West nile virus has the following characteristics except

Patients with flaccid paralysis have perivascular lymphocytic infiltration in the spinal cord, microglial nodules, and loss of anterior horn cells 9. Spinal cord inflammation was seen in 17 of 23 people who died with WNV neuroinvasive disease; inflammation was more prominent in the anterior horns than in the posterior horns of 9 patients 9.

Endoneural mononuclear inflammation of cranial nerve roots and spinal nerves can be found in a small percentage of persons. Foci of demyelination, gliosis, and occasional perivascular infiltrates may be found in persons with prolonged clinical courses. Before , attempts to isolate WNV from postmortem tissues in the United States had been unsuccessful. Recently, the virus has been isolated postmortem from 2 immunosuppressed patients with apparently high viral loads Viral antigens are usually found within neurons and neuronal processes, predominantly in the brain stem and anterior horns Figure , panel C.

In general, antigens are focal and sparse, except in immunosuppressed patients in whom they can be seen extensively throughout the CNS 9. Visualization of WNV particles by electron microscopy is rare. When found, they are seen within endoplasmic reticulum of neurons Figure , panel D. Routine clinical laboratory studies do not distinguish WNV infection from many other viral infections.

Patients with neuroinvasive disease generally have lymphocytic pleocytosis in the cerebrospinal fluid CSF , but neutrophils may predominate early in the course of illness 28 , Results of brain magnetic resonance imaging are frequently normal, but signal abnormalities may be seen in the basal ganglia, thalamus, and brain stem of patients with encephalitis, and in the anterior spinal cord in patients with poliomyelitislike syndrome 18 , 29 , Busch, pers.

Consequently, detectable IgM may occasionally reflect past rather than recent infection. Recently developed microsphere immunoassays for WNV antibody appear to be more accurate and efficient than current enzyme immunoassays EIAs J.

Johnson, pers. As with standard EIA, related flaviviral infection may elicit cross-reactive test results. A microsphere assay with nonstructural viral antigens appears to discriminate between primary flaviviral infections that elicit cross-reactive antibody to the E glycoprotein However, PRNT may not discriminate between WNV infection and other flaviviral infections in patients with previous flavivirus exposure, because the neutralizing antibody in such cases may broadly cross-react to several related flaviviruses.

WNV is best isolated in cell culture or suckling mice and identified by indirect immunofluorescence assay with specific monoclonal antibodies or by reverse transcriptase—polymerase chain reaction RT-PCR.

However, WNV is rarely isolated from the blood of patients with neuroinvasive WNV disease because viremia levels are typically low or absent by the time neurologic symptoms develop. The diagnosis of WNV encephalitis can be supported histopathologically, and there is no pathognomonic lesion.

Differential diagnoses include arboviral and other viral encephalitides, rickettsial infections, and various noninfectious diseases. When serum samples and frozen tissues are not available, IHC testing of formalin-fixed tissues with specific monoclonal and polyclonal antibodies is particularly useful. The clinical course of WNF ranges from a mild febrile illness of several days' duration to debilitating fatigue, aching, and weakness that may last for weeks or months 16 , 29 , Although cases of meningitis without alteration of the patient's mental status or other focal neurologic features have a favorable prognosis, persistent headaches and fatigue may be reported Patients with WNV encephalitis or focal neurologic manifestations often have persistent neurologic deficits for months or years 28 , Many patients with WNV-associated poliomyelitislike syndrome do not recover, but some improvement in limb strength may occur over time 42 , Management of severe WNV illness remains supportive.

Patients with severe meningeal symptoms often require pain control for headaches and antiemetic therapy and rehydration for associated nausea and vomiting.

Patients with severe encephalitis should be observed for development of elevated intracranial pressure and seizures, and patients with encephalitis or paralysis must be monitored for inability to protect the airway. Acute neuromuscular respiratory failure may develop rapidly, particularly in patients with prominent bulbar signs; prolonged ventilatory support may be required 22 , 30 , Two vaccines are available for vaccinating equines: an inactivated WNV vaccine and a recombinant vaccine that uses canarypox virus to express WNV antigens 44 , An inactivated vaccine is also being studied for use in humans A chimeric live virus vaccine incorporating the genetic sequences for E and prM antigens into a D yellow fever virus backbone has been shown to be efficacious in hamsters and is undergoing initial clinical trials in humans Another chimeric vaccine incorporating WNV genetic sequences into a backbone of attenuated serotype-4 dengue virus—induced protective immunity in monkeys Since the s, WNV has gained notoriety as a cause of severe neuroinvasive disease in humans.

As WNV isolates and genetic sequences accumulate over an increasing geographic and clinical range, the virus shows signs of genetic modifications that likely interact with host factors in causing different patterns of neuroinvasiveness and neurovirulence.

Several areas warrant research focus over the next few years. More efficient diagnostic assays will help with both clinical diagnosis and disease surveillance. Improved knowledge about the pathogenesis and natural history of WNV disease is crucial to developing effective treatment, and promising therapies need to be carefully evaluated in controlled clinical trials. Given the focal distribution of WNV outbreaks, and the uncertain distribution of future cases of WNV disease, prospective clinical studies need to be designed with the flexibility to gather information from widely dispersed and changing locations.

The development of a safe and effective vaccine for humans is a clear priority for prevention, and the public health strategies and recommendations for vaccination deserve careful thought. Given the relatively low incidence of WNV neuroinvasive disease and the focal occurrence of WNV epidemics thus far, vaccination will likely require targeting to higher risk groups to approach the cost-effectiveness of many recommended public health prevention strategies. His current research is focused on the epidemiology of arboviral and other vectorborne infectious diseases.

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Section Navigation. Facebook Twitter LinkedIn Syndicate. Article Metrics. Related Articles. Abstract West Nile virus WNV causes epidemics of febrile illness, meningitis, encephalitis, and flaccid paralysis.

Characteristics of West Nile Virus. See the New York State weekly arboviral surveillance report. Most people are infected in summer to early fall. While chances of anyone becoming seriously ill are small, people over 50 years of age are at the highest risk for severe illness.

WNV is usually spread through the bite of an infected mosquito. While there are about 70 different species of mosquitoes in New York State, only certain species have been associated with WNV. It is not spread from person to person through casual contact or from handling dead infected birds, although gloves should always be worn when handling any dead animal.

In a small number of cases, WNV has been spread by blood transfusion, which has resulted in the screening of blood donations for the virus in the US, or by organ transplantation. WNV can also be spread from mother to baby during pregnancy, delivery, or breast-feeding in a small number of cases. Pregnant women should consult their health care provider for more information. These symptoms typically last a few days - but may last several weeks. The symptoms of severe infection West Nile encephalitis or meningitis can include headache, high fever, neck stiffness, muscle weakness, stupor, disorientation, tremors, seizures, paralysis, and coma.

WNV can cause serious illness, and in some cases, death. Usually, symptoms occur from 3 to 14 days after being bitten by an infected mosquito. There is no specific treatment for viral infections, other than to treat the symptoms and provide supportive care. Individuals with concern should consult their health care provider for more information. Health care providers diagnose WNV based on the patient's clinical symptoms and laboratory diagnosis by testing blood or spinal fluids, which will show if the virus or antibodies against the virus are present in the person.

There is no specific treatment for WNV. Health care providers will usually attempt to relieve the symptoms of the illness. In severe cases, patients may need to be hospitalized and closely monitored. Currently there is no West Nile virus vaccine available for humans. It is likely that people with past infection of West Nile virus will be protected from getting the disease again. Pets occasionally get WNV from mosquito bites, but very rarely get sick.

Horses are more susceptible to serious illness from WNV than are dogs and cats; however, a vaccine is available for horses. Hall, Academic Editor.

Author information Article notes Copyright and License information Disclaimer. Received Mar 22; Accepted Jun Associated Data Supplementary Materials virusess Abstract West Nile virus disease WND is an arthropod-borne zoonosis responsible for nonspecific fever or severe encephalitis. Keywords: Japanese encephalitis virus, West Nile virus, chimera. Introduction West Nile virus disease is a wide-spread arboviral zoonosis. Materials and Methods 2.

Open in a separate window. Figure 1. Table 1 Primer sequences. Statistical Analysis Statistical analyses of growth curves, neutralizing antibody titer, and survival curves were drawn by the GraphPad Prism software, version 6. Results 3. Figure 2. Figure 3. Figure 4. Virus Distributions in Mice In order to detect virus proliferation in the blood and viscera, three mice in each group were identified for measurement of the viral titers in the plasmas, brains, livers, spleens, lungs, and kidneys by plaque assays on day 1,3, 5, 7, and 9, respectively.

Figure 5. Figure 6. Click here for additional data file. Author Contributions X. Institutional Review Board Statement All animal experiments were performed strictly in accordance with the welfare and ethical guidance on Chinese laboratory animals GB Informed Consent Statement Not applicable.

Conflicts of Interest The authors declare no conflict of interest. References 1. Gould E. Pathogenic flaviviruses. Smithburn K. Lanciotti R. Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States. Knipe D. Fields Virology. Kaiser J. Monath T. A live, attenuated recombinant West Nile virus vaccine.

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