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Archives of virology1986; 90(1-2); 111-124; doi: 10.1007/BF01314149

Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: equine stroke.

Abstract: Eight mares were infected with equid herpesvirus-1 subtype 1 isolated from a case of equine paresis. In two mares killed at 4 d.p.i. immunofluorescence showed endothelial cell infection together with thrombosis in the rete arteriosus of the nasal mucosa and also in the spinal cord of one of these mares. Circulating platelet counts in the other six mares fell as early as 2 d.p.i. and remained depressed for seven days. Circulating immune complexes started to appear at 2 d.p.i., reached maximum levels at 10 d.p.i., but were undetectable at 28 d.p.i. Three of the six remaining mares developed varying degrees of inco-ordination at 8 and 9 d.p.i. In the two inco-ordinate mares that were killed at 9 and 10 d.p.i. the haemorrhages in the spinal cord and brain were associated with extensive endothelial cell fluorescence and thrombus formation. Clinical paresis coincided with an increase in circulating complement fixing and neutralising antibodies which in all six mares were higher against the subtype 2 isolate than subtype 1. In five yearlings infected with a subtype 2 isolate of EHV-1 platelet counts remained normal and neither immune complexes nor viraemia, nor inco-ordination were detected.
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Publication Date: 1986-01-01 PubMed ID: 3015074DOI: 10.1007/BF01314149Google Scholar: Lookup
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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 research study investigates the relationship between equid herpesvirus-1 infection and the onset of paralysis in horses. The research specifically focused on thrombosis and endothelial cell infection, and involved infecting eight adult female horses with the virus, as well as observing its effects on five yearlings.

Methodology and Early Observations

  • The researchers infected eight adult female horses (mares) with equid herpesvirus-1 subtype 1, a virus responsible for equine paralysis. After four days of post-infection, two of the mares were euthanized to enable detailed examination of the virus’ effects.
  • Immunofluorescence was used to visualize the infection, revealing that the virus had invaded the endothelial cells, a single layer of cells lining the interior of blood vessels. Thrombosis, or blood clotting, was observed in the rete arteriosus of the nasal mucosa and the spinal cord of one mare.
  • Platelet counts in the remaining six mares started decreasing as early as the second day post-infection and stayed low for seven days. Platelets are the blood cells responsible for blood clotting, and a reduction in their count can cause excessive, sometimes dangerous, bleeding.

Circulating Immune Complexes and Paresis Development

  • Circulating immune complexes – proteins produced when antigens bind to antibodies – were detected as early as the second day post-infection. These complexes peaked at the tenth day post-infection and were undetectable by the 28th day.
  • Incoordination, a potential indicator of being at the onset of paralysis, was observed in three out of the six remaining mares at the 8th and 9th day post-infection.
  • The two incoordinate mares that were euthanized at the 9th and 10th day post-infection showed haemorrhages (excessive bleeding) in the spinal cord and brain. These damages were associated with extensive endothelial cell fluorescence, indicating a high level of virus activity, and thrombus (blood clot) formation.

Evidence of Immune Response and Subtype Differences

  • Researchers found that the development of clinical paresis (partial or complete paralysis) coincided with an increase in the levels of circulating complement fixing and neutralising antibodies. These antibodies, which play a crucial role in immune response, were higher against the subtype 2 isolate than subtype 1. This suggests that the virus subtype plays a role in the severity of the infection and the body’s immune response.
  • The researchers also infected five yearlings (young horses) with subtype 2 of the virus. These yearlings did not show any reduction in platelet counts, nor presence of immune complexes or viraemia (presence of viruses in the blood), and did not develop incoordination. These observations could imply differences in immune response between adult and young horses, or between virus subtypes.

This research contributes fundamental knowledge for understanding the pathology of equid herpesvirus-1 and may possibly prove useful for future treatments and preventative measures regarding equine paralysis.

Cite This Article

APA
Edington N, Bridges CG, Patel JR. (1986). Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: equine stroke. Arch Virol, 90(1-2), 111-124. https://doi.org/10.1007/BF01314149

Publication

Archives of virology
ISSN: 0304-8608
NlmUniqueID: 7506870
Country: Austria
Language: English
Volume: 90
Issue: 1-2
Pages: 111-124

Researcher Affiliations

Edington, N
    Bridges, C G
      Patel, J R

        MeSH Terms

        • Animals
        • Antibodies, Viral / analysis
        • Antigen-Antibody Complex / analysis
        • Cerebrovascular Disorders / etiology
        • Cerebrovascular Disorders / immunology
        • Cerebrovascular Disorders / veterinary
        • Endothelium / microbiology
        • Endothelium / pathology
        • Female
        • Herpesviridae Infections / complications
        • Herpesviridae Infections / immunology
        • Herpesviridae Infections / microbiology
        • Herpesviridae Infections / veterinary
        • Herpesvirus 1, Equid / immunology
        • Herpesvirus 1, Equid / isolation & purification
        • Horse Diseases / etiology
        • Horse Diseases / immunology
        • Horses
        • Nasal Mucosa / blood supply
        • Nasal Mucosa / pathology
        • Paresis / etiology
        • Paresis / veterinary
        • Platelet Count
        • Spinal Cord / blood supply
        • Thrombosis / etiology
        • Thrombosis / pathology
        • Thrombosis / veterinary

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