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Equine herpesvirus-1 infected peripheral blood mononuclear cell subpopulations during viremia.
Abstract: Infection with equine herpesvirus-1 (EHV-1) causes respiratory disease, late term abortions and equine herpesvirus myeloencephalitis (EHM) and remains an important problem in horses worldwide. Despite increasing outbreaks of EHM in recent years, our understanding of EHM pathogenesis is still limited except for the knowledge that a cell-associated viremia in peripheral blood mononuclear cells (PBMCs) is a critical link between primary respiratory EHV-1 infection and secondary complications such as late-term abortion or EHM. To address this question our objective was to identify which PBMC subpopulation(s) are infected during viremia and may therefore play a role in transmitting the virus to the vascular endothelium of the spinal cord or pregnant uterus. PBMCs from 3 groups of animals were collected between days 4 and 9 following experimental infection with EHV-1 strain Findlay/OH03 or strain Ab4. PBMCs were labeled with primary antibodies selective for CD4+ or CD8+ T lymphocytes, B-lymphocytes, or monocytes and positively selected using magnetic bead separation. Cell numbers and EHV-1 genome numbers in each subpopulation were then determined using quantitative PCR for β-actin and the EHV-1 glycoprotein B, respectively. Viral genomic DNA was found in all PBMC subpopulations; the CD8+ lymphocytes were most frequently positive for viral DNA, followed by B-lymphocytes. These differences were statistically significant in horses infected with the EHV-1 strain Findlay/OH03, and ponies with Ab4. These results differ from what has been reported in in vitro studies, and indicate that different PBMC subpopulations may play different roles in EHV-1 viremia.
Copyright © 2010 Elsevier B.V. All rights reserved.
Publication Date: 2010-10-28 PubMed ID: 21093993DOI: 10.1016/j.vetmic.2010.10.004Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research investigates which cells, in horse’s blood, equine herpesvirus-1 (EHV-1) infects. It has found that the EHV-1 virus most frequently infects CD8+ lymphocytes and B-lymphocytes and these cells may play different roles in spreading the virus.
Research Goals
- The main goal of this research was to identify the subpopulations of peripheral blood mononuclear cells (PBMCs) that are infected by equine herpesvirus-1 (EHV-1) during viremia. The researchers aimed to shed light on which cells could be responsible for transmitting the virus to vascular endothelium of either the spinal cord or the pregnant uterus, causing secondary complications like late-term abortion or equine herpesvirus myeloencephalitis (EHM).
Methods
- The researchers took PBMCs from three groups of animals between days 4 and 9 following their infection with either the EHV-1 strain Findlay/OH03 or strain Ab4.
- Upon harvesting, the cells were labeled with antibodies selective for CD4+ or CD8+ T lymphocytes, B-lymphocytes, or monocytes and separated using magnetic bead separation.
- Quantitative PCR was run for β-actin and the EHV-1 glycoprotein B to determine cell numbers and EHV-1 genome numbers in each PBMC subpopulation respectively.
Results
- It was found that viral genomic DNA was present in all PBMC subpopulations. However, the CD8+ lymphocytes were most frequently positive for viral DNA, followed by the B-lymphocytes.
- This prevalence ratio was statistically significant in horses infected with the EHV-1 strain Findlay/OH03, and ponies with Ab4.
- This indicates that different PBMC subpopulations may play different roles in EHV-1 viremia, and these findings differ from prior in vitro studies.
Conclusion
- This research has identified the PBMCs that EHV-1 infects during viremia, suggesting their potential role in disseminating the virus to the vascular endothelium. The underpinning mechanisms for this cell selection, however, remain unclear and further studies are required to understand the intricate interplay between EHV-1 and these cell subpopulations.
Cite This Article
APA
Wilsterman S, Soboll-Hussey G, Lunn DP, Ashton LV, Callan RJ, Hussey SB, Rao S, Goehring LS.
(2010).
Equine herpesvirus-1 infected peripheral blood mononuclear cell subpopulations during viremia.
Vet Microbiol, 149(1-2), 40-47.
https://doi.org/10.1016/j.vetmic.2010.10.004 Publication
Researcher Affiliations
- Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 300 West Drake Road, Fort Collins, CO 80523, USA.
MeSH Terms
- Animals
- B-Lymphocytes / immunology
- CD8-Positive T-Lymphocytes / immunology
- DNA, Viral / blood
- Female
- Herpesviridae Infections / immunology
- Herpesviridae Infections / veterinary
- Herpesviridae Infections / virology
- Herpesvirus 1, Equid / immunology
- Horse Diseases / immunology
- Horse Diseases / virology
- Horses / virology
- Leukocytes, Mononuclear / immunology
- Leukocytes, Mononuclear / virology
- Male
- Polymerase Chain Reaction / methods
- Polymerase Chain Reaction / veterinary
- Viremia / immunology
- Viremia / veterinary
- Viremia / virology
Citations
This article has been cited 12 times.- Klouth E, Zablotski Y, Petersen JL, de Bruijn M, Gröndahl G, Müller S, Goehring LS. Epidemiological Aspects of Equid Herpesvirus-Associated Myeloencephalopathy (EHM) Outbreaks. Viruses 2022 Nov 21;14(11).
- Thieulent CJ, Sutton G, Toquet MP, Fremaux S, Hue E, Fortier C, Pléau A, Deslis A, Abrioux S, Guitton E, Pronost S, Paillot R. Oral Administration of Valganciclovir Reduces Clinical Signs, Virus Shedding and Cell-Associated Viremia in Ponies Experimentally Infected with the Equid Herpesvirus-1 C(2254) Variant. Pathogens 2022 May 4;11(5).
- Samoilowa S, Giessler KS, Torres CEM, Hussey GS, Allum A, Fux R, Jerke C, Kiupel M, Matiasek K, Sledge DG, Goehring LS. Equid herpesvirus-1 Distribution in Equine Lymphoid and Neural Tissues 70 Days Post Infection. Pathogens 2021 Jun 5;10(6).
- Zarski LM, Weber PSD, Lee Y, Soboll Hussey G. Transcriptomic Profiling of Equine and Viral Genes in Peripheral Blood Mononuclear Cells in Horses during Equine Herpesvirus 1 Infection. Pathogens 2021 Jan 7;10(1).
- Giessler KS, Samoilowa S, Soboll Hussey G, Kiupel M, Matiasek K, Sledge DG, Liesche F, Schlegel J, Fux R, Goehring LS. Viral Load and Cell Tropism During Early Latent Equid Herpesvirus 1 Infection Differ Over Time in Lymphoid and Neural Tissue Samples From Experimentally Infected Horses. Front Vet Sci 2020;7:621.
- Pavulraj S, Kamel M, Stephanowitz H, Liu F, Plendl J, Osterrieder N, Azab W. Equine Herpesvirus Type 1 Modulates Cytokine and Chemokine Profiles of Mononuclear Cells for Efficient Dissemination to Target Organs. Viruses 2020 Sep 8;12(9).
- Brown LJ, Brown G, Kydd J, Stout TAE, Schulman ML. Failure to detect equid herpesvirus types 1 and 4 DNA in placentae and healthy new-born Thoroughbred foals. J S Afr Vet Assoc 2019 May 30;90(0):e1-e5.
- Poelaert KCK, Van Cleemput J, Laval K, Favoreel HW, Couck L, Van den Broeck W, Azab W, Nauwynck HJ. Equine Herpesvirus 1 Bridles T Lymphocytes To Reach Its Target Organs. J Virol 2019 Apr 1;93(7).
- Schnabel CL, Wimer CL, Perkins G, Babasyan S, Freer H, Watts C, Rollins A, Osterrieder N, Wagner B. Deletion of the ORF2 gene of the neuropathogenic equine herpesvirus type 1 strain Ab4 reduces virulence while maintaining strong immunogenicity. BMC Vet Res 2018 Aug 22;14(1):245.
- Stokol T, Serpa PBS, Brooks MB, Divers T, Ness S. Subcutaneous Administration of Low-Molecular-Weight Heparin to Horses Inhibits Ex Vivo Equine Herpesvirus Type 1-Induced Platelet Activation. Front Vet Sci 2018;5:106.
- Yeo WM, Osterrieder N, Stokol T. Equine herpesvirus type 1 infection induces procoagulant activity in equine monocytes. Vet Res 2013 Mar 11;44(1):16.
- Lunn DP, Burgess BA, Dorman DC, Goehring LS, Gross P, Osterrieder K, Pusterla N, Soboll Hussey G. Updated ACVIM consensus statement on equine herpesvirus-1. J Vet Intern Med 2024 May-Jun;38(3):1290-1299.
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