Differences in replication kinetics and cell tropism between neurovirulent and non-neurovirulent EHV1 strains during the acute phase of infection in horses.
Open accessAbstract
Equine herpesvirus 1 (EHV1) replicates in the respiratory tract of horses, after which infected leukocytes transport virus throughout the body, resulting in abortion or nervous system disorders. Two EHV1 strains circulate in the field: neurovirulent and non-neurovirulent. To investigate differences in replication in the upper respiratory tract (URT), an experimental inoculation study in ponies was performed with both strains. Two groups of six ponies, were inoculated intranasally with 10(6.5) TCID(50) of either strain. Clinical signs, nasal shedding and viremia were evaluated. At early time points post-inoculation (pi), one pony of each group was euthanized. Tissues were collected for titration and immunostainings. Number and size of EHV1-induced plaques were calculated, and individual EHV1-infected cells were quantified and characterized. Inoculation with either strain resulted in nasal shedding and replication in several tissues of the URT. Both strains replicated in a plaquewise manner in epithelium of the nasal mucosa, but replication in epithelium of the nasopharynx was largely limited to non-neurovirulent EHV1. Plaques were never able to cross the basement membrane, but individual infected cells were noticed in the connective tissue of all examined tissues for both strains. The total number of these cells however, was 3-7 times lower with non-neurovirulent EHV1 compared to neurovirulent EHV1. CD172a(+) cells and CD5(+) lymphocytes were important target cells for both strains. Interestingly, in lymph nodes, B-lymphocytes were also important target cells for EHV1, irrespective of the strain. Viremia was detected very early pi and infected cells were mainly CD172a(+) for both strains. In summary, these results are valuable for understanding EHV1 pathogenesis at the port of entry, the URT.
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Primary EHV-1 infection of several tissues of the upper respiratory tract results in destruction and erosion of the epithelium and in nasal shedding starting from 1 to 14 days post-inoculation.
“Primary EHV-1 infection of several tissues of the URT results in the destruction and erosion of the epithelium and in nasal shedding starting from 1 to 14 dpi (Gibson et al., 1992; Gryspeerdt et al., 2010; Figure 1.1b).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Results (section 3.3; page unavailable) report EHV-1 replication in upper-respiratory epithelium and nasal shedding beginning at 1 day post-inoculation. The paper reports shedding only through day 7, not day 14, and the cited passages describe epithelial plaques rather than destruction and erosion of the epithelium. (LLM, conf=0.88)
Experimental — accuracy not yet measuredUpon entry into the host, EHV-1 first replicates in a restricted plaquewise manner in epithelial cells lining the upper respiratory tract, including nasal septum, nasopharynx, and trachea.
“Upon entry into the host, EHV-1 first replicates in a restricted plaquewise manner in the epithelial cells lining the URT, including nasal septum, nasopharynx, and trachea (van Maanen, 2002; Gryspeerdt et al., 2010; Figure 1.1a).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Discussion (page not available in our copy) describes restricted, plaque-forming replication in the epithelium of the nasal septum and/or nasopharynx. It does not establish plaque-forming replication in the trachea, and the Results (section 3.2; page not available) specify that nasopharyngeal epithelial plaques were observed for the non-neurovirulent strain, not the neurovirulent strain. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe leukocytes that carry EHV-1 across the basement membrane are mainly CD172a+ cells of myeloid origin, followed by T lymphocytes and B lymphocytes.
“These cells were mainly identified as CD172a+ cells (myeloid origin) followed by T lymphocytes and B lymphocytes (Gryspeerdt et al., 2010; Vandekerckhove et al., 2010; Baghi et al., 2014).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Discussion identifies CD172a+ myeloid cells as the main carriers in upper-respiratory connective tissue and also reports infected T lymphocytes. But it describes transport across the epithelial basement membrane as a speculation, not a demonstrated route for each cell type. Section 3.4.4 says B lymphocytes were rarely infected except in lymph nodes, so the claimed sequence of cells crossing the membrane is not established. (LLM, conf=0.86)
Experimental — accuracy not yet measuredViremia can be detected starting from 1 day post-inoculation and persists for 14 days.
“Viremia can be detected starting from 1 dpi and persists for 14 days (Gryspeerdt et al., 2010).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Discussion reports that cell-associated viremia was detectable as early as 1 day after inoculation. The Fig. 8 caption lists blood sampling only through day 7, so the paper does not establish that viremia persists for 14 days. Page numbers were not available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn nasal mucosal explants, EHV-1 elicited the production of chemokines CCL2 and CCL5 already at 24 hours post-inoculation in order to attract target CD172a+ cells.
“In nasal mucosal explants, EHV-1 elicited the production of chemokines (e.g., CCL2 and CCL5), already at 24 hpi, in order to attract target CD172a+ cells (Gryspeerdt et al., 2010; Zhao et al., 2017).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Results (§3.2; page unavailable) report CD172a+ infected cells in nasal tissue at one day after inoculation, and the Discussion (§4; page unavailable) identifies them as important EHV-1 carrier cells. The paper does not report nasal mucosal explant experiments or production of CCL2 and CCL5 at 24 hours to attract those cells. (LLM, conf=0.86)
Experimental — accuracy not yet measured
The production of type I interferon was directly associated with a self-limited EHV-1 infection of the respiratory epithelium and short-duration of nasal shedding.
“The production of type I IFN was directly associated with a self-limited EHV-1 infection of the respiratory epithelium and short-duration of nasal shedding (Gryspeerdt et al., 2010).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
The Conclusion (section 5; page unavailable) describes epithelial EHV-1 infection as self-limiting, most likely because of IFN-α production. That is a proposed explanation, not a demonstrated direct association. The nasal-shedding results (section 3.3; page unavailable) report shedding through day 7, with high titers still present at day 7 for the non-neurovirulent strain; they do not establish that IFN-α production was associated with short-duration shedding. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vivo, EHV-1-induced plaques were observed in the epithelium of the nasal mucosa from 2 to 7 days post-inoculation.
“In vivo, EHV-1-induced plaques were observed in the epithelium of the nasal mucosa starting from 2 to 7 days post-inoculation (dpi) (Gryspeerdt et al., 2010).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
While EHV-1 can infect the respiratory epithelium, previous in vivo, ex vivo and in vitro studies showed that its replication is somehow restricted.
“While EHV-1 can infect the respiratory epithelium, previous in vivo, ex vivo and in vitro studies showed that its replication is somehow restricted (Gryspeerdt et al., 2010; Vandekerckhove et al., 2010; Hussey et al., 2014).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Gryspeerdt et al., 2010
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References 48 · Cited by 69
- Authors
- Gryspeerdt, A. C., Vandekerckhove, A. P., Garré, B., Barbé, F., Van de Walle, G. R., & Nauwynck, H. J.
- Affiliations
- Ghent University (BE)
- ORCID
- Nauwynck, H.J.
- Venue
- Veterinary Microbiology
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 142
- Issue
- 3-4
- Pages
- 242-253
- ISSN
- 0378-1135 (ISSN-L)
- OpenAlex
- W2063979108
- Cited by
- 69
- References
- 48
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 6 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 6 · 2014: 6 · 2013: 4 · 2012: 5
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Veterinary Microbiology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Funders
- Vlaamse regering
- Topics
- Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
- Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- equine herpesvirus 1, viral replication kinetics, cell tropism, upper respiratory tract, nasal mucosa, nasopharynx, viremia, nasal shedding, B cells, lymph nodes, plaque formation, horses, experimental infection
- MeSH terms
- Animals, Antibodies, Viral, Cell Line, Epithelium, Herpesvirus 1, Equid, Herpesviridae Infections, Horse Diseases, Horses, Male, Rabbits, Respiratory System, Viremia, Virus Replication
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