West nile virus historical perspective

History
Studies of phylogenetic lineages have determined that WNV 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, while Lineage 2 remains as an Africa zoonose.

WNV was first isolated from a feverish adult woman in the West Nile District of Uganda in 1937 during research on yellow fever. A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt and Israel. 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 and found to be widespread in southern Europe, southwest Asia and Australia.

The first appearance of West Nile virus in the Western hemisphere was 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 American outbreak began in the New York City area, including New Jersey and Connecticut, and the virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence. The US virus was very closely related to a lineage 1 strain found in Israel in 1998. 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 horse cases, and many birds are infected. Both the US and Israeli strains are marked by high mortality rates in infected avian populations, the presence of dead birds - especially corvidae - can be an early indicator of the arrival of the virus.

A very high level of media coverage through 2001/2002 raised public awareness of West Nile virus. This disproportionate coverage was most likely the result of successive appearances of the virus in new areas.

Environmentalists have condemned attempts to control the transmitting mosquitoes 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. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern U.S., Culex pipiens, is a canopy feeder. WNV was first isolated in the WN province of Uganda in 1937. Human and equine outbreaks have been recorded in portions of Africa, southern Europe, North America, and Asia.

In late summer 1999, the first domestically acquired human cases of West Nile (WN) encephalitis were documented in the U.S. The discovery of virus-infected, overwintering mosquitoes during the winter of 1999-2000 presaged renewed virus activity for the following spring and precipitated early season vector control and disease surveillance in New York City (NYC) and the surrounding areas. These surveillance efforts were focused on identifying and documenting WN virus (WNV) infections in birds, mosquitoes and equines as sentinel animals that could alert health officials to the occurrence of human disease. Surveillance tracked the spread of WNV throughout much of the U.S. between 2000 and 2002. By the end of 2002, WNV activity had been identified in 44 states and the District of Columbia. The 2002 WNV epidemic and epizootic resulted in reports of 4,156 reported human cases of WN disease (including 2,942 meningoencephalitis cases and 284 deaths), 16,741 dead birds, 6,604 infected mosquito pools, and 14,571 equine cases. The 2002 WNV epidemic was the largest recognized arboviral meningoencephalitis epidemic in the Western Hemisphere and the largest WN meningoencephalitis epidemic ever recorded. Significant human disease activity was recorded in Canada for the first time, and WNV activity was also documented in the Caribbean basin and Mexico. In 2002, 4 novel routes of WNV transmission to humans were documented for the first time: 1) blood transfusion, 2) organ transplantation, 3) transplacental transfer, and 4) breast-feeding.