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Cited by 19interferon and immune responsesHerpesvirus Infections and TreatmentsAnimal Virus Infections Studies

Abortigenic but not neurotropic equine Herpes Virus 1 modulates the interferon antiviral defense.

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Poelaert, Katrien C. K., Van Cleemput, Jolien, Laval, Kathlyn, Favoreel, Herman W., Soboll Hussey, Gisela, Maes, Roger K., Nauwynck, Hans J.·2018·Frontiers in Cellular and Infection Microbiology
DOI 10.3389/fcimb.2018.00312PMC PMC6144955
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Abstract

Equine herpesvirus 1 (EHV1) is considered as a major pathogen of Equidae, causing symptoms from mild respiratory disease to late-term abortion and neurological disorders. Different EHV1 strains circulating in the field have been characterized to be of abortigenic or neurovirulent phenotype. Both variants replicate in a plaque-wise manner in the epithelium of the upper respiratory tract (URT), where the abortigenic strains induce more prominent viral plaques, compared to the neurovirulent strains. Considering the differences in replication at the URT, we hypothesized that abortigenic strains may show an increased ability to modulate the type I IFN secretion/signaling pathway, compared to strains that display the neurovirulent phenotype. Here, we analyze IFN levels induced by abortigenic and neurovirulent EHV1 using primary respiratory epithelial cells (EREC) and respiratory mucosa ex vivo explants. Similar levels of IFNα (approx. 70 U/ml) were detected in explants inoculated with both types of EHV1 strains from 48 to 72 hpi. Second, EREC and mucosa explants were treated with recombinant equine IFNα (rEqIFNα) or Ruxolitinib (Rux), an IFN signaling inhibitor, prior to and during inoculation with abortigenic or neurovirulent EHV1. Replication of both EHV1 variants was suppressed by rEqIFNα. Further, addition of Rux increased replication in a concentration-dependent manner, indicating an IFN-susceptibility for both variants. However, in two out of three horses, at a physiological concentration of 100 U/ml of rEqIFNα, an increase in abortigenic EHV1 replication was observed compared to 10 U/ml of rEqIFNα, which was not observed for the neurovirulent strains. Moreover, in the presence of Rux, the plaque size of the abortigenic variants remained unaltered, whereas the typically smaller viral plaques induced by the neurovirulent variants became larger. Overall, our results demonstrate the importance of IFNα in the control of EHV1 replication in the URT for both abortigenic and neurovirulent variants. In addition, our findings support the speculation that abortigenic variants of EHV1 may have developed anti-IFN mechanisms that appear to be absent or less pronounced in neurovirulent EHV1 strains.

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  • EHV-1 activated the interferon response in the upper respiratory tract by upregulating the expression of IFN-α mRNA and protein levels in equine respiratory epithelial cells and respiratory mucosal explants.

    “EHV-1 activated the IFN response in the URT by upregulating the expression of IFN-α mRNA and protein levels in EREC and respiratory mucosal explants (Hussey et al., 2014; Poelaert et al., 2018).”

    From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Poelaert et al., 2018

    The Results section, “EHV1 activates IFN production in equine respiratory mucosa explants and EREC” (page not provided), reports increased IFNα protein in nasal and tracheal explants and increased IFNα staining in EREC. It does not report upregulation of IFNα mRNA; IFNα concentration in EREC supernatants showed no significant increase over time. (LLM, conf=0.88)

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Research works printed but not linked: 1

  1. Derksen F. (1999). Pathophysiology of respiratory disease. upper airway in Equine Medicine and Surgery, 1st Edn, eds Colahan P. Mayhewm I. Merritt A. (St Louis, MO: Mosby), 447– 48.

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Authors
Poelaert, K. C. K., Van Cleemput, J., Laval, K., Favoreel, H. W., Soboll Hussey, G., Maes, R. K., & Nauwynck, H. J.
Affiliations
  • Ghent University (BE)
  • Princeton University (US)
  • Michigan State University (US)
Corresponding author
Nauwynck, Hans J.
ORCID
Venue
Frontiers in Cellular and Infection Microbiology
Publisher
Frontiers Media SA
Published
2018-09-12
Volume
8
Pages
312-312
ISSN
2235-2988 (ISSN-L)
DOI
10.3389/fcimb.2018.00312
PMC
PMC6144955
OpenAlex
W2892355294
Cited by
19
References
87
Citations by year
2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 4 · 2019: 7
FWCI
1.18
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Cellular and Infection Microbiology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Ghent University Academic Bibliography (Ghent University) (publishedVersion, other-oa)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Agentschap voor Innovatie door Wetenschap en Technologie (141627)
  • Fonds Wetenschappelijk Onderzoek (11Y5415N)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
  • Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
Keywords
equine herpesvirus 1, type I interferon, interferon-alpha, interferon signaling, viral replication, upper respiratory tract, airway epithelial cells, ruxolitinib, horses
MeSH terms
Animals, Cells, Cultured, Epithelial Cells, Herpesvirus 1, Equid, Horses, Immunologic Factors, Models, Biological, Organ Culture Techniques, Viral Plaque Assay, Virus Replication, Interferon-alpha, Respiratory Mucosa, Host-Pathogen Interactions, Immune Evasion

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