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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.
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
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| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
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