Pathogen Safety Data Sheets: Infectious Substances – West Nile virus (WNV)



NAME: West Nile virus (WNV)

SYNONYM OR CROSS REFERENCE: WNV(1,2,3,4,5,6,7,8,9,10,11,12,13>), West Nile fever(6), West Nile encephalitis, WN fever(1,10), West Nile disease(12), and West Nile neuroinvasive disease(10).

CHARACTERISTICS: A member of the genus Flavivirus, and Flavivirida e family(1,3,4,6). West Nile virus is an icosahedral, enveloped virus of 40 to 50 nm in diameter(1,5,10) and has a single-stranded, positive-sense RNA genome(1,5,6,12). WNV belongs to the Japanese encephalitis antigenic complex(14).


PATHOGENICITY/TOXICITY: Most individuals infected with WNV remain asymptomatic(4,10,12). West Nile (WN) fever is typically a mild illness lasting 3 to 6 days(1,4,12). The main symptoms are sudden onset of fever with chills, rash, malaise, headache, backache, arthralgia, myalgia and eye pain(1,4,10). Other non-specific manifestations include nausea, vomiting, anorexia, diarrhoea, rhinorrhoea, sore throat, and cough(1,10). In some patients there is generalised lymphadenopathy, and an erythematous macular, papular, or morbilliform eruption involving the entire body(1,4,10).

Meningitis, encephalitis, and/or acute flaccid paralysis develop in less than 1% of WNV-infected individuals(2,10,14). Patients with neurological disease typically have a febrile prodrome of 1 to 7 days, which may be biphasic, before they develop neurological symptoms(1). Typically, neurological patients will present with a fever, stiff neck, headache, weak muscles, gastrointestinal symptoms, disorientation, tremors, convulsions, and paralysis(1,4,10).

A New York serological survey revealed that, of those infected, approximately 20% developed West Nile fever(14). The overall case fatality rate ranges from 4% to 14% in individuals exhibiting neuroinvasive disease, with a higher incidence of severe presentation and higher fatality rates in older populations(2,14).

EPIDEMIOLOGY: WNV was first discovered in 1937 from the blood of a febrile woman in the West Nile region of Uganda(5,9,10). WNV is now known to be enzootic in most of Africa, southern Europe, India, the Middle East, western and southeast Asia, Australia (known as Kunjin virus), and North America(1,8,9,15). WNV was first detected in North America in 1999, following an outbreak in New York City(8). The virus spread westwards across the United States, southward into Central America and the Caribbean, and northward into Canada(8,10,11), resulting in the largest epidemics of neuroinvasive WNV fever ever known(8,10). In temperate and subtropical regions, most infections in humans occur in summer or early fall when; whereas, infections in tropical regions tend to coincide with the rainy season when mosquito populations are most abundant(16).

HOST RANGE: Humans(1,2,3,4,5,6,7,8,9,10,11,12,13,17), mosquitoes(1,3,4,5,6,7,8,9,10,12), ticks(7,8), birds (particularly passerine species)(1,3,5,6,8,9,17), horses(1,6), alligators (Alligator mississippiensis )(6), tree squirrels (Sciurus spp.)(3), eastern chipmunks (Tamias striatus ), eastern cottontail rabbits (Sylvilagus floridanus ), lake frogs ( Rana ridibunda ); as well as a broad range of common North American wild and domestic mammals, such as dogs, deer, feral swine, coyotes, foxes, opossums, raccoons skunks, bats and other small rodents.

INFECTIOUS DOSE: One viral unit (via the intramuscular route)(18).

MODE OF TRANSMISSION: The main route of infection is via the bite of a mosquito that has been infected by feeding on WNV infected birds(1,3,6,9). Humans and most other mammals are regarded as dead-end hosts, since they do not produce sufficient viraemia to infect mosquitoes and thus do not significantly contribute to the transmission cycle(10,12).

Other possible routes include blood transfusion, vertical transmission, breast milk, organ transplantation(11), contact of the conjunctiva with contaminated bodily secretions of infected birds(17), and laboratory accidents involving injury with sharps(13).

INCUBATION PERIOD: Ranges from 2 to 6 days, but may extend to 14 days, or as long as 21 days for patients following organ transplantation(1,14).

COMMUNICABILITY: Human-to-human transmission can occur via infected breast milk, organ transplantation, blood transfusion, and via vertical transmission (from mother to child during pregnancy)(11).


RESERVOIR: Birds, particularly passerine species (jays, finches, grackles, sparrows, and crows)(3,6,11).

ZOONOSIS: Yes. Humans can contract WNV from the exposure of conjunctival membranes(17) and/or percutaneous injury to the body fluids or tissues of WNV infected birds(13), as well as indirectly by the bite of an infected mosquito(4,15,16).

VECTORS: The main vectors are Culex mosquitoes(1,3,4,9,10).
In North America: C. pipiens , C. restuans , C. salinarius , C. quinquefasciatus , and C. tarsalis(3,9,10).
In Africa and the Middle East: C. univittatus(5,9).
In Asia: C. vishnui(5).
In Europe: C. pipiens , C. modestus , and Coquillettidia richiardii(9).
Other mosquito species such as Culex nigripalpus , Aedes albopictus , Aedes vexans , and
Ochlerotatus triseriatus , may also be of importance in the transmission of WNV(3).


DRUG SUSCEPTIBILITY: Ribavirin and interferon can inhibit WNV in vitro(10,11).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to disinfectants such as 3 to 8% formaldehyde, 2% glutaraldehyde, 2 to 3% hydrogen peroxide, 500 to 5,000 ppm available chlorine, alcohol, 1% iodine, and phenol iodophors(19).

PHYSICAL INACTIVATION: Inactivated by heat (50 to 60°C for at least 30 minutes), ultraviolet light, and gamma irradiation(19).

SURVIVAL OUTSIDE HOST: Low temperatures preserve infectivity, with stability being greatest below -60°C(19). When added to ELISA wash buffer there is a 10-fold decrease in titre per 24 hour period at 28°C(20).


SURVEILLANCE: Monitor for symptoms. Confirmation is via virus isolation from blood(1,2,4,11) or cerebrospinal fluid(1,2,10,11) during the viraemic phase. Other methods of detection include PCR(2,3,4,13,18), haemagglutinin inhibition(1,12,17), plaque reduction neutralization(1,12), compliment fixation, indirect immunofluorescence assay(12), and IgM capture ELISA(1,2,3,10,12,17).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Currently there is no treatment of proven efficacy for WNV fever(10,11). Supportive therapy for encephalitis cases includes intravenous fluid, electrolyte management, assisted respiration if needed, anticonvulsants, management of cerebral oedema, and prevention of secondary bacterial infections(1,2). Studies have assessed ribavirin, interferon, osmotic agents, gamma globulins, and steroids for treatment of WN fever in open trials, but more definitive evidence is needed to determine their efficacy(1,2,4).

IMMUNIZATION: None currently available. An inactivated vaccine is available for horses, but human vaccines are unlikely to be available for several years(4,12), although a number of candidates are in clinical trials(10,12).

PROPHYLAXIS: None currently available. The most effective preventative measure it to avoid mosquito bites(2,3,4,8,10). There are no chemoprophylactic measures for individuals suspected of being in contact with WNV. To prevent transmission of WNV through blood transfusion and organ donations, blood products are screened for WNV in the United States(11).


LABORATORY-ACQUIRED INFECTIONS: Eighteen cases were reported up until 1980(21), with no deaths. Recently two more cases were reported of workers who acquired WNV following percutaneous inoculation whilst handling fluids and tissues infected with WNV(2).

SOURCES/SPECIMENS: Blood(2,3,10,12), cerebrospinal fluid(1,2,3,10,11,12), tissues(2,3,11,12,17), infected arthropods(1,2,3,4,5,6,7,8,9,10,11,12,13), oral and cloacal swabs, and feather pulp(3).

PRIMARY HAZARDS: Needlestick injuries, droplets, and aerosols(6,13,17).

SPECIAL HAZARDS: Faecal secretions of infected birds may present a hazard to humans(4,17).



CONTAINMENT REQUIREMENTS: Containment Level 3 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Personnel entering the laboratory should remove street clothing and jewellery, and change into dedicated laboratory clothing and shoes, or don full coverage protective clothing (i.e., completely covering all street clothing). Additional protection may be worn over laboratory clothing when infectious materials are directly handled, such as solid-front gowns with tight fitting wrists, gloves, and respiratory protection. Eye protection must be used where there is a known or potential risk to splashes(23).

OTHER PRECAUTIONS: All activities with infectious material should be conducted in a biological safety cabinet (BSC) or other appropriate primary containment device in combination with personal protective equipment. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are unloaded in a biological safety cabinet. The use of needles, syringes, and other sharp objects should be strictly limited. Open wounds, cuts, scratches, and grazes should be covered with waterproof dressings. The use of needles, syringes and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities(23).


SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (30 min).

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and/or incineration(23).

STORAGE: In sealed, leak-proof containers that are appropriately labelled and locked in a Containment Level 3 laboratory(23).


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: September 2010.

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2010


  1. Watts, D. M. (2006). Japanese Encephalitis and West Nile and Other Flavivirus Infections. In R. Guerrant, D. Walker & P. Weller (Eds.), Tropical Infectious Diseases: Principles, Pathogens, and Practice (2nd ed., pp. 823-830). Philadelphia, PA: Elsevier Churchill Livingston.
  2. Watson, J. T., & Gerber, S. I. (2004). West Nile Virus: A brief review. Pediatric Infectious Disease Journal, 23 (4), 357-358.
  3. Trevejo, R. T., & Eidson, M. (2008). West Nile virus. Journal of the American Veterinary Medical Association, 232 (9), 1302-1309.
  4. Petersen, L. R., Marfin, A. A., & Gubler, D. J. (2003). West Nile Virus. JAMA: The Journal of the American Medical Association, 290 (4), 524-528. doi:10.1001/jama.290.4.524
  5. Van Der Meulen, K. M., Pensaert, M. B., & Nauwynck, H. J. (2005). West Nile virus in the vertebrate world. Archives of Virology, 150 (4), 637-657.
  6. Briese, T., & Bernard, K. A. (2005). West Nile virus - An old virus learning new tricks? Journal of Neurovirology, 11 (5), 469-475.
  7. Glaser, A. (2004). West Nile virus and North America: An unfolding story. OIE Revue Scientifique Et Technique, 23 (2), 557-568.
  8. Hayes, E. B., Komar, N., Nasci, R. S., Montgomery, S. P., O'Leary, D. R., & Campbell, G. L. (2005). Epidemiology and transmission dynamics of West Nile virus disease. Emerging Infectious Diseases, 11 (8), 1167-1173.
  9. Mackenzie, J. S., Gubler, D. J., & Petersen, L. R. (2004). Emerging flaviviruses: The spread and resurgence of Japanese encephalitis, West Nile and dengue viruses. Nature Medicine, 10 (12 SUPPL.), S98-S109.
  10. Davis, L. E., DeBiasi, R., Goade, D. E., Haaland, K. Y., Harrington, J. A., Harnar, J. B., Pergam, S. A., King, M. K., DeMasters, B. K., & Tyler, K. L. (2006). West nile virus neuroinvasive disease. Annals of Neurology, 60 (3), 286-300.
  11. Hayes, E. B., & O'Leary, D. R. (2004). West Nile Virus Infection: A Pediatric Perspective. Pediatrics, 113 (5 I), 1375-1381.
  12. Dauphin, G., & Zientara, S. (2007). West Nile virus: Recent trends in diagnosis and vaccine development. Vaccine, 25 (30 SPEC. ISS.), 5563-5576.
  13. From the Centers for Disease Control and Prevention. Laboratory-acquired West Nile virus infections--United States, 2002. (2003). JAMA : The Journal of the American Medical Association, 289 (4), 414-415.
  14. Peterson, L. R., & Marfin, A. A. (2002). West Nile Virus: A Primer for the Clinician. Annals of Internal Medicine, 137 (3), E-173-E-179.
  15. Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th Edition ed.). Washington, D.C.: American Public Health Association.
  16. Campbell, G. L., Marfin, A. A., Lanciotti, R. S., & Gubler, D. J. (2002). West Nile virus. The Lancet Infectious Diseases, 2 (9), 519-529.
  17. Fonseca, K., Prince, G. D., Bratvold, J., Fox, J. D., Pybus, M., Preksaitis, J. K., & Tilley, P. (2005). West Nile virus infection and conjunctival exposure [8]. Emerging Infectious Diseases, 11 (10), 1648-1649.
  18. Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and routes of infection. Laboratory-Acquired Infections: History, incidence, causes and prevention (4th ed., pp. 52). Oxford U.K.: Butterworth Heinemann.
  19. Burke, D. S., & Monath, T. P. (2001). Flaviviruses . In D. M. Knipe, & P. A. Howley (Eds.), (4th ed., pp. 1043-1125). Philadelphia, PA: Lippincott Williams & Wilkins.
  20. Mayo, D. R., & Beckwith III, W. H. (2002). Inactivation of West Nile virus during serologic testing and transport. Journal of Clinical Microbiology, 40 (8), 3044-3046.
  21. Scherer, W. F., Eddy, G. A., & Monath, T. P. (1980). Laboratory safety for arboviruses and certain other viruses of vertebrates. American Journal of Tropical Medicine and Hygiene, 29 (6), 1359-1381.
  22. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57- 58 Elizabeth II, 2009. (2009).
  23. Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
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