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Veterinary immunology and immunopathology2018; 197; 24-30; doi: 10.1016/j.vetimm.2018.01.007

Absence of relationship between type-I interferon suppression and neuropathogenicity of EHV-1.

Abstract: Equine herpesvirus-1 (EHV-1) infection is an important and highly prevalent disease in equine populations worldwide. Previously we have demonstrated that a neuropathogenic strain of EHV-1, T953, suppresses the host cell's antiviral type-I interferon (IFN) response in vitro. Whether or not this is unique to EHV-1 strains possessing the neuropathogenic genotype has been undetermined. Here, we examined whether there is any direct relationship between neuropathogenic genotype and the induced IFN-β response in equine endothelial cells (EECs) infected with 10 different strains of EHV-1. The extent of virus cell-to-cell spread following infection in EECs was also compared between the neuropathogenic and the non-neuropathogenic genotype of EHV-1. We then compared IFN-β and the total type-I IFN protein suppression between T953, an EHV-1 strain that is neuropathogenic and T445, an EHV-4 strain mainly associated only with respiratory disease. Data from our study revealed no relationship between the neuropathogenic genotype of EHV-1 and the induced IFN-β mRNA by the host cell. Results also indicate no statistically significant difference in plaque sizes of both genotypes of EHV-1 produced in EECs. However, while the T953 strain of EHV-1 was able to suppress IFN-β mRNA and type-I IFN biological activity at 12 h post-infection (hpi), EHV-4 weakly induces both IFN-β mRNA and type-I IFN biological activity. This finding correlated with a statistically significant difference in the mean plaque sizes produced by the two EHV subtypes in EECs. Our data help illuminate how EHV-1, irrespective of its genotype, evades the host cell's innate immune response thereby enabling viral spread to susceptible cells.
Publication Date: 2018-02-25 PubMed ID: 29475503DOI: 10.1016/j.vetimm.2018.01.007Google Scholar: Lookup
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  • Journal Article

Summary

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This research examines whether there is a link between the neuropathogenic genotype of the Equine herpesvirus-1 (EHV-1) variant and the host cell’s immunological response, specifically its type-I interferon (IFN) response. The findings revealed no association between the neuropathogenic genotype of EHV-1 and the induced IFN-β mRNA by the host cell.

Objective of the Research

  • The primary goal of this study was to ascertain whether there’s a direct correlation between the neuropathogenic genotype of Equine herpesvirus-1 (EHV-1) and the host cell’s type-I interferon (IFN) response.

Methodology

  • The researchers compared the extent of the EHV-1 virus cell-to-cell transmission in equine endothelial cells (EECs) affected by 10 distinct EHV-1 strains.
  • They further compared IFN-β and the overall type-I IFN protein suppression between two EHV strains, one EHV-1 strain (T953) that is neuropathogenic and another EHV-4 strain (T445), primarily associated only with respiratory disease.

Results

  • The findings revealed no correlation between the neuropathogenic genotype of EHV-1 and the induction of IFN-β mRNA by the host cell.
  • The data showed no statistically significant discrepancy in the sizes of the plaques produced by both genotypes of EHV-1 in EECs.
  • Nevertheless, EHV-1 strain T953 managed to suppress IFN-β mRNA and type-I IFN biological activity 12 hours post-infection, while EHV-4 mildly induced IFN-β mRNA and type-I IFN biological activity.
  • This outcome correlated with a statistically significant difference in the mean plaque sizes produced by the two EHV subtypes in EECs.

Conclusion

  • The research revealed how EHV-1, irrespective of its genotype, circumvents the host cell’s innate immune response, thereby facilitating viral spread to susceptible cells.

Cite This Article

APA
Oladunni FS, Sarkar S, Reedy S, Balasuriya UBR, Horohov DW, Chambers TM. (2018). Absence of relationship between type-I interferon suppression and neuropathogenicity of EHV-1. Vet Immunol Immunopathol, 197, 24-30. https://doi.org/10.1016/j.vetimm.2018.01.007

Publication

ISSN: 1873-2534
NlmUniqueID: 8002006
Country: Netherlands
Language: English
Volume: 197
Pages: 24-30
PII: S0165-2427(17)30375-6

Researcher Affiliations

Oladunni, Fatai S
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA; Department of Veterinary Microbiology, University of Ilorin, Ilorin, Nigeria. Electronic address: kanmi01@gmail.com.
Sarkar, Sanjay
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.
Reedy, Stephanie
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.
Balasuriya, Udeni B R
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.
Horohov, David W
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.
Chambers, Thomas M
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.

MeSH Terms

  • Animals
  • Endothelial Cells / immunology
  • Endothelial Cells / virology
  • Genotype
  • Herpesviridae Infections / immunology
  • Herpesviridae Infections / veterinary
  • Herpesvirus 1, Equid / classification
  • Herpesvirus 1, Equid / pathogenicity
  • Horse Diseases / immunology
  • Horse Diseases / virology
  • Horses / immunology
  • Immune Evasion
  • Immunity, Innate
  • Interferon Type I / immunology
  • Interferon-beta / immunology

Citations

This article has been cited 2 times.
  1. Oladunni FS, Horohov DW, Chambers TM. EHV-1: A Constant Threat to the Horse Industry.. Front Microbiol 2019;10:2668.
    doi: 10.3389/fmicb.2019.02668pubmed: 31849857google scholar: lookup
  2. Oladunni FS, Sarkar S, Reedy S, Balasuriya UBR, Horohov DW, Chambers TM. Equid Herpesvirus 1 Targets the Sensitization and Induction Steps To Inhibit the Type I Interferon Response in Equine Endothelial Cells.. J Virol 2019 Dec 1;93(23).
    doi: 10.1128/JVI.01342-19pubmed: 31511388google scholar: lookup