JVI Email Content Delivery
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.02621-07v1
82/8/4164    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Dai, J.
Right arrow Articles by Fikrig, E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dai, J.
Right arrow Articles by Fikrig, E.
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.







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2008 by the American Society for Microbiology. All rights reserved.