Interventions Against West Nile Virus, Rift Valley Fever Virus, and Crimean-Congo Hemorrhagic Fever Virus: Where Are We?

2010 ◽  
Vol 10 (7) ◽  
pp. 709-718 ◽  
Author(s):  
Jeroen Kortekaas ◽  
Önder Ergönül ◽  
Rob J.M. Moormann
Keyword(s):  
West Nile Virus ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
West Nile ◽  
Valley Fever ◽  
Crimean Congo Hemorrhagic Fever ◽  
Hemorrhagic Fever Virus

scholarly journals Detection of the Northeastern African Rift Valley Fever Virus Lineage During the 2015 Outbreak in Mauritania

2017 ◽  
Vol 4 (2) ◽  
Author(s):  
Ndeye Sakha Bob ◽  
Hampâté Bâ ◽  
Gamou Fall ◽  
Elkhalil Ishagh ◽  
Mamadou Y. Diallo ◽  
...  
Keyword(s):  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Hemorrhagic Fever ◽  
Enzyme Linked Immunosorbent Assay ◽  
Rt Pcr ◽  
West Nile ◽  
Valley Fever ◽  
Blood Samples ◽  
Crimean Congo Hemorrhagic Fever

Abstract Background Rift Valley fever (RVF) is an acute viral anthropozoonosis that causes epizootics and epidemics among livestock population and humans. Multiple emergences and reemergences of the virus have occurred in Mauritania over the last decade. This article describes the outbreak that occurred in 2015 in Mauritania and reports the results of serological and molecular investigations of blood samples collected from suspected RVF patients. Methods An RVF outbreak was reported from 14 September to 26 November 2015 in Mauritania. Overall, 184 suspected cases from different localities were identified by 26 health facilities. Blood samples were collected and tested by enzyme-linked immunosorbent assay (ELISA) and real-time reverse-transcription polymerase chain reaction (RT-PCR) at the Institut Pasteur de Dakar (IPD). Sequencing of partial genomes and phylogenetic analyses were performed on RT-PCR–positive samples. As part of routine surveillance at IPD, samples were also screened for dengue, yellow fever, West Nile, Crimean Congo hemorrhagic fever, Zika, and Chikungunya viruses by ELISA and RT-PCR. Results Of the 184 suspected cases, there were 57 confirmed cases and 12 deaths. Phylogenetic analysis of the sequences indicated an emergence of a virus that originated from Northeastern Africa. Our results show co-circulation of other arboviruses in Mauritania—dengue, Crimean Congo hemorrhagic fever, and West Nile viruses. Conclusion The Northeastern Africa lineage of RVF was responsible for the outbreak in Mauritania in 2015. Co-circulation of multiples arboviruses was detected. This calls for systematic differential diagnosis and highlights the need to strengthen arbovirus surveillance in Africa.

scholarly journals First Serological Evidence of Crimean-Congo Hemorrhagic Fever Virus and Rift Valley Fever Virus in Ruminants in Tunisia

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 769
Author(s):  
Khaoula Zouaghi ◽  
Ali Bouattour ◽  
Hajer Aounallah ◽  
Rebecca Surtees ◽  
Eva Krause ◽  
...  
Keyword(s):  
Risk Factors ◽  
Potential Risk ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Valley Fever ◽  
Hemorrhagic Fever Virus ◽  
Potential Risk Factors

Crimean-Congo hemorrhagic fever virus (CCHFV, Nairoviridae family) and Rift Valley fever virus (RVFV, Phenuiviridae family) are zoonotic vector-borne pathogens with clinical relevance worldwide. Our study aimed to determine seroprevalences of these viruses and potential risk factors among livestock (cattle, sheep, and goats) in Tunisia. Sera were tested for antibodies against CCHFV (n = 879) and RVFV (n = 699) using various enzyme-linked immunosorbent assays (ELISAs) and indirect immunofluorescence assays (IIFA). The overall seroprevalence of IgG antibodies was 8.6% (76/879) and 2.3% (16/699) against CCHFV and RVFV, respectively. For CCHF seropositivity bioclimatic zones and breed were potential risk factors for the three tested animal species; while the season was associated with cattle and sheep seropositivity, tick infestation was associated with cattle and goats seropositivity and age as a risk factor was only associated with cattle seropositivity. Age and season were significantly associated with RVFV seropositivity in sheep. Our results confirm the circulation of CCHFV and RVFV in Tunisia and identified the principal risk factors in ruminants. This knowledge could help to mitigate the risk of ruminant infections and subsequently also human infections.

scholarly journals Experimental transmission of West Nile Virus and Rift Valley Fever Virus by Culex pipiens from Lebanon

2018 ◽  
Vol 12 (1) ◽  
pp. e0005983 ◽  
Author(s):  
Renée Zakhia ◽  
Laurence Mousson ◽  
Marie Vazeille ◽  
Nabil Haddad ◽  
Anna-Bella Failloux
Keyword(s):  
West Nile Virus ◽  
Rift Valley ◽  
Culex Pipiens ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
West Nile ◽  
Valley Fever ◽  
Experimental Transmission

scholarly journals A ΩXaV motif in the Rift Valley fever virus NSs protein is essential for degrading p62, forming nuclear filaments and virulence

2015 ◽  
Vol 112 (19) ◽  
pp. 6021-6026 ◽  
Author(s):  
Normand Cyr ◽  
Cynthia de la Fuente ◽  
Lauriane Lecoq ◽  
Irene Guendel ◽  
Philippe R. Chabot ◽  
...  
Keyword(s):  
Rift Valley ◽  
Rift Valley Fever ◽  
Excision Repair ◽  
Rna Virus ◽  
Nonstructural Protein ◽  
Rift Valley Fever Virus ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Valley Fever ◽  
Infected Cells

Rift Valley fever virus (RVFV) is a single-stranded RNA virus capable of inducing fatal hemorrhagic fever in humans. A key component of RVFV virulence is its ability to form nuclear filaments through interactions between the viral nonstructural protein NSs and the host general transcription factor TFIIH. Here, we identify an interaction between a ΩXaV motif in NSs and the p62 subunit of TFIIH. This motif in NSs is similar to ΩXaV motifs found in nucleotide excision repair (NER) factors and transcription factors known to interact with p62. Structural and biophysical studies demonstrate that NSs binds to p62 in a similar manner as these other factors. Functional studies in RVFV-infected cells show that the ΩXaV motif is required for both nuclear filament formation and degradation of p62. Consistent with the fact that the RVFV can be distinguished from otherBunyaviridae-family viruses due to its ability to form nuclear filaments in infected cells, the motif is absent in the NSs proteins of otherBunyaviridae-family viruses. Taken together, our studies demonstrate that p62 binding to NSs through the ΩXaV motif is essential for degrading p62, forming nuclear filaments and enhancing RVFV virulence. In addition, these results show how the RVFV incorporates a simple motif into the NSs protein that enables it to functionally mimic host cell proteins that bind the p62 subunit of TFIIH.

scholarly journals Wolbachia effects on Rift Valley fever virus infection in Culex tarsalis mosquitoes

2017 ◽  
Author(s):  
Brittany L. Dodson ◽  
Elizabeth S. Andrews ◽  
Michael J. Turell ◽  
Jason L. Rasgon
Keyword(s):  
West Nile Virus ◽  
Virus Infection ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Mosquito Species ◽  
West Nile Virus Infection ◽  
Fever Virus ◽  
Culex Tarsalis ◽  
Valley Fever

AbstractInnovative tools are needed to alleviate the burden of mosquito-borne diseases, and strategies that target the pathogen instead of the mosquito are being considered. A possible tactic is the use of Wolbachia, a maternally inherited, endosymbiotic bacterium that can suppress diverse pathogens when introduced to naive mosquito species. We investigated effects of somatic Wolbachia (strain wAlbB) infection on Rift Valley fever virus (RVFV) in Culex tarsalis mosquitoes. When compared to Wolbachia-uninfected mosquitoes, there was no significant effect of Wolbachia infection on RVFV infection, dissemination, or transmission frequencies, nor on viral body or saliva titers. Within Wolbachia-infected mosquitoes, there was a modest negative correlation between RVFV body titers and Wolbachia density, suggesting that Wolbachia may suppress RVFV in a density-dependent manner in this mosquito species. These results are contrary to previous work in the same mosquito species, showing Wolbachia-induced enhancement of West Nile virus infection rates. Taken together, these results highlight the importance of exploring the breadth of phenotypes induced by Wolbachia.Author SummaryAn integrated vector management program utilizes several practices, including pesticide application and source reduction, to reduce mosquito populations. However, mosquitoes are developing resistance to some of these methods and new control approaches are needed. A novel technique involves the bacterium Wolbachia that lives naturally in many insects. Wolbachia can be transferred to uninfected mosquitoes and can block pathogen transmission to humans. Additionally, Wolbachia is maternally inherited, allowing it to spread quickly through uninfected field populations of mosquitoes. We studied the impacts of Wolbachia on Rift Valley fever virus (RVFV) in the naturally uninfected mosquito, Culex tarsalis. Wolbachia had no effects on the ability of Culex tarsalis to become infected with or transmit RVFV. High densities of Wolbachia were associated with no virus infection or low levels of virus, suggesting that Wolbachia might suppress RVFV at high densities. These results contrast with our previous study that showed Wolbachia enhances West Nile virus infection in Culex tarsalis. Together, these studies highlight the importance of studying Wolbachia effects on a variety of pathogens so that control methods are not impeded.

scholarly journals A Haploid Genetic Screen Identifies Heparan Sulfate Proteoglycans Supporting Rift Valley Fever Virus Infection

2015 ◽  
Vol 90 (3) ◽  
pp. 1414-1423 ◽  
Author(s):  
Amber M. Riblett ◽  
Vincent A. Blomen ◽  
Lucas T. Jae ◽  
Louis A. Altamura ◽  
Robert W. Doms ◽  
...  
Keyword(s):  
Heparan Sulfate ◽  
Golgi Complex ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Hemorrhagic Fever ◽  
Cell Types ◽  
Fever Virus ◽  
Host Cells ◽  
Valley Fever

ABSTRACTRift Valley fever virus (RVFV) causes recurrent insect-borne epizootics throughout the African continent, and infection of humans can lead to a lethal hemorrhagic fever syndrome. Deep mutagenesis of haploid human cells was used to identify host factors required for RVFV infection. This screen identified a suite of enzymes involved in glycosaminoglycan (GAG) biogenesis and transport, including several components of thecis-oligomeric Golgi (COG) complex, one of the central components of Golgi complex trafficking. In addition, disruption ofPTAR1led to RVFV resistance as well as reduced heparan sulfate surface levels, consistent with recent observations that PTAR1-deficient cells exhibit altered Golgi complex morphology and glycosylation defects. A variety of biochemical and genetic approaches were utilized to show that both pathogenic and attenuated RVFV strains require GAGs for efficient infection on some, but not all, cell types, with the block to infection being at the level of virion attachment. Examination of other members of theBunyaviridaefamily for GAG-dependent infection suggested that the interaction with GAGs is not universal among bunyaviruses, indicating that these viruses, as well as RVFV on certain cell types, employ additional unidentified virion attachment factors and/or receptors.IMPORTANCERift Valley fever virus (RVFV) is an emerging pathogen that can cause severe disease in humans and animals. Epizootics among livestock populations lead to high mortality rates and can be economically devastating. Human epidemics of Rift Valley fever, often initiated by contact with infected animals, are characterized by a febrile disease that sometimes leads to encephalitis or hemorrhagic fever. The global burden of the pathogen is increasing because it has recently disseminated beyond Africa, which is of particular concern because the virus can be transmitted by widely distributed mosquito species. There are no FDA-licensed vaccines or antiviral agents with activity against RVFV, and details of its life cycle and interaction with host cells are not well characterized. We used the power of genetic screening in human cells and found that RVFV utilizes glycosaminoglycans to attach to host cells. This furthers our understanding of the virus and informs the development of antiviral therapeutics.

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