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Viruses
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Viral Cycle and Cell Host Interactions of Equine Viruses
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Viral Cycle and Cell Host Interactions of Equine Viruses

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

Deadline for manuscript submissions: 31 October 2024 | Viewed by 6898

Special Issue Editor

Dr. Jose Carlos Valle-Casuso

E-Mail Website
Guest Editor
Laboratoire de Santé Animale, Site de Normandie de l’Agence nationale de sécurité sanitaire de l’alimentation, de l’environnement et du travail (ANSES), Physiopathologie et épidémiologie des maladies équines (PhEED) Unit, 14430 Goustranville, France
Interests: equine viral infectious diseases, with particular emphasis on those that have an economic impact on livestock productivity, are responsible for zoonoses or can serve as animal models for human infections; Innovative diagnostic tools; NGS; metagenomics and virus discovery

Special Issue Information

Dear Colleagues,

Environmental changes, human and animal demography, pathogen changes, and farming practices are among the factors that lead to emerging diseases. Emerging diseases or known diseases affecting horses have economic repercussions beyond their direct health costs. Working equids (horses, ponies, donkeys, and mules) remain essential to ensure the livelihood of poor communities around the world. Some of the viruses affecting equids also infect humans, and others do not but are members of viruses families where some infect humans.

With this Special Issue, we intend to explore the viral cycle of equine viruses, to understand better their life cycle and viral–host cell interactions. This knowledge will highlight critical interactions that will help improve our understanding of the viral families that infect horses and infect other animals, including humans. The pathogenicity pathways and viral-cell host interactions identified in those studies will be a precious source of inspiration to develop future treatments for equine infectious diseases. However, it will also be useful, from a “One Health” perspective, to better understand those viruses from the same families that infect other animals, including humans.

Dr. Jose Carlos Valle-Casuso
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • equine
  • virus
  • viral – cell host interactions
  • emergence
  • viral pathogenicity
  • viral entry, assembly and release
  • latency / persistence
  • one health / translational research
  • antiviral drugs

Published Papers (4 papers)

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Research

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21 pages, 2933 KiB  
Article
Equine Arteritis Virus in Monocytic Cells Suppresses Differentiation and Function of Dendritic Cells
by Nathifa A. Moyo, Dave Westcott, Rachel Simmonds and Falko Steinbach
Viruses 2023, 15(1), 255; https://0-doi-org.brum.beds.ac.uk/10.3390/v15010255 - 16 Jan 2023
Viewed by 1620
Abstract
Equine viral arteritis is an infectious disease of equids caused by equine arteritis virus (EAV), an RNA virus of the family Arteriviridae. Dendritic cells (DC) are important modulators of the immune response with the ability to present antigen to naïve T cells and [...] Read more.
Equine viral arteritis is an infectious disease of equids caused by equine arteritis virus (EAV), an RNA virus of the family Arteriviridae. Dendritic cells (DC) are important modulators of the immune response with the ability to present antigen to naïve T cells and can be generated in vitro from monocytes (MoDC). DC are important targets for many viruses and this interaction is crucial for the establishment—or rather not—of an anti-viral immunity. Little is known of the effect EAV has on host immune cells, particularly DC. To study the interaction of eqDC with EAV in vitro, an optimized eqMoDC system was used, which was established in a previous study. MoDC were infected with strains of different genotypes and pathogenicity. Virus replication was determined through titration and qPCR. The effect of the virus on morphology, phenotype and function of cells was assessed using light microscopy, flow cytometry and in vitro assays. This study confirms that EAV replicates in monocytes and MoDC. The replication was most efficient in mature MoDC, but variable between strains. Only the virulent strain caused a significant down-regulation of certain proteins such as CD14 and CD163 on monocytes and of CD83 on mature MoDC. Functional studies conducted after infection showed that EAV inhibited the endocytic and phagocytic capacity of Mo and mature MoDC with minimal effect on immature MoDC. Infected MoDC showed a reduced ability to stimulate T cells. Ultimately, EAV replication resulted in an apoptosis-mediated cell death. Thus, EAV evades the host anti-viral immunity both by inhibition of antigen presentation early after infection and through killing infected DC during replication. Full article
(This article belongs to the Special Issue Viral Cycle and Cell Host Interactions of Equine Viruses)
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10 pages, 854 KiB  
Article
Identification of Equine Arteritis Virus Immunodominant Epitopes Using a Peptide Microarray
by Jo Mayers, David Westcott and Falko Steinbach
Viruses 2022, 14(9), 1880; https://0-doi-org.brum.beds.ac.uk/10.3390/v14091880 - 26 Aug 2022
Viewed by 1236
Abstract
Using the commercially available PEPperCHIP® microarray platform, a peptide microarray was developed to identify immunodominant epitopes for the detection of antibodies against Equine arteritis virus (EAV). For this purpose, the whole EAV Bucyrus sequence was used to design a total of 1250 [...] Read more.
Using the commercially available PEPperCHIP® microarray platform, a peptide microarray was developed to identify immunodominant epitopes for the detection of antibodies against Equine arteritis virus (EAV). For this purpose, the whole EAV Bucyrus sequence was used to design a total of 1250 peptides that were synthesized and spotted onto a microarray slide. A panel of 28 serum samples representing a selection of EAV strains was tested using the microarray. Of the 1250 peptides, 97 peptides (7.76%) showed reactivity with the EAV-positive samples. No single peptide was detected by all the positive serum samples. Seven peptides repeatedly showed reactivity above the cut-off and were considered to have diagnostic potential. Five of these peptides were within the immunodominant GP5 protein and two were within the replicase polyprotein regions NSP2 and NSP10, located in ORF1. The diagnostic sensitivity of the seven peptides selected was low, ranging from 5% to 55%; however, the combined diagnostic sensitivity and specificity of the seven peptides was 90% and 100%, respectively. This data demonstrate that multiple peptide sequences would be required to design a comprehensive serological test to cover the diversity of the EAV strains and the individual immune responses of horses. Full article
(This article belongs to the Special Issue Viral Cycle and Cell Host Interactions of Equine Viruses)
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19 pages, 1141 KiB  
Article
Clinical, Virological and Immunological Responses after Experimental Infection with African Horse Sickness Virus Serotype 9 in Immunologically Naïve and Vaccinated Horses
by Manuel Durán-Ferrer, Rubén Villalba, Paloma Fernández-Pacheco, Cristina Tena-Tomás, Miguel-Ángel Jiménez-Clavero, José-Antonio Bouzada, María-José Ruano, Jovita Fernández-Pinero, Marisa Arias, Javier Castillo-Olivares and Montserrat Agüero
Viruses 2022, 14(7), 1545; https://0-doi-org.brum.beds.ac.uk/10.3390/v14071545 - 15 Jul 2022
Cited by 1 | Viewed by 1408
Abstract
This study described the clinical, virological, and serological responses of immunologically naïve and vaccinated horses to African horse sickness virus (AHSV) serotype 9. Naïve horses developed a clinical picture resembling the cardiac form of African horse sickness. This was characterized by inappetence, reduced [...] Read more.
This study described the clinical, virological, and serological responses of immunologically naïve and vaccinated horses to African horse sickness virus (AHSV) serotype 9. Naïve horses developed a clinical picture resembling the cardiac form of African horse sickness. This was characterized by inappetence, reduced activity, and hyperthermia leading to lethargy and immobility–recumbency by days 9–10 post-infection, an end-point criteria for euthanasia. After challenge, unvaccinated horses were viremic from days 3 or 4 post-infection till euthanasia, as detected by serogroup-specific (GS) real time RT-PCR (rRT-PCR) and virus isolation. Virus isolation, antigen ELISA, and GS-rRT-PCR also demonstrated high sensitivity in the post-mortem detection of the pathogen. After infection, serogroup-specific VP7 antibodies were undetectable by blocking ELISA (b-ELISA) in 2 out of 3 unvaccinated horses during the course of the disease (9–10 dpi). Vaccinated horses did not show significant side effects post-vaccination and were largely asymptomatic after the AHSV-9 challenge. VP7-specific antibodies could not be detected by the b-ELISA until day 21 and day 30 post-inoculation, respectively. Virus neutralizing antibody titres were low or even undetectable for specific serotypes in the vaccinated horses. Virus isolation and GS-rRT-PCR detected the presence of AHSV vaccine strains genomes and infectious vaccine virus after vaccination and challenge. This study established an experimental infection model of AHSV-9 in horses and characterized the main clinical, virological, and immunological parameters in both immunologically naïve and vaccinated horses using standardized bio-assays. Full article
(This article belongs to the Special Issue Viral Cycle and Cell Host Interactions of Equine Viruses)
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Review

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16 pages, 360 KiB  
Review
Interactions of Equine Viruses with the Host Kinase Machinery and Implications for One Health and Human Disease
by Carol Anderson, Haseebullah Baha, Niloufar Boghdeh, Michael Barrera, Farhang Alem and Aarthi Narayanan
Viruses 2023, 15(5), 1163; https://0-doi-org.brum.beds.ac.uk/10.3390/v15051163 - 13 May 2023
Cited by 1 | Viewed by 2019
Abstract
Zoonotic pathogens that are vector-transmitted have and continue to contribute to several emerging infections globally. In recent years, spillover events of such zoonotic pathogens have increased in frequency as a result of direct contact with livestock, wildlife, and urbanization, forcing animals from their [...] Read more.
Zoonotic pathogens that are vector-transmitted have and continue to contribute to several emerging infections globally. In recent years, spillover events of such zoonotic pathogens have increased in frequency as a result of direct contact with livestock, wildlife, and urbanization, forcing animals from their natural habitats. Equines serve as reservoir hosts for vector-transmitted zoonotic viruses that are also capable of infecting humans and causing disease. From a One Health perspective, equine viruses, therefore, pose major concerns for periodic outbreaks globally. Several equine viruses have spread out of their indigenous regions, such as West Nile virus (WNV) and equine encephalitis viruses (EEVs), making them of paramount concern to public health. Viruses have evolved many mechanisms to support the establishment of productive infection and to avoid host defense mechanisms, including promoting or decreasing inflammatory responses and regulating host machinery for protein synthesis. Viral interactions with the host enzymatic machinery, specifically kinases, can support the viral infectious process and downplay innate immune mechanisms, cumulatively leading to a more severe course of the disease. In this review, we will focus on how select equine viruses interact with host kinases to support viral multiplication. Full article
(This article belongs to the Special Issue Viral Cycle and Cell Host Interactions of Equine Viruses)
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