West Nile virus

Abstract

West Nile virus (WNV) is responsible for thousands of cases of morbidity and mortality in birds, horses, and humans. Epidemics were localized to Europe, Africa, the Middle East, and parts of Asia, and primarily caused a mild febrile illness in humans. In the late 1990s, the virus became more virulent and spread to North America. In humans, the clinical presentation ranges from asymptomatic, seen frequently, to encephalitis/paralysis and death, seen rarely. There is no FDA (Food and Drug Administration)-licensed vaccine for human use, and the only recommended treatment is supportive care. Often, there is a long recovery period. This article reviews the current literature summarizing the molecular virology, epidemiology, clinical manifestations, pathogenesis, diagnosis, treatment, immunology, and protective measures against WNV and WNV infections in humans.

Figure 1. Schematic of WNV genome

A representation of the WNV genome including the 3 structural proteins that make up virion particle and the 7 non-structural proteins necessary for virus replication and immune evasion.

Figure 2. Scanned images are of West Nile virus isolated from brain tissue from an infected crow

The tissue was cultured in a Vero cell for a 3-day incubation period. The Vero cells were fixed in glutaraldehyde, dehyrated, placed in an Epon resin, thin sectioned, placed on a copper grid, and stained with uranyl acetate and lead citrate. The grids were then placed in the electron microscope and viewed. Total magnifications, image 65,625x. Image courtesy of CDC (Bruce Cropp, Microbiologist, Division of Vector-Borne Infectious Diseases).

Figure 3. Diagram of the WNV transmission cycle

The maintenance of WNV in nature depends upon many avian and mosquito species. Humans and other incidental hosts (like horses) become infected when WNV-infected mosquito takes a bloodmeal from them.

Figure 4. Culex mosquito

The Culex species of mosquito is the most common vector of WNV. Photograph of Culex species mosquito feeding. Courtesy of USGS.

Figure 5. Distribution of WNV

Countries with historic or recent (2007-present) WNV activity (isolations from mosquitoes, birds, horses or humans) are highlighted in red and blue, respectively.

Figure 6

The number of confirmed human cases of WNV disease in the United States in 2008. Courtesy of CDC.

Figure 7. Radiographic and neuropathologic findings in West Nile virus encephalitis

(A) Coronal fluid-attenuated inversion recovery (FLAIR) magnetic resonance image shows an area of abnormally increased signal in the thalami, substantia nigra (extending superiorly toward the subthalamic nuclei) and white matter. (B) Corresponding tissue section from the same patient at autopsy 15 days later, stained with Luxol fast blue–periodic acid Schiff for myelin, shows numerous ovoid foci of necrosis and pallor throughout the thalamus and subthalamic nucleus (arrows). (C) Axial proton density image at the level of the midbrain shows a bilaterally increased signal in the substantia nigra (arrows). (D) Corresponding tissue section at autopsy, stained with Luxol fast blue–periodic acid Schiff, illustrates multifocal involvement of the substantia nigra (arrows), with nearly 50% of the area destroyed; the red nuclei are clearly affected. (E) Axial FLAIR image at the level of the lateral ventricle bodies shows a bilaterally increased signal within the white matter. A scan performed approximately 5 months earlier demonstrated an abnormal signal in the left periventricular white matter. This signal increased once West Nile virus encephalitis developed, and the lesions in the right cerebral white matter (left side of photograph) were new. (F) Photomicrograph taken from the right periventricular white matter, immunostained with the HAM56 antibody, shows numerous macrophages, both in perivascular areas (lower right) and diffusely throughout the white matter (center). Permission: Kleinschmidt-DeMaster BK et al. (2004). Arch Neurology 61: 1210-1220.