This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnston, J. B.
Right arrow Articles by Power, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnston, J. B.
Right arrow Articles by Power, C.

 Previous Article  |  Next Article 

Journal of Virology, April 2002, p. 3626-3636, Vol. 76, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.8.3626-3636.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

J. B. Johnston and C. Power*

Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada

Received 25 May 2001/ Accepted 11 January 2002

The use of chemokine receptors as cell recognition signals is a property common to several lentiviruses, including feline, human, and simian immunodeficiency viruses. Previously, two feline immunodeficiency virus (FIV) isolates, V1CSF and Petaluma, were shown to use chemokine receptors in a strain-dependent manner to infect human peripheral blood mononuclear cells (PBMC) (J. Johnston and C. Power, J. Virol. 73:2491-2498, 1999). Since the sequences of these viruses differed primarily in regions of the FIV envelope gene implicated in receptor use and cell tropism, envelope chimeras of V1CSF and Petaluma were constructed to investigate the role of envelope diversity in the profiles of chemokine receptors used by FIV to infect primate cells. By use of a receptor-blocking assay, all viruses were found to infect human and macaque PBMC through a mechanism involving the CXCR4 receptor. However, infection by viruses encoding the V3-to-V5 region of the V1CSF surface unit was also inhibited by blockade of the CCR3 or CCR5 receptor. Similar results were obtained with GHOST cells, human osteosarcoma cells expressing specific combinations of chemokine receptors. CXCR4 was required for infection by all FIV strains, but viruses expressing the V3-to-V5 region of V1CSF required the concurrent presence of either CCR3 or CCR5. In contrast, CXCR4 alone was sufficient to allow infection of GHOST cells by FIV strains possessing the V3-to-V5 region of Petaluma. To assess the role of primate chemokine receptors in productive infection, Crandell feline kidney (CrFK) cells that expressed human CXCR4, CCR3, or CCR5 in addition to feline CXCR4 were generated. Sustained infection by viruses encoding the V3-to-V5 region of V1CSF was detected in CrFK cells expressing human CCR3 or CCR5 but not in cells expressing CXCR4 alone, while all CrFK cell lines were permissive to viruses encoding the V3-to-V5 region of Petaluma. These results indicate that FIV uses chemokine receptors to infect both human and nonhuman primate cells and that the profiles of these receptors are dependent on envelope sequence, and they provide insights into the mechanism by which xenoinfections may occur.

* Corresponding author. Mailing address: Department of Clinical Neurosciences, HMRB 150, 3330 Hospital Dr. NW, University of Calgary, Calgary, Alberta, Canada T2N 4N1. Phone: (403) 220-5572. Fax: (403) 283-8731. E-mail: power{at}ucalgary.ca.

Journal of Virology, April 2002, p. 3626-3636, Vol. 76, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.8.3626-3636.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Maingat, F., Vivithanaporn, P., Zhu, Y., Taylor, A., Baker, G., Pearson, K., Power, C. (2009). Neurobehavioral Performance in Feline Immunodeficiency Virus Infection: Integrated Analysis of Viral Burden, Neuroinflammation, and Neuronal Injury in Cortex. J. Neurosci. 29: 8429-8437 [Abstract] [Full Text]  
  • Yoshimura, F. K., Luo, X., Zhao, X., Gerard, H. C., Hudson, A. P. (2008). Up-regulation of a cellular protein at the translational level by a retrovirus. Proc. Natl. Acad. Sci. USA 105: 5543-5548 [Abstract] [Full Text]  
  • Zhu, Y., Antony, J., Liu, S., Martinez, J. A., Giuliani, F., Zochodne, D., Power, C. (2006). CD8+ lymphocyte-mediated injury of dorsal root ganglion neurons during lentivirus infection: CD154-dependent cell contact neurotoxicity.. J. Neurosci. 26: 3396-3403 [Abstract] [Full Text]  
  • Zhu, Y., Jones, G., Tsutsui, S., Opii, W., Liu, S., Silva, C., Butterfield, D. A., Power, C. (2005). Lentivirus Infection Causes Neuroinflammation and Neuronal Injury in Dorsal Root Ganglia: Pathogenic Effects of STAT-1 and Inducible Nitric Oxide Synthase. J. Immunol. 175: 1118-1126 [Abstract] [Full Text]  
  • Zhang, K., Rana, F., Silva, C., Ethier, J., Wehrly, K., Chesebro, B., Power, C. (2003). Human Immunodeficiency Virus Type 1 Envelope-Mediated Neuronal Death: Uncoupling of Viral Replication and Neurotoxicity. J. Virol. 77: 6899-6912 [Abstract] [Full Text]  
  • Willett, B. J., Cannon, C. A., Hosie, M. J. (2002). Upregulation of Surface Feline CXCR4 Expression following Ectopic Expression of CCR5: Implications for Studies of the Cell Tropism of Feline Immunodeficiency Virus. J. Virol. 76: 9242-9252 [Abstract] [Full Text]  
  • Patrick, M. K., Johnston, J. B., Power, C. (2002). Lentiviral Neuropathogenesis: Comparative Neuroinvasion, Neurotropism, Neurovirulence, and Host Neurosusceptibility. J. Virol. 76: 7923-7931 [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»