The Journal of Experimental Medicine
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Published online 1 May 2006 doi:10.1084/jem.20052388
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 5, 1371-1381
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ARTICLE

 Protective immune responses against West Nile virus are primed by distinct complement activation pathways

Erin Mehlhop1 and Michael S. Diamond1,2,3

1 Department of Pathology and Immunology, 2 Department of Medicine, and 3 Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110

CORRESPONDENCE Michael S. Diamond: diamond{at}borcim.wustl.edu

West Nile virus (WNV) causes a severe infection of the central nervous system in several vertebrate animals including humans. Prior studies have shown that complement plays a critical role in controlling WNV infection in complement (C) 3–/– and complement receptor 1/2–/– mice. Here, we dissect the contributions of the individual complement activation pathways to the protection from WNV disease. Genetic deficiencies in C1q, C4, factor B, or factor D all resulted in increased mortality in mice, suggesting that all activation pathways function together to limit WNV spread. In the absence of alternative pathway complement activation, WNV disseminated into the central nervous system at earlier times and was associated with reduced CD8+ T cell responses yet near normal anti-WNV antibody profiles. Animals lacking the classical and lectin pathways had deficits in both B and T cell responses to WNV. Finally, and somewhat surprisingly, C1q was required for productive infection in the spleen but not for development of adaptive immune responses after WNV infection. Our results suggest that individual pathways of complement activation control WNV infection by priming adaptive immune responses through distinct mechanisms.

Abbreviations used: C, complement; CNS, central nervous system; CR, complement receptor; E, envelope; fB, factor B; fD, factor D; LCMV, lymphocytic choriomeningits virus; MBL, mannose binding lectin; WNV, West Nile virus.


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