Updated: Septiembre 15, 2004
The West Nile Virus (WNV), was first identified in 1937. The disease is widespread in Africa, the Middle East, Europe, the former USSR, and parts of Asia. Its first appearance in North America was in New York in 1999, and 62 people were infected in that initial outbreak, seven of whom died.
The level of disease in the U.S. remained fairly steady in 2000 and 2001, but in 2002 WNV caused the largest recorded outbreak of arboviral encephalitis in the western hemisphere involving 4156 cases and 284 deaths.
In 2003, the western hemisphere saw a continuation of the epidemic with over 9100 cases including 231 deaths. However, much of the increase in numbers of cases was due to availability of commercial diagnostics that have identified West Nile fever cases. The numbers of West Nile neurological disease cases was about around 2500 in both 2002 and 2003.
The disease is spread by mosquitoes, which become infected when they ingest blood from birds (primarily crows and blue jays) that carry the virus. Humans and other animals, particularly horses, become infected when bitten by infected mosquitoes. WNV has now been found in more than 200 species of birds, and it is believed that migratory birds and mosquitoes will continue to spread the disease, possibly throughout the entire Western Hemisphere. The virus has been found throughout North America, including Canada and Mexico, and has spread into Central America, including the Caribbean and El Salvador.
WNV is not transmitted from person to person or from animals to humans. However, at least 20 U.S. cases became infected through organ transplants and WNV can also be transmitted by blood transfusion. Although the risk of such transmission is low (only 6 confirmed cases in 2003), the Food and Drug Administration (FDA) has issued new guidelines for screening blood donors to reduce the risk that infected blood enters the blood supply.
There is also evidence that WNV can be spread transplacentally but the risk is very low (CDC has issued guidelines for evaluation and management of perinatal infections; see MMWR 2/27/04). Also, WNV can be transmitted in breast milk, but it is not known what the risk of such transmission is, or how likely the infants of nursing mothers infected with WNV are to become infected themselves. Because the health benefits of breast-feeding are well established, breast-feeding recommendations are currently unchanged. Women who are breast-feeding who develop any illness that includes a fever should consult their physician.
The vast majority of people bitten by a WNV-infected mosquito do not become ill. Of the two-tenths of one percent (0.2%) of people bitten who do get sick, most have only mild symptoms that may include fever, headache, and body aches, and also may include a skin rash on the trunk and swollen lymph glands. A very small subset of those who become infected (about 1 in 150 persons infected) will develop a more severe form of disease. The symptoms of severe infection West Nile encephalitis or meningitis) include headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. The risk of serious disease is higher for people 50 years of age and older.
Unfortunately, there currently is no test that can rapidly identify the presence of WNV. Patients are diagnosed on the basis of their immune (antibody) response to the virus, which takes about 14 days from the time the infection occurs.
Mosquito control and protection against mosquito bites are currently the most effective means of preventing human WNV disease. There is no known effective antiviral therapy, and no licensed WNV vaccine for use in humans, though several experimental vaccines are under development. Research is also ongoing on anti-viral drugs against WNV disease, including alpha-interferon, a drug used in the treatment of hepatitis C.
Because the Japanese Encephalitis virus (JEV) is similar to WNV, the inactivated JEV vaccine has been evaluated as one possible way to protect humans against WNV disease but unfortunately it is not effective. Another approach being examined is using the current yellow fever vaccine as the template for a WNV vaccine. To make this vaccine, yellow fever vaccine genes are replaced with corresponding WNV genes. A weakened strain of the yellow fever virus is used as the backbone of the vaccine, and the gene that encodes the yellow fever virus’s protein coat is replaced with the corresponding gene from the WNV. The yellow fever vaccine used as the basis for this process has been safely and effectively given to millions of people, and initial WNV trials in animals have shown promising results and phase I human clinical trials are underway.
Somewhat similar efforts to produce a WNV vaccine based on the dengue type 4 vaccine are in process at The National Institutes of Health (NIH), and this vaccine appears to have some success in decreasing the severity of WNV disease in laboratory mice. The National Institute of Allergy and Infectious Diseases at the NIH is funding research on West Nile Virus vaccines and believes that one may be ready for human trials sometime in 2004.
Other vaccine candidates are undergoing preclinical development.
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