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J Virol, March 1998, p. 2097-2104, Vol. 72, No. 3
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Modulation of Feline Immunodeficiency Virus Infection by Stromal Cell-Derived Factor

Margaret J. Hosie,1,* Nelleke Broere,1 Joseph Hesselgesser,2 Julie D. Turner,3 James A. Hoxie,3 James C. Neil,1 and Brian J. Willett1

Department of Veterinary Pathology, University of Glasgow Veterinary School, Glasgow G61 1QH, United Kingdom1; Department of Immunology, Berlex Biosciences, Richmond, California 948062; and Hematology-Oncology Division, University of Pennsylvania, Philadelphia, Pennsylvania 191043

Received 26 September 1997/Accepted 19 November 1997

The alpha -chemokine receptor CXCR4 has recently been shown to support syncytium formation mediated by strains of feline immunodeficiency virus (FIV) that have been selected for growth in the Crandell feline kidney cell line (CrFK-tropic virus). Given that both human and feline CXCR4 support syncytium formation mediated by FIV, we investigated whether human stromal cell-derived factor (SDF-1) would inhibit infection with FIV. Human SDF-1alpha and SDF-1beta bound with a high affinity (KDs of 12.0 and 10.4 nM, respectively) to human cells stably expressing feline CXCR4, and treatment of CrFK cells with human SDF-1alpha resulted in a dose-dependent inhibition of infection by FIVPET. No inhibitory activity was detected when the interleukin-2 (IL-2)-dependent feline T-cell line Mya-1 was used in place of CrFK cells, suggesting the existence of a CXCR4-independent mechanism of infection. Furthermore, neither the human beta -chemokines RANTES, MIP-1alpha , MIP-1beta , and MCP-1 nor the alpha -chemokine IL-8 had an effect on infection of either CrFK or Mya-1 cells with CrFK-tropic virus. Envelope glycoprotein purified from CrFK-tropic virus competed specifically for binding of SDF-1alpha to feline CXCR4 and CXCR4 expression was reduced in FIV-infected cells, suggesting that the inhibitory activity of SDF-1alpha in CrFK cells may be the result of steric hindrance of the virus-receptor interaction following the interaction between SDF and CXCR4. Prolonged incubation of CrFK cells with SDF-1alpha led to an enhancement rather than an inhibition of infection. Flow cytometric analysis revealed that this effect may be due largely to up-regulation of CXCR4 expression by SDF-1alpha on CrFK cells, an effect mimicked by treatment of the cells with phorbol myristate acetate. The data suggest that infection of feline cells with FIV can be mediated by CXCR4 and that, depending on the assay conditions, infection can be either inhibited or enhanced by SDF-1alpha . Infection with FIV may therefore prove a valuable model in which to study the development of novel therapeutic interventions for the treatment of AIDS.

* Corresponding author. Mailing address: Department of Veterinary Pathology, University of Glasgow Veterinary School, Bearsden Road, Glasgow G61 1QH, United Kingdom. Phone: 44 141 330 5786. Fax: 44 141 330 5602. E-mail: m.hosie{at}vet.gla.ac.uk.




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