Icam-1 participates in the entry of west nile virus into the central nervous system.
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.
Dai
Jianfeng
J
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, P.O. Box 208031, New Haven, CT 06520-8031, USA.
Wang
Penghua
P
Bai
Fengwei
F
Town
Terrence
T
Fikrig
Erol
E
D000818:Animals; D001921:Brain / Q000473:pathology / Q000821:virology; D002490:Central Nervous System / Q000821:virology*; D016207:Cytokines / Q000096:biosynthesis; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000502:physiology*; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009474:Neurons / Q000473:pathology; D016019:Survival Analysis; D014901:West Nile Fever / Q000821:virology*; D014902:West Nile virus / Q000502:physiology*
D016207:Cytokines; D018799:Intercellular Adhesion Molecule-1