scholarly journals Pathogen-specific resistance to Rift Valley fever virus infection is induced in mosquito cells by expression of the recombinant nucleoprotein but not NSs non-structural protein sequences

2000 ◽  
Vol 81 (9) ◽  
pp. 2161-2166 ◽  
Author(s):  
A. Billecocq ◽  
M. Vazeille-Falcoz ◽  
F. Rodhain ◽  
M. Bouloy

Rift Valley fever virus (RVFV) is an arbovirus of the Bunyaviridae family, causing recurrent disease outbreaks in Africa. Natural vertebrate hosts include cattle and humans. Several mosquito species belonging to the Aedes and Culex generaact as vectors of this phlebovirus. To test whether pathogen-derived resistance against RVFV could be induced by expressing genomic sequences in mosquito cells, as has been shown for La Crosse and dengue 2 viruses, we generated various recombinant Semliki Forest viruses expressing the S segment (or its genes) in the genomic or antigenomic sense. Expression of the N but not the NSs gene interfered with the production of RVFV in mosquito cells and this phenomenon was RNA- but not protein-dependent. These results raise questions on the molecular mechanisms involved in virus resistance.

Author(s):  
Adel M. Gad ◽  
Mosaad M. Hassan ◽  
Sharif El Said ◽  
Mahmoud I. Moussa ◽  
Owen L. Wood

1988 ◽  
Vol 38 (2) ◽  
pp. 440-446 ◽  
Author(s):  
Thomas P. Gargan ◽  
David J. Dohm ◽  
Michael J. Turell ◽  
Charles L. Bailey ◽  
Gary G. Clark

Viruses ◽  
2010 ◽  
Vol 2 (2) ◽  
pp. 655-675 ◽  
Author(s):  
Valerie Vaughn ◽  
Cale Streeter ◽  
David Miller ◽  
Sonja Gerrard

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1079
Author(s):  
Sarah Lumley ◽  
Laura Hunter ◽  
Kirsty Emery ◽  
Roger Hewson ◽  
Anthony R. Fooks ◽  
...  

Rift Valley fever virus (RVFV) causes a zoonotic mosquito-borne haemorrhagic disease that emerges to produce rapid large-scale outbreaks in livestock within sub-Saharan Africa. A range of mosquito species in Africa have been shown to transmit RVFV, and recent studies have assessed whether temperate mosquito species are also capable of transmission. In order to support vector competence studies, the ability to visualize virus localization in mosquito cells and tissue would enhance the understanding of the infection process within the mosquito body. Here, the application of in situ hybridization utilizing RNAscope® to detect RVFV infection within the mosquito species, Culex pipiens, derived from the United Kingdom was demonstrated. Extensive RVFV replication was detected in many tissues of the mosquito with the notable exception of the interior of ovarian follicles.


2017 ◽  
Author(s):  
Brittany L. Dodson ◽  
Elizabeth S. Andrews ◽  
Michael J. Turell ◽  
Jason L. Rasgon

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.


2021 ◽  
Author(s):  
Dina R. Weilhammer ◽  
Nicholas R. Hum ◽  
Feliza A. Bourguet ◽  
Aimy Sebastian ◽  
Doris Lam ◽  
...  

Rift Valley fever virus (RVFV) is a highly pathogenic mosquito-borne virus capable of causing hepatitis, encephalitis, blindness, hemorrhagic syndrome, and death in humans and livestock. Upon aerosol infection with RVFV, the brain is a major site of viral replication and tissue damage, yet pathogenesis in this organ has been understudied. Here, we investigated the immune response in the brain of RVFV infected mice. In response to infection, microglia initiate robust transcriptional upregulation of antiviral immune genes, as well as increased levels of activation markers and cytokine secretion that is dependent on mitochondrial antiviral-signaling protein (MAVS) and independent of toll-like receptors 3 and 7. In vivo, Mavs-/- mice displayed enhanced susceptibility to RVFV as determined by increased brain viral burden and higher mortality. Single-cell RNA sequence analysis identified microglia-specific defects in type I interferon and interferon responsive gene expression in Mavs-/- mice, as well as dysregulated lymphocyte infiltration. The results of this study provide a crucial step towards understanding the precise molecular mechanisms by which RVFV infection is controlled in the brain and will help inform the development of vaccines and antiviral therapies that are effective in preventing encephalitis.


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