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Journal of Virology, September 2005, p. 11045-11052, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11045-11052.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Alpha/Beta Interferon Differentially Modulates the Clearance of Cytoplasmic Encapsidated Replication Intermediates and Nuclear Covalently Closed Circular Hepatitis B Virus (HBV) DNA from the Livers of Hepatocyte Nuclear Factor 1{alpha}-Null HBV Transgenic Mice{dagger}

Aimee L. Anderson,1 Krista E. Banks,1 Marco Pontoglio,2 Moshe Yaniv,2 and Alan McLachlan1*

Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037,1 Gene Expression and Disease Unit, FRE 2850 du CNRS, Developmental Biology Department, Institut Pasteur, 75724 Paris Cedex, France2

Received 23 February 2005/ Accepted 26 May 2005

Treatment with alpha interferon is a standard therapy for patients with chronic hepatitis B virus (HBV) infections. This treatment can reduce virus load and ameliorate disease symptoms. However, in the majority of cases, alpha interferon therapy fails to resolve the chronic HBV infection. The reason alpha interferon therapy is inefficient at resolving chronic HBV infections is assumed to be because it fails to eliminate covalently closed circular (CCC) HBV DNA from the nuclei of infected hepatocytes. In an attempt to address this issue, the stability of HBV CCC DNA in response to alpha/beta interferon induction was examined in HNF1{alpha}-null HBV transgenic mice. Alpha/beta interferon induction by polyinosinic-polycytidylic acid [poly(I-C)] treatment efficiently eliminated encapsidated cytoplasmic HBV replication intermediates while only modestly reducing nuclear HBV CCC DNA. These observations indicate that nuclear HBV CCC DNA is more stable than cytoplasmic replication intermediates in response to alpha/beta interferon induction. Consequently it appears that for therapies to resolve chronic HBV infection efficiently, they will have to target the elimination of the most stable HBV replication intermediate, nuclear HBV CCC DNA.

* Corresponding author. Mailing address: Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. Phone: (858) 784-8097. Fax: (858) 784-2513. E-mail: mclach{at}scripps.edu.

{dagger} Publication number 17195-CB from the Scripps Research Institute.

Journal of Virology, September 2005, p. 11045-11052, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11045-11052.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Gao, W., Hu, J. (2007). Formation of Hepatitis B Virus Covalently Closed Circular DNA: Removal of Genome-Linked Protein. J. Virol. 81: 6164-6174 [Abstract] [Full Text]  


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