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      West Nile virus and its emergence in the United States of America

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          Abstract

          Zoonotic West Nile virus (WNV) circulates in natural transmission cycles involving certain mosquitoes and birds, horses, humans, and a range of other vertebrates are incidental hosts. Clinical infections in humans can range in severity from uncomplicated WNV fever to fatal meningoencephalitis. Since its introduction to the Western Hemisphere in 1999, WNV had spread across North America, Central and South America and the Caribbean, although the vast majority of severe human cases have occurred in the United States of America (USA) and Canada. By 2002–2003, the WNV outbreaks have involved thousands of patients causing severe neurologic disease (meningoencephalitis and poliomyelitis-like syndrome) and hundreds of associated fatalities in USA. The purpose of this review is to present recent information on the epidemiology and pathogenicity of WNV since its emergence in North America.

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          Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States.

          R S Lanciotti, J. Roehrig, V. Deubel … (1999)
          In late summer 1999, an outbreak of human encephalitis occurred in the northeastern United States that was concurrent with extensive mortality in crows (Corvus species) as well as the deaths of several exotic birds at a zoological park in the same area. Complete genome sequencing of a flavivirus isolated from the brain of a dead Chilean flamingo (Phoenicopterus chilensis), together with partial sequence analysis of envelope glycoprotein (E-glycoprotein) genes amplified from several other species including mosquitoes and two fatal human cases, revealed that West Nile (WN) virus circulated in natural transmission cycles and was responsible for the human disease. Antigenic mapping with E-glycoprotein-specific monoclonal antibodies and E-glycoprotein phylogenetic analysis confirmed these viruses as WN. This North American WN virus was most closely related to a WN virus isolated from a dead goose in Israel in 1998.
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            Experimental Infection of North American Birds with the New York 1999 Strain of West Nile Virus

            Nicholas Komar, Stanley Langevin, Steven Hinten … (2003)
            To evaluate transmission dynamics, we exposed 25 bird species to West Nile virus (WNV) by infectious mosquito bite. We monitored viremia titers, clinical outcome, WNV shedding (cloacal and oral), seroconversion, virus persistence in organs, and susceptibility to oral and contact transmission. Passeriform and charadriiform birds were more reservoir competent (a derivation of viremia data) than other species tested. The five most competent species were passerines: Blue Jay (Cyanocitta cristata), Common Grackle (Quiscalus quiscula), House Finch (Carpodacus mexicanus), American Crow (Corvus brachyrhynchos), and House Sparrow (Passer domesticus). Death occurred in eight species. Cloacal shedding of WNV was observed in 17 of 24 species, and oral shedding in 12 of 14 species. We observed contact transmission among four species and oral in five species. Persistent WNV infections were found in tissues of 16 surviving birds. Our observations shed light on transmission ecology of WNV and will benefit surveillance and control programs.
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              The outbreak of West Nile virus infection in the New York City area in 1999.

              Denis Nash, Farzad Mostashari, Annie Fine … (2001)
              In late August 1999, an unusual cluster of cases of meningoencephalitis associated with muscle weakness was reported to the New York City Department of Health. The initial epidemiologic and environmental investigations suggested an arboviral cause. Active surveillance was implemented to identify patients hospitalized with viral encephalitis and meningitis. Cerebrospinal fluid, serum, and tissue specimens from patients with suspected cases underwent serologic and viral testing for evidence of arboviral infection. Outbreak surveillance identified 59 patients who were hospitalized with West Nile virus infection in the New York City area during August and September of 1999. The median age of these patients was 71 years (range, 5 to 95). The overall attack rate of clinical West Nile virus infection was at least 6.5 cases per million population, and it increased sharply with age. Most of the patients (63 percent) had clinical signs of encephalitis; seven patients died (12 percent). Muscle weakness was documented in 27 percent of the patients and flaccid paralysis in 10 percent; in all of the latter, nerve conduction studies indicated an axonal polyneuropathy in 14 percent. An age of 75 years or older was an independent risk factor for death (relative risk adjusted for the presence or absence of diabetes mellitus, 8.5; 95 percent confidence interval, 1.2 to 59.1), as was the presence of diabetes mellitus (age-adjusted relative risk, 5.1; 95 percent confidence interval, 1.5 to 17.3). This outbreak of West Nile meningoencephalitis in the New York City metropolitan area represents the first time this virus has been detected in the Western Hemisphere. Given the subsequent rapid spread of the virus, physicians along the eastern seaboard of the United States should consider West Nile virus infection in the differential diagnosis of encephalitis and viral meningitis during the summer months, especially in older patients and in those with muscle weakness.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Vet Res
                Journal ID (publisher-id): vetres
                Title: Veterinary Research
                Publisher: EDP Sciences
                ISSN (Print): 0928-4249
                ISSN (Electronic): 1297-9716
                Publication date (Electronic): 24 June 2010
                Publication date (Print): Nov-Dec 2010
                Publication date PMC-release: 24 June 2010
                Volume: 41
                Issue: 6 , Emerging and re-emerging animal viruses ( publisher-idID: vetres/2010/06 )
                Electronic Location Identifier: 67
                Affiliations
                [1 ] The University of Texas Health Science Center at Houston, Center for Infectious Diseases, School of Public Health Houston Texas USA
                [2 ] Institut Pasteur, Department of Virology 25 rue du Dr Roux 75724 Paris Cedex 15 France
                Author notes
                [* ]Corresponding author: philippe.despres@ 123456pasteur.fr
                Article
                Publisher ID: v100010 Other ID: 10.1051/vetres/2010039
                DOI: 10.1051/vetres/2010039
                PMC ID: 2913730
                PubMed ID: 21188801
                SO-VID: 9a6228c4-ff8f-42e4-af0c-df045997dbb2
                Copyright © © INRA, EDP Sciences, 2010
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted use, distribution, and reproduction in any noncommercial medium, provided the original work is properly cited.

                History
                Date received : 02 February 2010
                Date accepted : 23 June 2010
                Page count
                Figures: 3, Tables: 1, Equations: 0, References: 170, Pages: 14
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Veterinary medicine
                Keywords: epidemiology,pathogenicity,west nile virus,arbovirus,zoonosis
                Data availability:
                ScienceOpen disciplines: Veterinary medicine
                Keywords: epidemiology, pathogenicity, west nile virus, arbovirus, zoonosis

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