The West Nile Virus





The West Nile Virus


BACKGROUND AND DISTRIBUTION
A West Nile (WN) virus was first isolated in 1937 from the peripheral blood of a woman in the West Nile province of Uganda in Central Africa. Since then, WN viruses have been reported from North Africa (Egypt, Israel), East, Central, and South Africa, Asia (India, Pakistan), Borneo, Europe (Cyprus, France, Romania) and, most recently, the northeastern USA. Tests for antibody to WN suggest it has also been present in Thailand, the Philippines, Malaysia, Turkey, and Albania.
West Nile viruses are members of the virus family Flaviviridae and are closely related to Japanese encephalitis viruses from the Old World and St. Louis encephalitis (SLE) viruses from the New World. In addition, WN cross-reacts in a variety of serological tests, including the plaque reduction neutralization test, with Murray Valley encephalitis (MVE), Usutu, Kunjin, Kokobera, Stratford, and Alfuy viruses. It was this cross reactivity of the New York City (NYC) WN with SLE serologic reagents that initially confused this virus with SLE. Additional tests that used direct examination of the gene sequence of the NYC virus identified it as a WN-like virus, not SLE.
West Nile is represented by at least 2 distinct antigenic groups. One, the African-Middle Eastern group, contains WN isolates from the Congo, Egypt, Israel, Uganda, South Africa, Pakistan, France, and Eastern Europe. The second antigenic group contains WN isolates from India and South Africa.
HISTORY
The earliest reported epidemics caused by WN were in Israel. The first involved more than 500 clinical cases in 1950. Additional epidemics were reported from Israel in 1951, 1952, 1953, and 1957. The 1950 and 1957 epidemics were reported from a site 40 miles north of Tel Aviv, while the 1951 epidemic occurred at a site 15 miles southeast of Tel Aviv. In 1952, 1953, and 1954, cases were reported from both areas, indicting the ability of this virus to be extremely focal in its epidemic transmission patterns.
Epidemics of WN occurred in the Rhone delta region of France in 1962, 1963, and 1964. The largest epidemic of WN, involving thousands of clinical cases, was reported in South Africa in 1974. Epidemic activity was again reported in South Africa in 1983 and 1984. Human cases were reported in southeast Romania in 1996 and 1997. Most recently, WN virus(es) was apparently introduced into the northeastern region of the borough of Queens in NYC during the summer of 1999.
West Nile is more mobile than other closely related viruses like the SLE viruses in North America and MVE viruses in Australia. West Nile viruses have spread from Africa to Western Europe, the Middle East, Eastern Europe, and now North America. To date, close relatives of WN like SLE and MVE have remained confined to their home regions.
THE DISEASE
In humans, infection with WN can cause clinical or subclincal symptoms. Clinical symptoms vary from temporary fever to serious encephalitis. The disease can be severe in the elderly, but is usually mild in healthy adults and children. The incubation period for WN is 3-6 days. Onset of disease symptoms is usually sudden, beginning with a sustained, elevated fever. Clinical infection can include severe headache; a rash, usually on the trunk; and swollen lymph nodes. Symptoms of WN infection can also include eye, muscular and back pains, and gastrointestinal problems. In severe cases, there are often symptoms of encephalitis with eventual neurological involvement and sometimes death. Humans experience a low-level viremia that lasts about 6 days. Mortality rates in humans range from 5 to 13%.
In domestic animals, clinical signs of WN infection have only been observed in horses, even though most horse infections are asymptomatic. However, in the WN epidemic in France during 1962-64, horses experienced 25% mortality. As with horses, cattle, sheep, and camels can also be infected with WN, but clinical symptoms and viremia capable of infecting arthropod vectors have not been reported from these hosts. Birds, however, do experience viremias capable of infecting arthropod vectors.

TRANSMISSION BY ARTHROPODS
Mosquitoes and ticks serve as natural vectors of WN. Most virus isolates have been from mosquitoes, suggesting that they serve as primary vectors. Culex univittatus appears to be the major WN vector in Africa. Culex pipiens is a secondary vector in South Africa and may be the primary vector in Israel. Members of the Cx. vishnui