The pathology of human West Nile virus infection

Sampson, Barbara A.; Ambrosi, Corinne; Charlot, Aglae; Reiber, Kaki; Veress, Joseph F.; Armbrustmacher, Vernon W.

doi:10.1053/hp.2000.8047

Cited by 209 publications

(152 citation statements)

References 11 publications

Supporting

Mentioning

140

Contrasting

Unclassified

Order By: Relevance

“…1 Humans can become infected when bitten by a mosquito and the infection can result in the development of fatal encephalitis. 2 Since an outbreak of WN encephalitis in humans and horses in New York City in 1999, WN virus has spread throughout North America very rapidly. 3 In European Russia, WN virus was first isolated from humans and ticks in 1963.…”

Section: Introductionmentioning

confidence: 99%

Seroprevalence of West Nile Virus in Wild Birds in Far Eastern Russia Using a Focus Reduction Neutralization Test

Murata

Hashiguchi²,

Yoshii³

et al. 2011

The American Society of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. West Nile (WN) virus has been spreading geographically to non-endemic areas in various parts of the world. However, little is known about the extent of WN virus infection in Russia. Japanese encephalitis (JE) virus, which is closely related to WN virus, is prevalent throughout East Asia. We evaluated the effectiveness of a focus reduction neutralization test in young chicks inoculated with JE and WN viruses, and conducted a survey of WN infection among wild birds in Far Eastern Russia. Following single virus infection, only neutralizing antibodies specific to the homologous virus were detected in chicks. The neutralization test was then applied to serum samples from 145 wild birds for WN and JE virus. Twenty-one samples were positive for neutralizing antibodies to WN. These results suggest that WN virus is prevalent among wild birds in the Far Eastern region of Russia.

show abstract

Section: Introductionmentioning

confidence: 99%

Seroprevalence of West Nile Virus in Wild Birds in Far Eastern Russia Using a Focus Reduction Neutralization Test

Murata

Hashiguchi²,

Yoshii³

et al. 2011

The American Society of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

show abstract

“…In Israel and the United States, where the Isr98͞NY99 variant of WN virus was frequently isolated during recent outbreaks, approximately 20% of infected persons developed febrile illness, with a high rate of mortality among patients with neurological symptoms (2,3). This result suggests that susceptibility and sensitivity to WN virus infections might depend, at least in part, on host genetic factors (4).…”

mentioning

confidence: 99%

A nonsense mutation in the gene encoding 2′-5′-oligoadenylate synthetase/L1 isoform is associated with West Nile virus susceptibility in laboratory mice

Mashimo

Lucas²,

Simon-Chazottes³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

256

215

View full text Add to dashboard Cite

A mouse model has been established to investigate the genetic determinism of host susceptibility to West Nile (WN) virus, a member of the genus flavivirus and family Flaviviridae. Whereas WN virus causes encephalitis and death in most laboratory inbred mouse strains after peripheral inoculation, most strains derived from recently trapped wild mice are completely resistant. The phenotype of resistance͞susceptibility is determined by a major locus, Wnv, mapping to chromosome 5 within the 0.4-cM-wide interval defined by markers D5Mit408 and D5Mit242. We constructed a high resolution composite͞consensus map of the interval by merging the data from the mouse T31 Radiation Hybrid map and those from the homologous region of human chromosome 12q, and found the cluster of genes encoding 2 -5 -oligoadenylate synthetases (2 -5 -OAS) to be the most prominent candidate. This cluster encodes a multimember family of IFN-inducible proteins that is known to play an important role in the established endogenous antiviral pathway. Comparing the cDNA sequences of 2 -5 -OAS L1, L2, and L3 isoforms, between susceptible and resistant strains, we identified a STOP codon in exon 4 of the gene encoding the L1 isoform in susceptible strains that can lead to a truncated form with amputation of one domain, whereas all resistant mice tested so far have a normal copy of this gene. The observation that WN virus sensitivity of susceptible mice was completely correlated with the occurrence of a point mutation in 2 -5 -OAS L1 suggests that this isoform may play a critical role in WN pathogenesis.F lavivirus is a genus of the Flaviviridae family that comprises over 70 positive-sense, single-stranded, and enveloped RNA viruses, most of which are arthropod-borne (1). Mosquito-borne flaviviruses such as dengue (DEN), Japanese encephalitis (JE), yellow fever (YF), and West Nile (WN) viruses can cause epidemic outbreaks in humans, and patients infected may exhibit a wide range of acute diseases, from nonspecific febrile illness to severe hemorrhagic manifestations (DEN and YF) or encephalitic syndromes (JE and WN), sometimes associated with a high (up to 50%) fatality rate. The reasons why flaviviruses cause clinical manifestations only in a small percentage of infected individuals have not yet been clearly elucidated but are supposed to involve host-dependent genetic factors.Over the past 5 years, WN fever has been an emerging concern for public health in Europe, in the Middle East, and more recently in the United States. In Israel and the United States, where the Isr98͞NY99 variant of WN virus was frequently isolated during recent outbreaks, approximately 20% of infected persons developed febrile illness, with a high rate of mortality among patients with neurological symptoms (2, 3). This result suggests that susceptibility and sensitivity to WN virus infections might depend, at least in part, on host genetic factors (4). In the present study we investigated the influence of the host genetic constitution on the severity of WN virus infection, by using...

show abstract

“…12,16,17 In fatal cases, the most common inflammatory focus is brainstem, but thalamus, cerebellum, and cerebral cortex are also involved. 18 In contrast to other arboviral infections, the inflammatory infiltrate is minimal and there is no vasculitis. 16 Until recently, autopsies of fatal cases have not included sectioning of spinal cord, and neuropathology of this portion of the central nervous system had been lacking.…”

Section: Viral Epidemiologymentioning

confidence: 99%

West Nile Virus Infection and its Neurological Manifestations

Madden

2003

Clinical Medicine & Research

View full text Add to dashboard Cite

The West Nile virus caused an epidemic of meningoencephalitis in Midwest North America during 2002. The peak incidence coincided with the highest activity period of mosquito vectors in affected states. This epidemic followed recent established trends, not only of increased central nervous system involvement by the virus, but also increased incidence of dramatic neuromuscular impairment. Two cases are presented which illustrate the most concerning types of neuromuscular sequelae, diffuse weakness leading to respiratory insufficiency, and the development of focal weakness similar to poliomyelitis. The epidemiology and clinical characteristics of West Nile virus infection are also reviewed. Concern is expressed regarding the possibility of epidemics in other Midwestern states during future seasons of increased mosquito activity.

show abstract

The pathology of human West Nile virus infection

Cited by 209 publications

References 11 publications

Seroprevalence of West Nile Virus in Wild Birds in Far Eastern Russia Using a Focus Reduction Neutralization Test

Seroprevalence of West Nile Virus in Wild Birds in Far Eastern Russia Using a Focus Reduction Neutralization Test

A nonsense mutation in the gene encoding 2′-5′-oligoadenylate synthetase/L1 isoform is associated with West Nile virus susceptibility in laboratory mice

West Nile Virus Infection and its Neurological Manifestations

Contact Info

Product

Resources

About