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    Taxonomic name: West Nile virus (WNV)
    Common names: West Nile virus (English)
    Organism type: micro-organism
    West Nile virus (WNV) is a mosquito-borne flavivirus native to Africa, Europe, and Western Asia. WNV is mostly transmitted by Culex mosquitoes in a cycle involving birds as amplifying hosts. However infected mosquitoes can also transmit the virus to other animals and humans. Most animals are “dead-end” hosts and do not contribute to virus spread or evolution in nature, because infection in non-avian species results in low virus levels that is insufficient for infection of mosquitoes.
    Since its introduction into the United States in the New York City area in 1999 WNV has continued to expand its range across the United States and into Canada, Mexico and Central and South America. WNV causes severe disease humans, horses and other vertebrates. Most people infected with West Nile virus have only mild illness. However the virus can also cause severe neuroinvasive diseases, often leading to death. No specific medication exists to treat West Nile virus infection, and there is currently no vaccine available for humans. Control measures focus on reducing mosquito breeding habitat: standing water in urban areas, agricultural areas, and wetlands.
    According to Solomon et al. (2003), like other flaviviruses, West Nile virus is a small virus, with a single stranded, positive sense RNA genome comprising about 11,000 nucleotides wrapped in a nucleocapsid and surrounded by a lipid membrane. Under a microscope the virions appear roughly as spheres 40-65 nm in diameter.
    Similar Species
    Japanese encephalitis virus, Kunjin Virus, Murray Valley encephalitis virus, St. Louis encephalitis virus

    Occurs in:
    agricultural areas, urban areas, wetlands
    Habitat description
    WNV cycles enzootically between Culex mosquitoes and birds, although it also can infect and cause illness in a range of vertebrate species including humans and horses (Hayes et al. 2005a; Kile et al. 2005; Miller et al. 2003). These vertebrate animals act as dead-end hosts and generally do not contribute to virus spread or evolution in nature because infection in nonavian species results in a low-level, transient viremia that is generally insufficient for infection of mosquitoes (Hubalek et alCulex spp. of mosquito, which commonly breed in urban areas and prefer to feed on birds. Mosquitoes thrive wherever standing water exists, including wetland and agricultural areas. Mosquitoes also breed effectively in artificial containers and storm drain systems and thus often exhibit high abundance in urban areas (Allan et al. 2009).
    General impacts
    According to the CDC (2003), most people infected with the West Nile virus will not display any symptoms. It is estimated that only 20% of the people who become infected will develop symptoms, which usually occur after an incubation period of 2-14 days. These are often flu-like including fever, headache, body aches, malaise, myalgia, fatigue, lymphadenopathy, vomiting, diarrhea and occasionally a skin rash. This relatively mild condition is known as West Nile fever (WNF), and most patients completely recover within days to months (Bode et al. 2003; Watson et al. 2004; Klee et al. 2004 in Kramer et al. 2007).

    Please follow this link for detailed information on the impacts of the West Nile virus (WNV) on humans, horses and birds, compiled by the IUCN SSC Invasive Species Specialist Group.

    Temperature and rainfall are important determinants of the activity of arboviruses. Recent West Nile virus epidemics have occurred during unusually hot and dry periods (e.g. Platonov et al. 2008; Paz 2006), thereby driving speculation that climate change could result in increased incidences of WNV and other vector-borne diseases (Epstein 2001; Lazar et al. 2002 in Torrence et al. 2006).
    Geographical range
    West Nile virus is recognized as the most widespread virus among flaviviruses. WNV was first discovered in Uganda in 1937, and subsequently, Africa, Europe, Australia, and Asia were recognized as regions in which the virus was endemic (Trevejo et al. 2008). It was discovered in the United States in 1999 (Solomon et al. 2003). The geographic range of the virus has since increased rapidly, and now includes 47 states,Canada, Mexico and Central and South America.

    A distribution map of WNV in the United States is provided by USGS.

    Introduction pathways to new locations
    Other: West Nile virus is introduced to new locations through infected birds (CDC, 2003).

    Local dispersal methods
    Consumption/excretion: When Culex spp. feed on the blood of infected birds, the mosquitoes ingest the virus and can pass the virus into humans (CDC, 2003).
    Management information
    Because of the large impact of WNV on human and animal health, it is critical to develop effective methods to limit WNV transmission and prevent and/or treat WN disease.

    Currently, control measures to curtail WNV transmission include reducing mosquito vector populations and limiting exposure to mosquito bites with protective clothing and repellents. Vector control agencies often use a combination of approaches (mosquito population monitoring, mosquito source reduction, larvicide and adulticide application, and public education) to reduce mosquito populations.

    Please follow this link for detailed information on the control and management of the West Nile virus (WNV), compiled by the IUCN SSC Invasive Species Specialist Group.

    West Nile virus can grow in a variety of cells from different tissues depending on the host species. These tissues include neurons, glial cells, and cells from spleen, liver, heart, lymph nodes and lung (Cantile et al. 2001 in Castillo-Olivares and Wood 2004). Virus replication takes place in the perinuclear region of the rough endoplasmic reticulum (ER) of cells. Newly synthesised E, NS1 and prM proteins are translocated to the ER lumen where prM and E heterodimerise. The immature virions are transported through the secretory pathway to the cell membrane where the final cleavage of the prM protein takes place (Castillo-Olivares and Wood 2004). It takes about 20-30 hours for the assembly and release of flaviviruses. The virions are finally released by exocytosis or by budding or when the cell lyses (Solomon et al. 2003).
    Lifecycle stages
    Enzootic Cycle: The natural WNV replication cycle involves culicine mosquitoes and different bird species. Wild bird species vary in their competence as hosts, depending on the duration and magnitude of infection and ability to transmit the virus to mosquitoes (Trevejo et al. 2008). It appears that only a small proportion of WNV-positive birds are competent (amplifying) hosts for the virus. Humans, horses and other mammalian species are so-called ‘‘dead-end’’ hosts characterised by WNV infections with potential clinical symptoms, but transient and low virus levels that are insufficient to establish a mosquito mammalian WNV replication cycle (Pfleiderer et al. 2008). “Although they are typically referred to as “dead-end” hosts (Komar 2000), occasional individuals, given sufficient numbers, may in fact be able to infect mosquitoes” (Castillo-Olivares and Wood 2004).

    There is evidence that tree squirrels (Sciurus spp), eastern chipmunks (Tamias striatus), and eastern cottontail rabbits (Sylvilagus floridanus) may be sufficient to provide a source of infection for mosquitoes(Padgett et al. 2007; Platt et al. 2007; Tiawsirisup et al. 2005 in Trevejo et al. 2008). Alligators (Alligator mississippiensis) and in Russia the lake frog Rana ridibunda may be competent reservoirs (Hayes et al. 2005 in Trevejo et al. 2008). More studies are needed to determine how important these species are in WNV epidemiology.

    Mosquito species vary in their vector competence. Culex quinquefasciatus, Culex pipiens, Culex restuans, Culex salinarius, and Culex tarsalis are the most significant vectors of WNV in the United States (CDC 2006; Hayes et al. 2005 in Trevejo et al. 2008), although Culex nigripalpus, Aedes albopictus, Aedes vexans, and Ochlerotatus triseriatus, may be important (CDC 2003 in Trevejo et al. 2008). Feeding preference of mosquitoes plays an important role in transmission and spread of WNV. While Culex spp. typically feed on birds, opportunistic feeding and transmission by secondary routes can cause mammalian hosts to become infected.

    Allan et al (2009) tested the hypothesis that high bird diversity reduces WNV transmission because mosquito blood-meals are distributed across a wide range of bird species, many of which have low reservoir competence. A study in Saint Louis, MO determined that prevalence of WNV infection in mosquitoes and humans increased with decreasing bird diversity and with increasing reservoir competence of the bird community. The results suggest that “conservation of avian diversity might help ameliorate the current West Nile virus epidemic in the USA” (Allan et al. 2009).

    Other Routes of Transmission: Non-mosquito borne transmission of WNV to animals and humans can also occur. Transmission to fetuses can occur via the placenta during pregnancy, as was reported in a human infant born in 2002; although this is extremely rare (CDC 2002; O’Leary et al 2006 in Trevejo et al. 2008). Transmission via breastfeeding was reported in 2002 (CDC 2002), although further studies found no evidence of this, and suggest that this is also extremely rare (Hinckley et al. 2007). There have also been reports of WNV transmission in humans following blood transfusion, organ transplantation and dialysis (CDC 2002; Kotton 2007; CDC 2003 in Trevejo et al. 2008).

    Birds with high levels of WNV can excrete large quantities of virus in oral and cloacal secretions and in feces (Komar et al. 2003; Nemeth et al. 2006 in Bowen and Nemeth 2007).

    Theoretically companion animals such as dogs or cats could become infected through contact with or ingesting an infected bird or small mammal, but studies are needed to confirm such a route for transmission (Trevejo et al. 2008).

    Reviewed by: Michael Holbrook. Department of Pathology, Center for Biodefense and Emerging Infectious Diseases, and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston. USA
    Compiled by: National Biological Information Infrastructure (NBII) & IUCN/SSC Invasive Species Specialist Group (ISSG)
    Updates completed with support from the Ministry of Agriculture and Forestry (MAF)- Biosecurity New Zealand
    Last Modified: Friday, 31 March 2006

ISSG Landcare Research NBII IUCN University of Auckland