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Journal of Virology, April 2008, p. 4164-4168, Vol. 82, No. 8
0022-538X/08/$08.00+0     doi:10.1128/JVI.02621-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System{triangledown}

Jianfeng Dai,1 Penghua Wang,1 Fengwei Bai,1 Terrence Town,2,3 and Erol Fikrig1*

Section of Infectious Diseases, Department of Internal Medicine,1 Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520,2 Department of Biomedical Sciences and Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 900483

Received 10 December 2007/ Accepted 18 January 2008

Determining how West Nile virus crosses the blood-brain barrier is critical to understanding the pathogenesis of encephalitis. Here, we show that ICAM-1–/– mice are more resistant than control animals to lethal West Nile encephalitis. ICAM-1–/– mice have a lower viral load, reduced leukocyte infiltration, and diminished neuronal damage in the brain compared to control animals. This is associated with decreased blood-brain barrier leakage after viral infection. These data suggest that ICAM-1 plays an important role in West Nile virus neuroinvasion and that targeting ICAM-1 signaling may help control viral encephalitis.

* Corresponding author. Mailing address: Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, P.O. Box 208031, New Haven, CT 06520-8031. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: erol.fikrig{at}yale.edu

{triangledown} Published ahead of print on 6 February 2008.

Journal of Virology, April 2008, p. 4164-4168, Vol. 82, No. 8
0022-538X/08/$08.00+0     doi:10.1128/JVI.02621-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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