West Nile Virus ‐ Where did It Come from and Where Might It Go?

Bl, Johnston; Conly, JM

doi:10.1155/2000/856598

Cited by 20 publications

(16 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A still unsettled question is how the virus was brought into the US [44]. The primary mechanism by which dengue and Zika viruses spread around the world is the long-distance travel of infected humans (e.g., [16,45]).…”

Section: Emergence Of An Exotic Virusmentioning

confidence: 99%

Twenty years of West Nile virus spread and evolution in the Americas visualized by Nextstrain

et al. 2019

View full text Add to dashboard Cite

It has been 20 years since West Nile virus first emerged in the Americas, and since then, little progress has been made to control outbreaks caused by this virus. After its first detection in New York in 1999, West Nile virus quickly spread across the continent, causing an epidemic of human disease and massive bird die-offs. Now the virus has become endemic to the United States, where an estimated 7 million human infections have occurred, making it the leading mosquito-borne virus infection and the most common cause of viral encephalitis in the country. To bring new attention to one of the most important mosquito-borne viruses in the Americas, we provide an interactive review using Nextstrain: a visualization tool for real-time tracking of pathogen evolution (nextstrain.org/WNV/NA). Nextstrain utilizes a growing database of more than 2,000 West Nile virus genomes and harnesses the power of phylogenetics for students, educators, public health workers, and researchers to visualize key aspects of virus spread and evolution. Using Nextstrain, we use virus genomics to investigate the emergence of West Nile virus in the U S, followed by its rapid spread, evolution in a new environment, establishment of endemic transmission, and subsequent international spread. For each figure, we include a link to Nextstrain to allow the readers to directly interact with and explore the underlying data in new ways. We also provide a brief online narrative that parallels this review to further explain the data and highlight key epidemiological and evolutionary features (nextstrain.org/narratives/twenty-years-of-WNV). Mirroring the dynamic nature of outbreaks, the Nextstrain links provided within this paper are constantly updated as new West Nile virus genomes are shared publicly, helping to stay current with the research. Overall, our review showcases how genomics can track West Nile virus spread and evolution, as well as potentially uncover novel targeted control measures to help alleviate its public health burden.

show abstract

Section: Emergence Of An Exotic Virusmentioning

confidence: 99%

Twenty years of West Nile virus spread and evolution in the Americas visualized by Nextstrain

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Langerhans cells immigrate to the local lymph nodes, where the WNV cycle in the blood stream begins causing primary viremia, 14 which is followed by the secondary viremia after its distribution in peripheral tissues like spleen and kidney. 15 The WNV can be detected in the blood one or two days post-infection, while it could largely disappear by the seventh day after inoculation, accompanied with the appearance of IgM (Immunoglobulin M) neutralizing antibodies.…”

Section: Pathogenesismentioning

confidence: 99%

Development and Characterization of New Peptidomimetic Inhibitors of the West Nile Virus NS2B–NS3 Protease

et al. 2013

View full text Add to dashboard Cite

A series of new substrate analogue inhibitors of the WNV NS2B–NS3 protease containing decarboxylated arginine mimetics at the P1 position was developed. Among the various analogues, trans‐(4‐guanidino)cyclohexylmethylamide (GCMA) was identified as the most suitable P1 residue. In combination with dichloro‐substituted phenylacetyl groups at the P4 position, three inhibitors with inhibition constants of <0.2 μM were obtained. These GCMA inhibitors have a better selectivity profile than the previously described agmatine analogues, and possess negligible affinity for the trypsin‐like serine proteases thrombin, factor Xa, and matriptase. A crystal structure in complex with the WNV protease was determined for one of the most potent inhibitors, 3,4‐dichlorophenylacetyl‐Lys‐Lys‐GCMA (Ki=0.13 μM). The inhibitor adopts a horseshoe‐like conformation, most likely due to a hydrophobic contact between the P4 phenyl ring and the P1 cyclohexyl group, which is further stabilized by an intramolecular hydrogen bond between the P1 guanidino group and the P4 carbonyl oxygen atom. These inhibitors are stable, readily accessible, and have a noncovalent binding mode. Therefore, they may serve as suitable lead structures for further development.

show abstract

“…An introduction of WSLV into an immunologically naive population, particularly during the breeding season, could however result in rapid dissemination and unprecedented disease manifestation. Such "virgin soil" arbovirus outbreaks tend to be severe, as previously exemplified by the Bluetongue and Schmallenberg outbreaks in Europe and the West Nile virus (WNV) and ZIKV outbreaks in the Americas [21][22][23][24]. It is therefore important to further assess WSLV virulence for animals and humans and its ability to be disseminated by mosquito vectors indigenous to currently unaffected areas.…”

Section: Discussionmentioning

confidence: 99%

Early Pathogenesis of Wesselsbron Disease in Pregnant Ewes

et al. 2020

View full text Add to dashboard Cite

Wesselsbron virus (WSLV) is a neglected, mosquito-borne flavivirus that is endemic to the African continent. The virus is teratogenic to ruminants and causes a self-limiting febrile illness in humans. Wesselsbron disease manifests with similar clinical signs and occurs in the same areas under the same climatic conditions as Rift Valley fever, which is therefore included in the differential diagnosis. Although the gross pathology of WSLV infection in pregnant ewes is reported in literature, the pathogenesis that leads to stillbirths, congenital malformations and abortion has remained undescribed. In the present study, pregnant ewes were inoculated with WSLV and subjected to detailed clinical- and histopathology 8 days later. The virus was mainly detected in foetal trophoblasts of the placenta and in neural progenitor cells, differentiated neurons, oligodendrocytes, microglia and astrocytes. Our study demonstrates that WSLV efficiently crosses the maternal–foetal interface and is highly neuroinvasive in the ovine foetus.

show abstract

West Nile Virus ‐ Where did It Come from and Where Might It Go?

Cited by 20 publications

References 23 publications

Twenty years of West Nile virus spread and evolution in the Americas visualized by Nextstrain

Twenty years of West Nile virus spread and evolution in the Americas visualized by Nextstrain

Development and Characterization of New Peptidomimetic Inhibitors of the West Nile Virus NS2B–NS3 Protease

Early Pathogenesis of Wesselsbron Disease in Pregnant Ewes

Contact Info

Product

Resources

About