West Nile Virus: Epidemiology and Clinical Features of an Emerging Epidemic in the United States*

Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado 80522, USA.
Annual Review of Medicine (Impact Factor: 12.93). 02/2006; 57(1):181-94. DOI: 10.1146/
Source: PubMed


West Nile virus (WNV) was first detected in North America in 1999 during an outbreak of encephalitis in New York City. Since then the virus has spread across North America and into Canada, Latin America, and the Caribbean. The largest epidemics of neuroinvasive WNV disease ever reported occurred in the United States in 2002 and 2003. This paper reviews new information on the epidemiology and clinical aspects of WNV disease derived from greatly expanded surveillance and research on WNV during the past six years.

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    • "WNV specific T cells recognize a broad range of epitopes WNV, like other arboviruses in the Flaviridae family, contains a single-stranded RNA genome that encodes the capsid (C), envelope (E), premembrane (prM), and membrane (M) proteins, as well as seven nonstructural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5) that likely contribute to viral replication[12]. We utilized a tetramer guided approach (S1 Fig) tocomprehensively identify CD4 + T cells epitopes across the entire WNV proteome, utilizing peripheral blood samples from subjects with documented WNV infection (Table 1). "
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    ABSTRACT: Most West Nile virus (WNV) infections are asymptomatic, but some lead to neuroinvasive disease with symptoms ranging from disorientation to paralysis and death. Evidence from animal models suggests that neuroinvasive infections may arise as a consequence of impaired immune protection. However, other data suggest that neurologic symptoms may arise as a consequence of immune mediated damage. We demonstrate that elevated immune responses are present in neuroinvasive disease by directly characterizing WNV-specific T cells in subjects with laboratory documented infections using human histocompatibility leukocyte antigen (HLA) class II tetramers. Subjects with neuroinvasive infections had higher overall numbers of WNV-specific T cells than those with asymptomatic infections. Independent of this, we also observed age related increases in WNV-specific T cell responses. Further analysis revealed that WNV-specific T cell responses included a population of atypically polarized CXCR3+CCR4+CCR6- T cells, whose presence was highly correlated with neuroinvasive disease. Moreover, a higher proportion of WNV-specific T cells in these subjects co-produced interferon-γ and interleukin 4 than those from asymptomatic subjects. More globally, subjects with neuroinvasive infections had reduced numbers of CD4+FoxP3+ Tregs that were CTLA4 positive and exhibited a distinct upregulated transcript profile that was absent in subjects with asymptomatic infections. Thus, subjects with neuroinvasive WNV infections exhibited elevated, dysregulated, and atypically polarized responses, suggesting that immune mediated damage may indeed contribute to pathogenic outcomes.
    Full-text · Article · Jan 2016 · PLoS Pathogens
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    • "Since its emergence in North America in 1999, WNV has become endemic across southern Canada, particularly in the prairies , where the highest rates of human infection in Canada have occurred (Chen et al. 2013). A mosquito-borne flavivirus, WNV is primarily maintained and amplified in bird populations through transmission by mosquitoes (especially Culex species), with occasional spillover to horses and humans, which are dead end hosts (Hayes and Gubler 2006). Since its introduction into North America, WNV has been reported in .200 "
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    ABSTRACT: The Canadian prairies are one of the most important breeding and staging areas for migratory waterfowl in North America. Hundreds of thousands of waterfowl of numerous species from multiple flyways converge in and disperse from this region annually; therefore this region may be a key area for potential intra- and interspecific spread of infectious pathogens among migratory waterfowl in the Americas. Using Blue-winged Teal (Anas discors, BWTE), which have the most extensive migratory range among waterfowl species, we investigated ecologic risk factors for infection and antibody status to avian influenza virus (AIV), West Nile virus (WNV), and avian paramyxovirus-1 (APMV-1) in the three prairie provinces (Alberta, Saskatchewan, and Manitoba) prior to fall migration. We used generalized linear models to examine infection or evidence of exposure in relation to host (age, sex, body condition, exposure to other infections), spatiotemporal (year, province), population-level (local population densities of BWTE, total waterfowl densities), and environmental (local pond densities) factors. The probability of AIV infection in BWTE was associated with host factors (e.g., age and antibody status), population-level factors (e.g., local BWTE population density), and year. An interaction between age and AIV antibody status showed that hatch year birds with antibodies to AIV were more likely to be infected, suggesting an antibody response to an active infection. Infection with AIV was positively associated with local BWTE density, supporting the hypothesis of density-dependent transmission. The presence of antibodies to WNV and APMV-1 was positively associated with age and varied among years. Furthermore, the probability of being WNV antibody positive was positively associated with pond density rather than host population density, likely because ponds provide suitable breeding habitat for mosquitoes, the primary vectors for transmission. Our findings highlight the importance of spatiotemporal, environmental, and host factors at the individual and population levels, all of which may influence dynamics of these and other viruses in wild waterfowl populations.
    Full-text · Article · Nov 2015 · Journal of wildlife diseases
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    • "The incubation period for WNV ranges from 2 to 14 days and about 80% of WNV cases are asymptomatic but a few progress from mild to severe disease[13]. In mild cases of the disease the patient presents with fever, headache, myalgia, lymphodenopathy and a maculopapular rash[26]. In severe cases of the disease the patients may progress to a more serious neurological illness of meningitis and/or encephalitis characterized by headache, neck stiffness, disorientation, muscle weakness, seizures, flaccid paralysis or coma[27]. "

    Full-text · Article · Mar 2015
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