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Journal of Virology, June 2007, p. 5527-5536, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.02586-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Generation and Characterization of a Recombinant Vesicular Stomatitis Virus Expressing the Glycoprotein of Borna Disease Virus{triangledown}

Mar Perez,1 Roberto Clemente,1 Clinton S. Robison,2,{dagger} E. Jeetendra,2,{ddagger} Himangi R. Jayakar,2 Michael A. Whitt,2 and Juan C. de la Torre1*

Department of Molecular Integrative Neuroscience, The Scripps Research Institute, La Jolla, California 92037,1 Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, Tennessee 381632

Received 22 November 2006/ Accepted 7 March 2007

Borna disease virus (BDV) is an enveloped virus with a nonsegmented negative-strand RNA genome whose organization is characteristic of mononegavirales. However, based on its unique genetics and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. BDV cell entry occurs via receptor-mediated endocytosis, a process initiated by the recognition of an as yet unidentified receptor at the cell surface by the BDV surface glycoprotein (G). The paucity of cell-free virus associated with BDV infection has hindered studies aimed at the elucidation of cellular receptors and detailed mechanisms involved in BDV cell entry. To overcome this problem, we generated and characterized a replication-competent recombinant vesicular stomatitis virus expressing BDV G (rVSV{Delta}G*/BDVG). Cells infected with rVSV{Delta}G*/BDVG produced high titers (107 PFU/ml) of cell-free virus progeny, but this virus exhibited a highly attenuated phenotype both in cell culture and in vivo. Attenuation of rVSV{Delta}G*/BDVG was associated with a delayed kinetics of viral RNA replication and altered genome/N mRNA ratios compared to results for rVSV{Delta}G*/VSVG. Likewise, incorporation of BDV G into virions appeared to be restricted despite its high levels of expression and efficient processing in rVSV{Delta}G*/BDVG-infected cells. Notably, rVSV{Delta}G*/BDVG recreated the cell tropism and entry pathway of bona fide BDV. Our results indicate that rVSV{Delta}G*/BDVG represents a unique tool for the investigation of BDV G-mediated cell entry, as well as the roles of BDV G in host immune responses and pathogenesis associated with BDV infection.

* Corresponding author. Mailing address: The Scripps Research Institute, IMM6, 10550 N. Torrey Pines Rd., La Jolla, CA 92037. Phone: (858) 784-9462. Fax: (858) 784-9981. E-mail: juanct{at}scripps.edu

{triangledown} Published ahead of print on 21 March 2007.

{dagger} Current address: Dept. of Biological Sciences & Pittsburgh NMR Center for Biomedical Research, Carnegie Mellon University, Mellon Institute, 4400 Fifth Ave., Pittsburgh, PA 15213.

{ddagger} Current address: GTx, Inc., 3 N. Dunlap St., Memphis, TN 38163.

Journal of Virology, June 2007, p. 5527-5536, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.02586-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Clemente, R., de la Torre, J. C. (2009). Cell Entry of Borna Disease Virus Follows a Clathrin-Mediated Endocytosis Pathway That Requires Rab5 and Microtubules. J. Virol. 83: 10406-10416 [Abstract] [Full Text]  
  • Clemente, R., de Parseval, A., Perez, M., de la Torre, J. C. (2009). Borna Disease Virus Requires Cholesterol in both Cellular Membrane and Viral Envelope for Efficient Cell Entry. J. Virol. 83: 2655-2662 [Abstract] [Full Text]  
  • Rojek, J. M., Perez, M., Kunz, S. (2008). Cellular Entry of Lymphocytic Choriomeningitis Virus. J. Virol. 82: 1505-1517 [Abstract] [Full Text]  


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