Journal article
Replication of the hepatitis B virus requires a calcium-dependent HBx-induced G1 phase arrest of hepatocytes
Virology (New York, N.Y.), v 407(1)
2010
PMID: 20719353
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Chronic HBV infections cause hepatocellular carcinoma (HCC). Activities of the HBV HBx protein regulate HBV replication and may contribute to the development of HCC. We previously reported that HBx causes primary rat hepatocytes to exit G0 but stall in G1 phase of the cell cycle; entry into G1 stimulated HBV replication. We now report that the activity of the mitochondria permeability transition pore is required for HBx regulation of cell cycle proteins and HBV replication in primary rat hepatocytes, that progression from G0 to G1 stimulates HBV polymerase activity, and that HBV replication is facilitated by the HBx-induced G1 arrest. HBx stimulation of HBV replication was linked to elevation of the R2 subunit of ribonucleotide reductase. Our studies suggest that HBx uses mitochondrial-dependent calcium signaling to cause hepatocytes to exit G0 but stall in G1 and that this HBx activity alters the cellular environment and stimulates HBV replication.
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Details
- Title
- Replication of the hepatitis B virus requires a calcium-dependent HBx-induced G1 phase arrest of hepatocytes
- Creators
- Tricia L Gearhart - Graduate Program in Molecular and Cellular Biology and Genetics, Drexel University College of Medicine, Philadelphia, PA 19102, USAMichael J Bouchard - Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA
- Publication Details
- Virology (New York, N.Y.), v 407(1)
- Publisher
- Elsevier
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biochemistry and Molecular Biology
- Web of Science ID
- WOS:000282486300003
- Scopus ID
- 2-s2.0-77956941978
- Other Identifier
- 991014877901204721
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- Web of Science research areas
- Virology