West Nile virus

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Key facts

  • West Nile virus can cause a fatal neurological disease in humans.
  • However, approximately 80% of people who are infected will not show any symptoms.
  • West Nile virus is mainly transmitted to people through the bites of infected mosquitoes.
  • The virus can cause severe disease and death in horses.
  • Vaccines are available for use in horses but not yet available for people.
  • Birds are the natural hosts of West Nile virus.

West Nile Virus (WNW) can cause neurological disease and death in people. WNW is commonly found in Africa, Europe, the Middle East, North America and West Asia. WNW is maintained in nature in a cycle involving transmission between birds and mosquitoes. Humans, horses and other mammals can be infected.

West Nile Virus (WNW) is a member of the antivirus genus and belongs to the Japanese encephalitis antigenic complex of the family Riboflavin.


West Nile Virus (WNW) was first isolated in a woman in the West Nile district of Uganda in 1937. It was identified in birds (crows and columbines) in Nile delta region in 1953. Before 1997 WNW was not considered pathogenic for birds, but at that time in Israel a more virulent strain caused the death of different bird species presenting signs of encephalitis and paralysis. Human infections attributable to WNV have been reported in many countries in the World for over 50 years.

In 1999 a WNW circulating in Israel and Tunisia was imported in New York producing a large and dramatic outbreak that spread throughout the continental United States of America (USA) in the following years. The WNW outbreak in USA (1999-2010) highlighted that importation and establishment of vector-borne pathogens outside their current habitat represent a serious danger to the world.

The largest outbreaks occurred in Greece, Israel, Romania, Russia and USA. Outbreak sites are on major birds migratory routes. In its original range, WNW was prevalent throughout Africa, parts of Europe, Middle East, West Asia, and Australia. Since its introduction in 1999 into USA, the virus has spread and is now widely established from Canada to Venezuela.


Human infection is most often the result of bites from infected mosquitoes. Mosquitoes become infected when they feed on infected birds, which circulate the virus in their blood for a few days. The virus eventually gets into the mosquito’s salivary glands. During later blood meals (when mosquitoes bite), the virus may be injected into humans and animals, where it can multiply and possibly cause illness.

The virus may also be transmitted through contact with other infected animals, their blood, or other tissues.

A very small proportion of human infections have occurred through organ transplant, blood transfusions and breast milk. There is one reported case of trans placental (mother-to-child) WNV transmission.

To date, no human-to-human transmission of WNW through casual contact has been documented, and no transmission of WNW to health care workers has been reported when standard infection control precautions have been put in place.

Transmission of WNW to laboratory workers has been reported.

Signs and symptoms

Infection with WNV is either asymptomatic (no symptoms) in around 80% of infected people, or can lead to West Nile fever or severe West Nile disease.

About 20% of people who become infected with WNW will develop West Nile fever. Symptoms include fever, headache, tiredness, and body aches, nausea, vomiting, occasionally with a skin rash (on the trunk of the body) and swollen lymph glands.

The symptoms of severe disease (also called noninvasive disease, such as West Nile encephalitis or meningitis or West Nile poliomyelitis) include headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. It is estimated that approximately 1 in 150 persons infected with the West Nile virus will develop a more severe form of disease. Serious illness can occur in people of any age, however people over the age of 50 and some uncompromising persons (for example, transplant patients) are at the highest risk for getting severely ill when infected with WNW.

The incubation period is usually 3 to 14 days.


West Nile virus can be diagnosed by a number of different tests:

  • IgG antibody sore-conversion (or significant increase in antibody titters) in two serial specimen collected at a one week interval by enzyme-linked immunodeficient assay (ELISA);
  • IgM antibody capture enzyme-linked immunodeficient assay (ELISA);
  • neutralization assays;
  • viral detection by reverse transcription polymer chain reaction (RT-PCT) assay, and
  • virus isolation by cell culture.

IgM can be detected in nearly all cerebrovascular fluid (C SF) and serum specimens received from WNW infected patients at the time of their clinical presentation. Serum IgM antibody may persist for more than a year.

Treatment and vaccine

Treatment is supportive for patients with n euro-invasive West Nile virus, often involving hospitalization, intravenous fluids, respiratory support, and prevention of secondary infections. No vaccine is available for humans.

Vector and animal hosts

WN virus is maintained in nature in a mosquito-bird-mosquito transmission cycle. Mosquitoes of the genus Culley are generally considered the principal vectors of WNW, in particular C. Sapiens. WNW is maintained in mosquito populations through vertical transmission (adults to eggs).

Birds are the reservoir hosts of WNW. In Europe, Africa, Middle East and Asia, mortality in birds associated with WNW infection is rare. In striking contrast, the virus is highly pathogenic for birds in the Americas. Members of the crow family (Cordage) are particularly susceptible, but virus has been detected in dead and dying birds of more than 250 species. Birds can be infected by a variety of routes other than mosquito bites, and different species may have different potential for maintaining the transmission cycle.

Horses, just like humans, are “dead-end” hosts, meaning that while they become infected, they do not spread the infection. Symptomatic infections in horses are also rare and generally mild, but can cause neurological disease, including fatal electroencephalograms.

Life cycle

Once WNW has successfully entered the bloodstream of a host animal, the envelope protein, E, binds to attachment factors called glycosaminoglycans on the host cell.These attachment factors aid entry into the cell, however, binding to primary receptors is also necessary.Primary receptors include DC-SIGN, DC-SIGN-R, and the integrity By binding to these primary receptors, WNW enters the cell through clarinet-mediated endometriosis. As a result of endometriosis, WNW enters the cell within an endoscope.

The acidity of the endoscope catalyzes the fusion of the endometrial and viral membranes, allowing the genome to be released into the cytoplasm.Translation of the positive-sense single-stranded RNA occurs at the cytoplasmic reticulum; the RNA is translated into a poly protein which is then cleaved by viral pro teases NS2B-N23 to produce mature proteins.

In order to replicate its genome, NS5, a RNA polymerase, forms a replication complex with other nonstructural proteins to produce an intermediary negative-sense single-stranded RNA; the negative-sense strand serves as a template for synthesis of the final positive-sense RNA.Once the positive-sense RNA has been synthesized, the caps id protein, C, encloses the RNA strands into immature visions.The rest of the virus is assembled along the cytoplasmic reticulum and through the Golgi apparatus, and results in non-infectious immature visions. The E protein is then syllabicated and p Rm is cleaved by furn, a host cell pro tease, into the M protein, thereby producing an infectious mature vision.The mature viruses are then secreted out of the cell.


Phylogeny tree of West Nile viruses based on sequencing of the envelopment during complete genome sequencing of the virus

WNV is one of the Japanese encephalitis antigenic complexion of viruses, together with Japanese encephalitis virus, Murray Valley encephalitis virus, Saint Louis encephalitis virus and some other retroviruses Studies of phylogeny lineages have determined that WNW emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages. Lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an African stenosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Maraca sylvan us, was the first nonhuman primate to contract WNW.[33] Both the American and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Cordage—can be an early indicator of the arrival of the virus.

Host range and transmission

Culley pippins mosquitoes are a vector for WNW.

The natural hosts for WNW are birds and mosquitoes.Over 300 different species of bird have been shown to be infected with the virus. Some birds, including the American crow (Corvus brachyrhynchos), blue jay (Cyanobacteria sacristan) and greater sage-grouse (Cysticercus claustrophobia), are killed by the infection, but others survive. The American robin (Turds migrators) and house sparrow (Passer domestics) are thought to be among the most important reservoir species in N. American and European cities.Brown thrashers (Myxomatosis rum), gray catbirds (Dumbbell carcinogens), northern cardinals (Cardinals cardinals), northern mockingbirds (Minus polyglots), wood thrushes (Staphylococci mustiness) and the dove family are among the other common N. American birds in which high levels of antibodies against WNW have been found.

WNW has been demonstrated in a large number of mosquito species, but the most significant for viral transmission are Culley species that feed on birds, including Culley pippins, C. restaurant, C. sanitariums, C. quintessential, C. principals, C. erratic us and C. tarsals. Experimental infection has also been demonstrated with soft tick vectors, but is unlikely to be important in natural transmission.

WNW has a broad host range, and is also known to be able to infect at least 30 mammalian species, including humans, some non-human primates,horses, dogs and cats. Some infected humans and horses experience disease but dogs and cats rarely show symptoms.Reptiles and amphibians can also be infected, including some species of crocodiles, alligators, snakes, lizards and frogs.Mammals are considered incidental or dead-end hosts for the virus: they do not usually develop a high enough level of virus in the blood (uremia) to infect another mosquito feeding on them and carry on the transmission cycle; some birds are also dead-end hosts

In the normal rural or enzymatic transmission cycle, the virus alternates between the bird reservoir and the mosquito vector. It can also be transmitted between birds via direct contact, by eating an infected bird carcass or by drinking infected water Vertical transmission between female and offspring is possible in mosquitoes, and might potentially be important in overwintering. In the urban or spillover cycle, infected mosquitoes that have fed on infected birds transmit the virus to humans. This requires mosquito species that bite both birds and humans, which are termed bridge vectors. The virus can also rarely be spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding.Unlike in birds, it does not otherwise spread directly between people.

Mild infection signs and symptoms

About 20 percent of people develop a mild infection called West Nile fever. Common signs and symptoms include:

  • Fever
  • Headache
  • Body aches
  • Vomiting
  • Diarrhea
  • Fatigue
  • Skin rash

Serious infection signs and symptoms

In less than 1 percent of infected people, the virus causes a serious neurological infection, including inflammation of the brain (encephalitis) and of the membranes surrounding the brain and spinal cord (meningitis).

Signs and symptoms of neurological infections include:

  • High fever
  • Severe headache
  • Stiff neck
  • Disorientation or confusion
  • Stupor or coma
  • Tremors or muscle jerking
  • Seizures
  • Partial paralysis or muscle weakness

Signs and symptoms of West Nile fever usually last a few days, but signs and symptoms of encephalitis or meningitis can linger for weeks or months. Certain neurological effects, such as muscle weakness, can be permanent.

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