West Nile virus
West Nile virus
West Nile virus (WNV) is a member of the family of viruses that is called Flaviviridae. The virus is similar to other members of this viral family, and is passed to humans from birds by the bite of a mosquito. West Nile Virus is capable of causing West Nile fever, West Nile encephalitis, or West Nile meningitis in humans.
West Nile virus is endemic (naturally present) in Africa. Periodic outbreaks have occurred in Europe for decades, although it has become more prominent in Europe and North America in the late 1990s. The virus was first discovered in North America in September 1999, during an investigation of an encephalitis outbreak in New York City.
Encephalitis is a swelling of the brain. The malady occurs in domestic animals such as horses, dogs, cats, wild animals, and wild birds. The virus can be transferred from an infected bird to humans by the bite of a mosquito. When transferred to a human, the viral infection produces encephalitis and inflammation of membranes surrounding the brain and spinal cord (meningitis).
In 1999, 62 cases of the disease were reported in New York City. Seven people died. The following spring, 21 more cases occurred, and two of the people died. It is thought that infected mosquitoes that survived the winter were responsible for the renewed outbreak. In 1999 and 2000, the West Nile virus was confined to the northeastern region of the United States. Since then, the virus has spread to all of the continental United States and some provinces of Canada. As of November 2006, there were 4028 confirmed and reported cases of West Nile disease resulting in 135 deaths for the 2006 year alone.
Infected migratory birds may have aided the rapid spread of the virus. As well, the presence of the virus or infected mosquitoes in transported equipment, trains and airplanes, luggage, and on people is thought to be a factor in the spread. Many epidemiologists
(scientists who track and study disease outbreaks) now consider West Nile virus to be endemic to the continental United States.
The symptoms of infection begin three to 15 days following the bite of an infected mosquito. Most people with West Nile fever experience only mild symptoms that mimic the flu (i.e., fever, headache, body aches). Others will also develop a mild rash or have swollen lymph glands.
In about 3–15% of those who are infected with the virus, the infection is more serious. This is particularly the case for the elderly or those whose immune systems are not functioning properly. These are the people who are at greatest risk for developing encephalitis or meningitis. Symptoms of West Nile encephalitis and West Nile meningitis appear suddenly, and include a severe headache, high fever, stiff neck, vomiting, confusion, and loss of consciousness. Even after recovery, a person may have muscle weakness and brain related complications for months or years.
The origin of the virus dates back to 1937, when the virus was isolated from a woman in the West Nile District of Uganda. This is the basis for the name of the virus. The disease causing nature of the virus for humans was discovered in the 1950s, and in animals during the 1960s. It is unclear whether the virus radiated out from Uganda, or whether it has long been present in North America and was previously undetected. However, the pattern of detection suggested that the virus spread globally from one region.
Numerous species of mosquito can become infected with the virus. Three species in particular have been most commonly associated with outbreaks. These species are Culex pipiens, Culex restuans, and Culex quinquefasciatus.
Mosquitoes acquire the virus when they obtain a blood meal from an infected animal. The virus resides in the salivary glands of the mosquito and can be passed into a human from which the mosquito subsequently obtains a blood meal.
The number of bird species involved in transmission of the West Nile virus is not known. It is known that over 138 species of birds can be infected with the virus, and that the infection kills many crows, blue jays, magpies, and ravens.
The virus enters the host’s bloodstream and, by a mechanism that is not yet known, is able to cross the barrier between the blood and the brain. Multiplication of the virus in brain tissue disrupts the cells, causing the nervous system to malfunction and the brain tissue to become inflamed.
Despite the publicity of public fear surrounding the spread of the West Nile virus in North America, the chance of acquiring West Nile virus via a mosquito bite is small. The available data from surveys of mosquito populations indicates that around 1% of mosquitoes carry the virus, even in areas where the virus is known to be present.
Because the mosquito will not survive cold northerly winters in the wild, the spread of the virus in colder climates is slow. However, if mosquitoes can find protection from the winter, such as in buildings or sewer pipelines, they can survive over the winter.
Another climatic factor may be hot and dry spring and summer seasons. The dry conditions limit the open water supplies that are frequented by mosquitoes. The large mosquito populations that gather at the available water supplies make it easier for the virus to become established in large numbers of the insects.
The mosquito-to-human route of infection is overwhelmingly the major route of WNV disease transmission in humans. While ticks can be infected with the virus, a tick-borne outbreak of the disease has not been documented in humans. Person to person transmission through direct contact has occurred in only two observed cases, once via mother to her unborn child, and once via breast milk. In 2002, however, several people became ill after receiving blood from a donor who was subsequently found to be infected with West Nile virus. All blood donations in the United States are now screened for the presence of West Nile virus.
No vaccine for the West Nile virus currently exists for humans, although researchers have recently reported on the success of a weakened West Nile virus-dengue virus construct in stimulating an immune response in experimental animals. A vaccine for horses has been developed, and over seven million horses were vaccinated against West Nile virus in 2002, the first year the vaccine was available. Prevention of infection in humans consists mainly of environmental control of mosquitoes, use of chemical mosquito repellent and insecticide, use of protective clothing, and simply avoiding being outside at places or times when mosquitoes are typically present.
See also Microorganisms; Zoonoses.
Resources
BOOKS
Despommier, D. West Nile Story. New York: Apple Trees Productions, LLC, 2001.
White, D. J., and D. L. Morse. West Nile Virus: Detection, Surveillance, and Control. Baltimore: Johns Hopkins University Press, 2002.
PERIODICALS
Pletnev, A. G., R. Putnak, J. Speicher, et al. “West Nile Virus/Dengue Type 4 Virus Chimeras that are Reduced in Neurovirulence and Peripheral Virulence Without Loss of Immunogenicity or Protective Efficacy.” Proceedings of the National Academy of Sciences 99 (March 2002): 3036–3041.
OTHER
Centers for Disease Control and Prevention, Division of Vector-Borne Infectious Diseases, P.O. Box 2087, Fort Collins, CO 80522. (888) 246–2675. <http://www.cdc.gov/ncidod/dvbid/westnile/> (accessed November 27, 2006).
Brian Hoyle
