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Journal of Virology, March 2009, p. 2655-2662, Vol. 83, No. 6
0022-538X/09/$08.00+0     doi:10.1128/JVI.02206-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Borna Disease Virus Requires Cholesterol in both Cellular Membrane and Viral Envelope for Efficient Cell Entry{triangledown}

Roberto Clemente,1 Aymeric de Parseval,2 Mar Perez,3 and Juan C. de la Torre1*

Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037,1 Public Health Research Institute, UMDNJ, NJMS 225 Warren Street, Newark, New Jersey 07103,2 Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro, 3, 28029 Madrid, Spain3

Received 17 October 2008/ Accepted 18 December 2008

Borna disease virus (BDV), the prototypic member of the family Bornaviridae within the order Mononegavirales, provides an important model for the investigation of viral persistence within the central nervous system (CNS) and of associated brain disorders. BDV is highly neurotropic and enters its target cell via receptor-mediated endocytosis, a process mediated by the virus surface glycoprotein (G), but the cellular factors and pathways determining BDV cell tropism within the CNS remain mostly unknown. Cholesterol has been shown to influence viral infections via its effects on different viral processes, including replication, budding, and cell entry. In this work, we show that cell entry, but not replication and gene expression, of BDV was drastically inhibited by depletion of cellular cholesterol levels. BDV G-mediated attachment to BDV-susceptible cells was cholesterol independent, but G localized to lipid rafts (LR) at the plasma membrane. LR structure and function critically depend on cholesterol, and hence, compromised structural integrity and function of LR caused by cholesterol depletion likely inhibited the initial stages of BDV cell internalization. Furthermore, we also show that viral-envelope cholesterol is required for BDV infectivity.

* 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 7 January 2009.

Journal of Virology, March 2009, p. 2655-2662, Vol. 83, No. 6
0022-538X/09/$08.00+0     doi:10.1128/JVI.02206-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Honda, T., Horie, M., Daito, T., Ikuta, K., Tomonaga, K. (2009). Molecular Chaperone BiP Interacts with Borna Disease Virus Glycoprotein at the Cell Surface. J. Virol. 83: 12622-12625 [Abstract] [Full Text]  
  • 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]  


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