West Nile Virus Infection Associated with Central Nervous System Vasculitis and Strokes (P03.264)

Neurology ◽  
2012 ◽  
Vol 78 (Meeting Abstracts 1) ◽  
pp. P03.264-P03.264 ◽  
Author(s):  
S. Zafar ◽  
D. Dash ◽  
M. Chachere ◽  
J. Cowart ◽  
J. Kass
2011 ◽  
Vol 12 (1) ◽  
pp. 6 ◽  
Author(s):  
Barbara S Stewart ◽  
Valerie L Demarest ◽  
Susan J Wong ◽  
Sharone Green ◽  
Kristen A Bernard

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 105 ◽  
Author(s):  
Evandro R. Winkelmann ◽  
Huanle Luo ◽  
Tian Wang

West Nile virus (WNV), a neurotropic single-stranded flavivirus has been the leading cause of arboviral encephalitis worldwide.  Up to 50% of WNV convalescent patients in the United States were reported to have long-term neurological sequelae.  Neither antiviral drugs nor vaccines are available for humans.  Animal models have been used to investigate WNV pathogenesis and host immune response in humans.  In this review, we will discuss recent findings from studies in animal models of WNV infection, and provide new insights on WNV pathogenesis and WNV-induced host immunity in the central nervous system.


2003 ◽  
Vol 198 (12) ◽  
pp. 1853-1862 ◽  
Author(s):  
Michael S. Diamond ◽  
Elizabeth M. Sitati ◽  
Lindzy D. Friend ◽  
Stephen Higgs ◽  
Bimmi Shrestha ◽  
...  

In humans, the elderly and immunocompromised are at greatest risk for disseminated West Nile virus (WNV) infection, yet the immunologic basis for this remains unclear. We demonstrated previously that B cells and IgG contributed to the defense against disseminated WNV infection (Diamond, M.S., B. Shrestha, A. Marri, D. Mahan, and M. Engle. 2003. J. Virol. 77:2578–2586). In this paper, we addressed the function of IgM in controlling WNV infection. C57BL/6J mice (sIgM−/−) that were deficient in the production of secreted IgM but capable of expressing surface IgM and secreting other immunoglobulin isotypes were vulnerable to lethal infection, even after inoculation with low doses of WNV. Within 96 h, markedly higher levels of infectious virus were detected in the serum of sIgM−/− mice compared with wild-type mice. The enhanced viremia correlated with higher WNV burdens in the central nervous system, and was also associated with a blunted anti-WNV IgG response. Passive transfer of polyclonal anti-WNV IgM or IgG protected sIgM−/− mice against mortality, although administration of comparable amounts of a nonneutralizing monoclonal anti-WNV IgM provided no protection. In a prospective analysis, a low titer of anti-WNV IgM antibodies at day 4 uniformly predicted mortality in wild-type mice. Thus, the induction of a specific, neutralizing IgM response early in the course of WNV infection limits viremia and dissemination into the central nervous system, and protects against lethal infection.


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