEK293 Cells
Hepatitis B virus
Hepatocyte Nuclear Factor 4
Humans
Liver
Molecular Sequence Data
Nucleocapsid Proteins
Promoter Regions, Genetic
Receptors, Cytoplasmic and Nuclear
Virus Replication
