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Home / Equine Research Bank / J Virol / Equid Herpesvirus 1 Targets the Sensitization and Induction ...
Journal of virology2019; 93(23); e01342-19; doi: 10.1128/JVI.01342-19

Equid Herpesvirus 1 Targets the Sensitization and Induction Steps To Inhibit the Type I Interferon Response in Equine Endothelial Cells.

Abstract: Equid herpesvirus 1 (EHV-1) is a viral pathogen of horse populations worldwide spread by the respiratory route and is known for causing outbreaks of neurologic syndromes and abortion storms. Previously, we demonstrated that an EHV-1 strain of the neuropathogenic genotype, T953, downregulates the beta interferon (IFN-β) response in equine endothelial cells (EECs) at 12 h postinfection (hpi). In the present study, we explored the molecular correlates of this inhibition as clues toward an understanding of the mechanism. Data from our study revealed that EHV-1 infection of EECs significantly reduced both Toll-like receptor 3 (TLR3) and TLR4 mRNA expression at 6 hpi and 12 hpi. While EHV-1 was able to significantly reduce IRF9 mRNA at both 6 hpi and 12 hpi, the virus significantly reduced IFN regulatory factor 7 (IRF7) mRNA only at 12 hpi. EHV-1 did not alter the cellular level of Janus-activated kinase 1 (JAK1) at any time point. However, EHV-1 reduced the cellular level of expression of tyrosine kinase 2 (TYK2) at 12 hpi. Downstream of JAK1-TYK2 signaling, EHV-1 blocked the phosphorylation and activation of signal transducer and activator of transcription 2 (STAT2) when coincubated with exogenous IFN, at 12 hpi, although not at 3 or 6 hpi. Immunofluorescence staining revealed that the virus prevented the nuclear translocation of STAT2 molecules, confirming the virus-mediated inhibition of STAT2 activation. The pattern of suppression of phosphorylation of STAT2 by EHV-1 implicated viral late gene expression. These data help illuminate how EHV-1 strategically inhibits the host innate immune defense by limiting steps required for type I IFN sensitization and induction. To date, no commercial vaccine label has a claim to be fully protective against the diseases caused by equid herpesvirus 1 (EHV-1), especially the neurologic form. The interferon (IFN) system, of which type I IFN is of great importance, still remains a viable immunotherapeutic option against EHV-1 infection. The type I IFN system has been exploited successfully to treat other viral infections, such as chronic hepatitis B and C in humans. The current state of research on how EHV-1 interferes with the protective effect of type I IFN has indicated transient induction of type I IFN production followed by a rapid shutdown in equine endothelial cells (EECs). The significance of our study is the identification of certain steps in the type I IFN signaling pathway targeted for inhibition by EHV-1. Understanding this pathogen-host relationship is essential for the long-term goal of developing effective immunotherapy against EHV-1.
Copyright © 2019 American Society for Microbiology.
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Publication Date: 2019-11-13 PubMed ID: 31511388PubMed Central: PMC6854505DOI: 10.1128/JVI.01342-19Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study examines how Equid Herpesvirus 1 (EHV-1), a pathogen known for causing diseases in horses, inhibits the host’s defensive type I Interferon response. It aims to understand this process to support the future development of effective immunotherapies against EHV-1 infection.

Research Purpose and Background

  • The research addresses EHV-1, a virus affecting horse populations globally, causing neurological syndromes and ‘abortion storms’ where multiple mares miscarry.
  • Previously, it was established that the EHV-1 strain, T953, downregulates or reduces the beta interferon (IFN-β) response in equine endothelial cells (EECs) 12 hours post-infection.
  • The present study seeks to understand the molecular aspects associated with this inhibition to unravel how the virus impedes the host’s defensive response.

Main Findings of the Study

  • One of the most crucial findings was EHV-1’s significant reduction of Toll-like receptor 3 (TLR3) and TLR4 mRNA expressions at 6 and 12 hours post-infection.
  • The virus was also found to considerably reduce IRF9 mRNA at both 6 and 12 hours post-infection. It did also reduce IFN regulatory factor 7 (IRF7) mRNA but only at 12 hours post-infection.
  • The presence of EHV-1 did not affect the cellular level of Janus-activated kinase 1 (JAK1) at any point. However, it did lower the cellular level of expression of tyrosine kinase 2 (TYK2) at 12 hours post-infection.
  • Downstream of the JAK1-TYK2 signaling pathway, the virus blocked the phosphorylation and activation of signal transducer and activator of transcription 2 (STAT2) at 12 hours post-infection, but not at 3 or 6 hours post-infection.
  • The virus’s late gene expression was implicated in this suppression of phosphorylation of STAT2.

Implications of the Study

  • Currently, no effective commercial vaccine provides full protection against diseases caused by EHV-1.
  • The Type I Interferon system remains a potential immunotherapeutic option against EHV-1 infection. It has worked successfully against viral infections like chronic hepatitis B and C in humans.
  • This study’s findings identify certain steps in the type I IFN signaling pathway targeted for inhibition by EHV-1. This knowledge is vital for developing effective immunotherapy against the virus in the future.

Cite This Article

APA
Oladunni FS, Sarkar S, Reedy S, Balasuriya UBR, Horohov DW, Chambers TM. (2019). Equid Herpesvirus 1 Targets the Sensitization and Induction Steps To Inhibit the Type I Interferon Response in Equine Endothelial Cells. J Virol, 93(23), e01342-19. https://doi.org/10.1128/JVI.01342-19

Publication

Journal of virology
ISSN: 1098-5514
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 93
Issue: 23
PII: e01342-19

Researcher Affiliations

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

MeSH Terms

  • Animals
  • Endothelial Cells / metabolism
  • Endothelial Cells / virology
  • Gene Expression Regulation
  • Hepatitis B, Chronic
  • Herpesviridae Infections / immunology
  • Herpesviridae Infections / metabolism
  • Herpesviridae Infections / virology
  • Herpesvirus 1, Equid / genetics
  • Herpesvirus 1, Equid / immunology
  • Horse Diseases / virology
  • Horses
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate
  • Interferon Type I / metabolism
  • Janus Kinase 1 / metabolism
  • RNA, Messenger / metabolism
  • STAT2 Transcription Factor / metabolism
  • Signal Transduction
  • TYK2 Kinase / metabolism
  • Toll-Like Receptor 3 / metabolism
  • Toll-Like Receptor 4 / metabolism

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Citations

This article has been cited 9 times.
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