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Journal of Virology, May 2005, p. 5653-5664, Vol. 79, No. 9
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.9.5653-5664.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Evolution of the Equine Infectious Anemia Virus Long Terminal Repeat during the Alteration of Cell Tropism{dagger}

Wendy Maury,1* Robert J. Thompson,1 Quentin Jones,1 Sarahann Bradley,2 Tara Denke,2,{ddagger} Prasith Baccam,3 Matthew Smazik,1 and J. Lindsay Oaks4

Department of Microbiology, University of Iowa, Iowa City, Iowa 52242,1 Division of Biomedical Sciences, University of South Dakota, Vermillion, South Dakota 57069,2 Innovative Emergency Management, 2014 South Tollgate Road, Suite 208, Bel Air, Maryland 21015,3 Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 991644

Received 21 June 2004/ Accepted 15 December 2004

Equine infectious anemia virus (EIAV) is a lentivirus with in vivo cell tropism primarily for tissue macrophages; however, in vitro the virus can be adapted to fibroblasts and other cell types. Tropism adaptation is associated with both envelope and long terminal repeat (LTR) changes, and findings strongly suggest that these regions of the genome influence cell tropism and virulence. Furthermore, high levels of genetic variation have been well documented in both of these genomic regions. However, specific EIAV nucleotide or amino acid changes that are responsible for cell tropism changes have not been identified. A study was undertaken with the highly virulent, macrophage-tropic strain of virus EIAVwyo to identify LTR changes associated with alterations in cell tropism. We found the stepwise generation of a new transcription factor binding motif within the enhancer that was associated with adaptation of EIAV to endothelial cells and fibroblasts. An LTR that contained the new motif had enhanced transcriptional activity in fibroblasts, whereas the new site did not alter LTR activity in a macrophage cell line. This finding supports a previous prediction that selection for new LTR genetic variants may be a consequence of cell-specific selective pressures. Additional investigations of the EIAVwyo LTR were performed in vivo to determine if LTR evolution could be detected over the course of a 3-year infection. Consistent with previous in vivo findings, we observed no changes in the enhancer region of the LTR over that time period, indicating that the EIAVwyo LTR was evolutionarily stable in vivo.

* Corresponding author. Mailing address: Department of Microbiology, 3403 Bowen Science Building, University of Iowa, Iowa City, IA 52242-1109. Phone: (319) 335-8021. Fax: (319) 335-9006. E-mail: wendy-maury{at}uiowa.edu.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: Department of Obstetrics, Gynecology and Women's Health, 12-211 Malcolm Moos Health Center Tower, University of Minnesota, Minneapolis, MN 55455.

Journal of Virology, May 2005, p. 5653-5664, Vol. 79, No. 9
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.9.5653-5664.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Brindley, M. A., Maury, W. (2008). Equine Infectious Anemia Virus Entry Occurs through Clathrin-Mediated Endocytosis. J. Virol. 82: 1628-1637 [Abstract] [Full Text]  
  • Oskarsson, T., Hreggvidsdottir, H. S., Agnarsdottir, G., Matthiasdottir, S., Ogmundsdottir, M. H., Jonsson, S. R., Georgsson, G., Ingvarsson, S., Andresson, O. S., Andresdottir, V. (2007). Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence. J. Virol. 81: 4052-4057 [Abstract] [Full Text]  


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