Shared Usage of the Chemokine Receptor CXCR4 by Primary and Laboratory-Adapted Strains of Feline Immunodeficiency Virus

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Journal of Virology, May 1999, p. 3661-3671, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Shared Usage of the Chemokine Receptor CXCR4 by Primary and Laboratory-Adapted Strains of Feline Immunodeficiency Virus

Jennifer Richardson,¹ Gianfranco Pancino,¹ Rastine Merat,¹ Thierry Leste-Lasserre,¹ Anne Moraillon,² Jens Schneider-Mergener,³ Marc Alizon,⁴ Pierre Sonigo,¹ and Nikolaus Heveker⁴^,^*

Génétique des Virus (ICGM-CNRS UPR 0415)¹ and Signalisation, Inflammation et Transformation Cellulaires (ICGM-INSERM U 332),⁴ Institut Cochin de Génétique Moléculaire, 75014 Paris, and Génétique Moléculaire Génétique Virale (INRA), Ecole Nationale Vétérinaire d'Alfort, 94704 Maisons-Alfort,² France, and Institut für Medizinische Immunologie, Universitätsklinikum Charité, Humboldt-Universität, 10098 Berlin, Germany³

Received 19 October 1998/Accepted 10 February 1999

Strains of the feline immunodeficiency virus (FIV) presently under investigation exhibit distinct patterns of in vitro tropism.In particular, the adaptation of FIV for propagation in Crandellfeline kidney (CrFK) cells results in the selection of strainscapable of forming syncytia with cell lines of diverse speciesorigin. The infection of CrFK cells by CrFK-adapted strains appearsto require the chemokine receptor CXCR4 and is inhibited by itsnatural ligand, stromal cell-derived factor 1 $alpha$ (SDF-1 $alpha$ ). Herewe found that inhibitors of CXCR4-mediated infection by humanimmunodeficiency virus type I (HIV-1), such as the bicyclam AMD3100and short peptides derived from the amino-terminal region of SDF-1 $alpha$ ,also blocked infection of CrFK by FIV. Nevertheless, we observeddifferences in the ranking order of the peptides as inhibitorsof FIV and HIV-1 and showed that such differences are relatedto the species origin of CXCR4 and not that of the viral envelope.These results suggest that, although the envelope glycoproteinsof FIV and HIV-1 are substantially divergent, FIV and HIV-1 interactwith CXCR4 in a highly similar manner. We have also addressedthe role of CXCR4 in the life cycle of primary isolates of FIV.Various CXCR4 ligands inhibited infection of feline peripheralblood mononuclear cells (PBMC) by primary FIV isolates in a concentration-dependentmanner. These ligands also blocked the viral transduction of felinePBMC by pseudotyped viral particles when infection was mediatedby the envelope glycoprotein of a primary FIV isolate but notby the G protein of vesicular stomatitis virus, indicating thatthey act at an envelope-mediated step and presumably at viralentry. These findings strongly suggest that primary and CrFK-adaptedstrains of FIV, despite disparate in vitro tropisms, share usageofCXCR4.

^* Corresponding author. Mailing address: INSERM U 332, Institut Cochin de Génétique Moléculaire, 22 rue Méchain, 75014 Paris,France. Phone: (33)-(0)1-40 51 64 96. Fax: (33)-(0)1-40 51 7749. E-mail: heveker{at}cochin.inserm.fr.

Journal of Virology, May 1999, p. 3661-3671, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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