Science Fair Project Encyclopedia
West Nile virus
West Nile virus is a newly emergent virus of the family Flaviviridae, found in both tropical and temperate regions. It mainly infects birds, but is also the cause of a number of conditions in humans, horses, and some other mammals. It is transmitted by bites of infected mosquitoes.
Photographs from a high resolution electron microscope published in the journal Science reveal the virus as spherical with a slightly bumpy surface but no projecting protein arms. It is said to have a strong resemblance in appearance to dengue fever virus.
In most people (80%), infection causes no symptoms. In others, the virus causes mild flu-like symptoms known as West Nile fever. The virus is able to pass the blood-brain barrier, and the most serious effects (in 0.7% of the infected) are encephalitis (inflammation of the brain) and meningitis (inflammation of the lining of the brain and spinal cord), both of which can be fatal. Persons over 50 years of age are at higher risk of developing severe disease, the symptoms of which include fever, nausea, stiff neck and changes in mental status. In rare cases (first reported October 2002), patients develop sudden-onset paralysis.
Symptoms develop 3-14 days after infection. No effective treatment is known.
The virus is mostly maintained in birds. Female mosquitos, mainly of the species Culex pipiens, Culex restuan and Culex quinquefasciatus, bite infected birds, carry the virus in their salivary glands, and infect other birds when they bite again. Culex pipiens is thought to be the main mosquito species transmit the virus from birds to mammals. In mammals the virus does not multiply as readily, and it is believed that mosquitos biting infected mammals do not further transmit the virus. A paper in the journal Science in 2004 found that Culex pipiens mosquitos existed in two population in Europe, one which bites birds and one which bites humans. In North America 40% of Culex pipiens were found to be hybrid of the two types which bites both birds and humans, providing a vector for West Nile virus. This is thought to provide an explanation of why the West Nile disease has spread more quickly in North America than Europe.
It was initially believed that direct human-to-human transmission was impossible, but in 2002 the Centers for Disease Control and Prevention (CDC) discovered the transmission of West Nile virus through blood transfusion and organ transplants as well as through breast milk and prenatal infection.
West Nile virus was first isolated from a feverish adult woman in the West Nile District of Uganda in 1937. The ecology was characterized in Egypt in the 1950s. The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s.
The first appearance of West Nile virus in North America in 1999, with encephalitis reported in humans and horses, and the subsequent spread in the United States, may be an important milestone in the evolving history of this virus. The US outbreak began in the New York City area, and the virus is believed to have entered via an air traveler. Since the first North American cases in 1999, the virus has been reported throughout the United States and Canada east of the Rocky Mountains. There have been human cases and horse cases, and many birds--especially crows and other corvids--are infected.
A very high level of media coverage through 2001/2002 raised public fears of West Nile virus, even though common diseases such as influenza take far more lives each year. This disproportionate coverage is most likely the result of the novelty of the disease and the successive announcements of the disease's initial appearance in new areas.
Environmentalists have condemned attempts to control the transmitting mosquitos by spraying pesticide, saying that the detrimental health effects of spraying outweigh the relatively few lives which may be saved, and that there are more environmentally friendly ways of controlling mosquitoes. There are also questions about the effectiveness of insecticide spraying, because mosquitos that are resting or flying above the level of spraying will not be killed; the commonest vector in the northeastern U.S., Culex pipiens , is a canopy feeder.
West Nile virus has been described in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin), and most recently, North America. Recent outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), the Democratic Republic of the Congo (1998), Russia (1999), the United States (1999 to 2003), Canada (1999 to 2003), and Israel (2000). Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000).
In the US in 2002, West Nile virus was documented in animals in 44 states and the District of Columbia with Illinois, Louisiana, Michigan and Ohio reporting the most deaths. By 2003, 45 states and DC had reported human cases.
United States: From 1999 through 2001, the CDC confirmed 149 cases of human West Nile virus infection, including 18 deaths. In 2002 a total of 4156 cases were reported, including 284 fatalities. 13 cases in 2002 were contracted through blood transfusion. The cost of West Nile-related health care in 2002 was estimated at $200 million. The first human West Nile disease in 2003 occurred in June and one West Nile-infected blood transfusion was also identified that month. In the 2003 outbreak, 9858 cases and 262 deaths were reported by the CDC. At least 30% of those cases were considered severe involving meningitis or encephalitis. In 2004, there were only 2470 reported cases and 88 deaths.
Canada: One human death occurred in 1999. In 2002, ten human deaths out of 416 confirmed and probable cases were reported by Canadian health officials. In 2003, 14 deaths and 1388 confirmed and probable cases were reported. Cases were reported in 2003 in Nova Scotia, Quebec, Ontario, Manitoba, Saskatchewan, Alberta, British Columbia, and the Yukon. In 2004, through November 1, only 29 cases were reported and zero deaths.
Israel: In 2000 Israel reported 10 deaths and 120 cases of West Nile disease.
West Nile Virus can be sampled from the environment by the pooling of trapped mosquitoes, testing avian blood samples drawn from wild birds and sentinel chickens, as well as testing dead birds found by various animal control agencies and the public. Testing of the mosquito samples requires the use of PCR to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild bird and sentinel chickens, you must test for the presence of West Nile Virus antibodies by use of Immunohistochemistry (IHC) (Jozan et. al. 2003) or Enzyme-Linked Immunosorbent Assay (ELISA) (Hall 1995, Jozan et. al. 2003). Dead birds after necropsy, have their various tissues tested for virus by either PCR, or Immunohistochemistry were virus shows up as brown stained tissue.
- 2003 case count from CDC
- US map of West Nile virus
- World map of West Nile and related viruses
- Canadian case count
- L. Peterson, M. Marphin: "West Nile Virus: A Primer for the Clinician", Annals of Internal Medicine, Vol 137 No 3, August 2002, http://www.cfe.cornell.edu/erap/WNV/WNVEducDocs/Petersen-Marfin2002.pdf
- D. J. White, D. L. Morse (eds.): "West Nile Virus: Detection, Surveillance, and Control", Annals of the New York Academy of Sciences, vol. 951 (2001), http://www.annalsnyas.org/content/vol951/issue1/
- Nature news article on West Nile paralysis
Hall, R. 1995. Immunodominant epitopes on the NS1 protein of Murray Valley encephalitis and Kunjin viruses serve as targets for a blocking ELISA to detect virus specific antibodies in sentinel animal serum. J. Virol Methods. 51:201-210.
Jozan, M., Evans, R., Mclean, R. Hall, R. Tangredi, B., Reed, L., Scott, J.. 2003. Detection of West Nile virus infection in birds in the United States by blocking ELISA and immunohistochemistry. Vector-borne and Zoonotic Diseases. 3(3):99-110.
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