scholarly journals First Detection of the West Nile Virus Koutango Lineage in Sandflies in Niger

Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 257
Author(s):  
Gamou Fall ◽  
Diawo Diallo ◽  
Hadiza Soumaila ◽  
El Hadji Ndiaye ◽  
Adamou Lagare ◽  
...  
Keyword(s):  
West Nile Virus ◽  
West Nile ◽  
Biting Midges ◽  
Valley Fever ◽  
Genetic Traits ◽  
Replication Studies ◽  
High Virulence ◽  
In The Wild ◽  
Great Genetic Diversity

West Nile virus (WNV), belonging to the Flaviviridae family, causes a mosquito-borne disease and shows great genetic diversity, with at least eight different lineages. The Koutango lineage of WNV (WN-KOUTV), mostly associated with ticks and rodents in the wild, is exclusively present in Africa and shows evidence of infection in humans and high virulence in mice. In 2016, in a context of Rift Valley fever (RVF) outbreak in Niger, mosquitoes, biting midges and sandflies were collected for arbovirus isolation using cell culture, immunofluorescence and RT-PCR assays. Whole genome sequencing and in vivo replication studies using mice were later conducted on positive samples. The WN-KOUTV strain was detected in a sandfly pool. The sequence analyses and replication studies confirmed that this strain belonged to the WN-KOUTV lineage and caused 100% mortality of mice. Further studies should be done to assess what genetic traits of WN-KOUTV influence this very high virulence in mice. In addition, given the risk of WN-KOUTV to infect humans, the possibility of multiple vectors as well as birds as reservoirs of WNV, to spread the virus beyond Africa, and the increasing threats of flavivirus infections in the world, it is important to understand the potential of WN-KOUTV to emerge.

scholarly journals The recently identified flavivirus Bamaga virus is transmitted horizontally by Culex mosquitoes and interferes with West Nile virus replication in vitro and transmission in vivo

2018 ◽  
Vol 12 (10) ◽  
pp. e0006886 ◽  
Author(s):  
Agathe M. G. Colmant ◽  
Sonja Hall-Mendelin ◽  
Scott A. Ritchie ◽  
Helle Bielefeldt-Ohmann ◽  
Jessica J. Harrison ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Virus Replication ◽  
West Nile ◽  
Culex Mosquitoes

scholarly journals Human Monoclonal Fab Antibodies Against West Nile Virus and its Neutralizing Activity Analyzed in Vitro and in Vivo

2009 ◽  
Vol 01 (01) ◽  
pp. 036-042 ◽  
Author(s):  
Tao Duan ◽  
Monique Ferguson ◽  
Lintian Yuan ◽  
Fangling Xu ◽  
Guangyu Li
Keyword(s):  
West Nile Virus ◽  
West Nile ◽  
Neutralizing Activity

scholarly journals Insecticide resistance genes affect Culex quinquefasciatus vector competence for West Nile virus

2019 ◽  
Vol 286 (1894) ◽  
pp. 20182273 ◽  
Author(s):  
Célestine M. Atyame ◽  
Haoues Alout ◽  
Laurence Mousson ◽  
Marie Vazeille ◽  
Mawlouth Diallo ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Insecticide Resistance ◽  
Culex Quinquefasciatus ◽  
Rift Valley Fever Virus ◽  
Vector Competence ◽  
Resistance Mechanisms ◽  
Transmission Efficiency ◽  
West Nile ◽  
Valley Fever ◽  
Resistant Lines

Insecticide resistance has been reported to impact the interactions between mosquitoes and the pathogens they transmit. However, the effect on vector competence for arboviruses still remained to be investigated. We examined the influence of two insecticide resistance mechanisms on vector competence of the mosquito Culex quinquefasciatus for two arboviruses, Rift Valley Fever virus (RVFV) and West Nile virus (WNV). Three Cx. quinquefasciatus lines sharing a common genetic background were used: two insecticide-resistant lines, one homozygous for amplification of the Ester 2 locus (SA2), the other homozygous for the acetylcholinesterase ace-1 G119S mutation (SR) and the insecticide-susceptible reference line Slab. Statistical analyses revealed no significant effect of insecticide-resistant mechanisms on vector competence for RVFV. However, both insecticide resistance mechanisms significantly influenced the outcome of WNV infections by increasing the dissemination of WNV in the mosquito body, therefore leading to an increase in transmission efficiency by resistant mosquitoes. These results showed that insecticide resistance mechanisms enhanced vector competence for WNV and may have a significant impact on transmission dynamics of arboviruses. Our findings highlight the importance of understanding the impacts of insecticide resistance on the vectorial capacity parameters to assess the overall consequence on transmission.

scholarly journals A Molecular Determinant of West Nile Virus Secretion and Morphology as a Target for Viral Attenuation

2020 ◽  
Vol 94 (12) ◽  
Author(s):  
Justine Basset ◽  
Julien Burlaud-Gaillard ◽  
Maxence Feher ◽  
Philippe Roingeard ◽  
Félix A. Rey ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Rational Design ◽  
Surface Membrane ◽  
Public Health Problem ◽  
M Protein ◽  
Membrane Glycoprotein ◽  
Wild Type ◽  
West Nile ◽  
Viral Attenuation

ABSTRACT West Nile virus (WNV), a member of the Flavivirus genus and currently one of the most common arboviruses worldwide, is associated with severe neurological disease in humans. Its high potential to reemerge and rapidly disseminate makes it a bona fide global public health problem. The surface membrane glycoprotein (M) has been associated with Flavivirus-induced pathogenesis. Here, we identified a key amino acid residue at position 36 of the M protein whose mutation impacts WNV secretion and promotes viral attenuation. We also identified a compensatory site at position M-43 whose mutation stabilizes M-36 substitution both in vitro and in vivo. Moreover, we found that introduction of the two mutations together confers a full attenuation phenotype and protection against wild-type WNV lethal challenge, eliciting potent neutralizing-antibody production in mice. Our study thus establishes the M protein as a new viral target for rational design of attenuated WNV strains. IMPORTANCE West Nile virus (WNV) is a worldwide (re)emerging mosquito-transmitted Flavivirus causing fatal neurological diseases in humans. However, no human vaccine has been yet approved. One of the most effective live-attenuated vaccines was empirically obtained by serial passaging of wild-type yellow fever Flavivirus. However, such an approach is not acceptable nowadays, and the development of a rationally designed vaccine is necessary. Generating molecular infectious clones and mutating specific residues known to be involved in Flavivirus virulence constitute a powerful tool to promote viral attenuation. WNV membrane glycoprotein is thought to carry such essential determinants. Here, we identified two residues of this protein whose substitutions are key to the full and stable attenuation of WNV in vivo, most likely through inhibition of secretion and possible alteration of morphology. Applied to other flaviviruses, this approach should help in designing new vaccines against these viruses, which are an increasing threat to global human health.

scholarly journals Mutations in West Nile virus nonstructural proteins that facilitate replicon persistence in vitro attenuate virus replication in vitro and in vivo

Virology ◽  
2007 ◽  
Vol 364 (1) ◽  
pp. 184-195 ◽  
Author(s):  
Shannan L. Rossi ◽  
Rafik Fayzulin ◽  
Nathan Dewsbury ◽  
Nigel Bourne ◽  
Peter W. Mason
Keyword(s):  
West Nile Virus ◽  
Virus Replication ◽  
Nonstructural Proteins ◽  
West Nile

scholarly journals Rift Valley fever virus lacking NSm proteins retains high virulence in vivo and may provide a model of human delayed onset neurologic disease

Virology ◽  
2007 ◽  
Vol 362 (1) ◽  
pp. 10-15 ◽  
Author(s):  
Brian H. Bird ◽  
César G. Albariño ◽  
Stuart T. Nichol
Keyword(s):  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Neurologic Disease ◽  
Valley Fever ◽  
Delayed Onset ◽  
High Virulence

scholarly journals Point mutations in the West Nile virus (Flaviviridae; Flavivirus) RNA-dependent RNA polymerase alter viral fitness in a host-dependent manner in vitro and in vivo

Virology ◽  
2012 ◽  
Vol 427 (1) ◽  
pp. 18-24 ◽  
Author(s):  
Greta A. Van Slyke ◽  
Alexander T. Ciota ◽  
Graham G. Willsey ◽  
Joachim Jaeger ◽  
Pei-Yong Shi ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Rna Polymerase ◽  
Point Mutations ◽  
Viral Fitness ◽  
Dependent Manner ◽  
The West ◽  
Rna Dependent Rna Polymerase ◽  
West Nile

scholarly journals Interferon Regulatory Factor IRF-7 Induces the Antiviral Alpha Interferon Response and Protects against Lethal West Nile Virus Infection

2008 ◽  
Vol 82 (17) ◽  
pp. 8465-8475 ◽  
Author(s):  
Stephane Daffis ◽  
Melanie A. Samuel ◽  
Mehul S. Suthar ◽  
Brian C. Keller ◽  
Michael Gale ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Cortical Neurons ◽  
Interferon Regulatory Factor ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn ◽  
Regulatory Factor ◽  
West Nile

ABSTRACT Type I interferon (IFN-α/β) comprises a family of immunomodulatory cytokines that are critical for controlling viral infections. In cell culture, many RNA viruses trigger IFN responses through the binding of RNA recognition molecules (RIG-I, MDA5, and TLR-3) and induction of interferon regulatory factor IRF-3-dependent gene transcription. Recent studies with West Nile virus (WNV) have shown that type I IFN is essential for restricting infection and that a deficiency of IRF-3 results in enhanced lethality. However, IRF-3 was not required for optimal systemic IFN production in vivo or in vitro in macrophages. To begin to define the transcriptional factors that regulate type I IFN after WNV infection, we evaluated IFN induction and virus control in IRF-7−/− mice. Compared to congenic wild-type mice, IRF-7−/− mice showed increased lethality after WNV infection and developed early and elevated WNV burdens in both peripheral and central nervous system tissues. As a correlate, a deficiency of IRF-7 blunted the systemic type I IFN response in mice. Consistent with this, IFN-α gene expression and protein production were reduced and viral titers were increased in IRF-7−/− primary macrophages, fibroblasts, dendritic cells, and cortical neurons. In contrast, in these cells the IFN-β response remained largely intact. Our data suggest that the early protective IFN-α response against WNV occurs through an IRF-7-dependent transcriptional signal.

scholarly journals Early Production of Type I Interferon during West Nile Virus Infection: Role for Lymphoid Tissues in IRF3-Independent Interferon Production

2007 ◽  
Vol 81 (17) ◽  
pp. 9100-9108 ◽  
Author(s):  
Nigel Bourne ◽  
Frank Scholle ◽  
Maria Carlan Silva ◽  
Shannan L. Rossi ◽  
Nathan Dewsbury ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Type I Interferon ◽  
High Titer ◽  
West Nile Virus Infection ◽  
Lymphoid Tissues ◽  
Genome Replication ◽  
Type I ◽  
West Nile

ABSTRACT Infection of cells with flaviviruses in vitro is reduced by pretreatment with small amounts of type I interferon (IFN-α/β). Similarly, pretreatment of animals with IFN and experiments using mice defective in IFN signaling have indicated a role for IFN in controlling flavivirus disease in vivo. These data, along with findings that flavivirus-infected cells block IFN signaling, suggest that flavivirus infection can trigger an IFN response. To investigate IFN gene induction by the very first cells infected during in vivo infection with the flavivirus West Nile virus (WNV), we infected mice with high-titer preparations of WNV virus-like particles (VLPs), which initiate viral genome replication in cells but fail to spread. These studies demonstrated a brisk production of IFN in vivo, with peak levels of over 1,000 units/ml detected in sera between 8 and 24 h after inoculation by either the intraperitoneal or footpad route. The IFN response was dependent on genome replication, and WNV genomes and WNV antigen-positive cells were readily detected in the popliteal lymph nodes (pLN) of VLP-inoculated mice. High levels of IFN mRNA transcripts and functional IFN were also produced in VLP-inoculated IFN regulatory factor 3 null (IRF3−/−) mice, indicating that IFN production was independent of the IRF3 pathways to IFN gene transcription, consistent with the IFN type produced (predominantly α).

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