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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.

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.
Published ahead of print on 6 February 2008.
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