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Journal of Virology, December 2008, p. 11859-11868, Vol. 82, No. 23
0022-538X/08/$08.00+0     doi:10.1128/JVI.00868-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Equine Herpesvirus 1 Entry via Endocytosis Is Facilitated by {alpha}V Integrins and an RSD Motif in Glycoprotein D {triangledown}

Gerlinde R. Van de Walle,1,2 Sarah T. Peters,1 Brian C. VanderVen,1 Dennis J. O'Callaghan,3 and Nikolaus Osterrieder1,4*

Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853,1 Department of Virology, Parasitology, and Immunology, Faculty of Veterinary Medicine, Ghent University, 9820 Merelbeke, Belgium,2 Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130,3 Institut für Virologie, Freie Universität Berlin, 10115 Berlin, Germany4

Received 24 April 2008/ Accepted 12 September 2008

Equine herpesvirus 1 (EHV-1) is a member of the Alphaherpesvirinae, and its broad tissue tropism suggests that EHV-1 may use multiple receptors to initiate virus entry. EHV-1 entry was thought to occur exclusively through fusion at the plasma membrane, but recently entry via the endocytic/phagocytic pathway was reported for Chinese hamster ovary cells (CHO-K1 cells). Here we show that cellular integrins, and more specifically those recognizing RGD motifs such as {alpha}Vβ5, are important during the early steps of EHV-1 entry via endocytosis in CHO-K1 cells. Moreover, mutational analysis revealed that an RSD motif in the EHV-1 envelope glycoprotein D (gD) is critical for entry via endocytosis. In addition, we show that EHV-1 enters peripheral blood mononuclear cells predominantly via the endocytic pathway, whereas in equine endothelial cells entry occurs mainly via fusion at the plasma membrane. Taken together, the data in this study provide evidence that EHV-1 entry via endocytosis is triggered by the interaction between cellular integrins and the RSD motif present in gD and, moreover, that EHV-1 uses different cellular entry pathways to infect important target cell populations of its natural host.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853. Phone: (607) 253-4045. Fax: (607) 253-3384. E-mail: no34{at}cornell.edu

{triangledown} Published ahead of print on 24 September 2008.

Journal of Virology, December 2008, p. 11859-11868, Vol. 82, No. 23
0022-538X/08/$08.00+0     doi:10.1128/JVI.00868-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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