Emerging Highlights in the Study of Rift Valley Fever Virus

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 3058

Special Issue Editors


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Guest Editor
Department of Microbiology, Immunology and Pathology, Colorado State University, Campus Delivery 1690, Fort Collins, CO 80523, USA
Interests: vector biology; arboviruses; mosquito anti-viral responses; molecular biology; mosquito immunity; genomic regulatory regions
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Guest Editor
Department of Microbiology, Immunology and Pathology, Colorado State University, Campus Delivery 1690, Fort Collins, CO 80523, USA
Interests: vector competence; arboviruses; tick-borne disease; mosquito biology

Special Issue Information

Dear Colleagues,

The Rift Valley Fever virus periodically emerges in explosive epizootics in Eastern Africa and parts of the Arabian Peninsula. Viral transmission from competent mosquitoes, e.g., Aedes and Culex spp., to vertebrate hosts, can cause severe illness in humans and abortion storms in ungulates. Threats posed by current and shifting dynamics in RVFV transmission necessitate many lines of research, including, but not limited to: 1) knowledge of vector–virus interactions, 2) development of efficient vaccines for vertebrates, 3) viral strain replication kinetics, and 4) pathogenesis models. This Special Issue seeks to cover the gamut of RVFV research areas and will reveal knowledge gaps that need to be further addressed.

Dr. Corey L. Campbell
Dr. Emma K. Harris
Guest Editors

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Keywords

  • Rift Valley fever virus
  • emerging diseases
  • viral reassortment
  • neglected tropical diseases
  • vaccine development
  • vector–virus interactions

Published Papers (2 papers)

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Research

14 pages, 4814 KiB  
Article
Safety and Efficacy upon Infection in Sheep with Rift Valley Fever Virus ZH548-rA2, a Triple Mutant Rescued Virus
by Sandra Moreno, Gema Lorenzo, Álvaro López-Valiñas, Nuria de la Losa, Celia Alonso, Elena Charro, José I. Núñez, Pedro J. Sánchez-Cordón, Belén Borrego and Alejandro Brun
Viruses 2024, 16(1), 87; https://doi.org/10.3390/v16010087 - 05 Jan 2024
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Abstract
The introduction of three single nucleotide mutations into the genome of the virulent RVFV ZH548 strain allows for the rescue of a fully attenuated virus in mice (ZH548-rA2). These mutations are located in the viral genes encoding the RdRp and the non-structural protein [...] Read more.
The introduction of three single nucleotide mutations into the genome of the virulent RVFV ZH548 strain allows for the rescue of a fully attenuated virus in mice (ZH548-rA2). These mutations are located in the viral genes encoding the RdRp and the non-structural protein NSs. This paper shows the results obtained after the subcutaneous inoculation of ZH548-rA2 in adult sheep and the subsequent challenge with the parental virus (ZH548-rC1). Inoculation with the ZH548-rA2 virus caused no detectable clinical or pathological effect in sheep, whereas inoculation of the parental rC1 virus caused lesions compatible with viral infection characterised by the presence of scattered hepatic necrosis. Viral infection was confirmed via immunohistochemistry, with hepatocytes within the necrotic foci appearing as the main cells immunolabelled against viral antigen. Furthermore, the inoculation of sheep with the rA2 virus prevented the liver damage expected after rC1 virus inoculation, suggesting a protective efficacy in sheep which correlated with the induction of both humoral and cell-mediated immune responses. Full article
(This article belongs to the Special Issue Emerging Highlights in the Study of Rift Valley Fever Virus)
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13 pages, 1603 KiB  
Article
Identification of Host Factors for Rift Valley Fever Phlebovirus
by Velmurugan Balaraman, Sabarish V. Indran, Yonghai Li, David A. Meekins, Laxmi U. M. R. Jakkula, Heidi Liu, Micheal P. Hays, Jayme A. Souza-Neto, Natasha N. Gaudreault, Philip R. Hardwidge, William C. Wilson, Friedemann Weber and Juergen A. Richt
Viruses 2023, 15(11), 2251; https://doi.org/10.3390/v15112251 - 13 Nov 2023
Cited by 1 | Viewed by 1451
Abstract
Rift Valley fever phlebovirus (RVFV) is a zoonotic pathogen that causes Rift Valley fever (RVF) in livestock and humans. Currently, there is no licensed human vaccine or antiviral drug to control RVF. Although multiple species of animals and humans are vulnerable to RVFV [...] Read more.
Rift Valley fever phlebovirus (RVFV) is a zoonotic pathogen that causes Rift Valley fever (RVF) in livestock and humans. Currently, there is no licensed human vaccine or antiviral drug to control RVF. Although multiple species of animals and humans are vulnerable to RVFV infection, host factors affecting susceptibility are not well understood. To identify the host factors or genes essential for RVFV replication, we conducted CRISPR-Cas9 knockout screening in human A549 cells. We then validated the putative genes using siRNA-mediated knock-downs and CRISPR-Cas9-mediated knock-out studies. The role of a candidate gene in the virus replication cycle was assessed by measuring intracellular viral RNA accumulation, and the virus titers were analyzed using plaque assay or TCID50 assay. We identified approximately 900 genes with potential involvement in RVFV infection and replication. Further evaluation of the effect of six genes on viral replication using siRNA-mediated knock-downs revealed that silencing two genes (WDR7 and LRP1) significantly impaired RVFV replication. For further analysis, we focused on the WDR7 gene since the role of the LRP1 gene in RVFV replication was previously described in detail. WDR7 knockout A549 cell lines were generated and used to dissect the effect of WRD7 on a bunyavirus, RVFV, and an orthobunyavirus, La Crosse encephalitis virus (LACV). We observed significant effects of WDR7 knockout cells on both intracellular RVFV RNA levels and viral titers. At the intracellular RNA level, WRD7 affected RVFV replication at a later phase of its replication cycle (24 h) when compared with the LACV replication, which was affected in an earlier replication phase (12 h). In summary, we identified WDR7 as an essential host factor for the replication of two different viruses, RVFV and LACV, both of which belong to the Bunyavirales order. Future studies will investigate the mechanistic role through which WDR7 facilitates phlebovirus replication. Full article
(This article belongs to the Special Issue Emerging Highlights in the Study of Rift Valley Fever Virus)
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