Evidence map›Paper›PMID 41572601›Full record

ArticleEquine veterinary journal2026

Experimental infection of horses with African horse sickness virus results in overt disseminated intravascular coagulation.

Eva Christina Schliewert, Emma H Hooijberg, Amelia Goddard

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Article in Equine veterinary journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Eva Christina SchliewertDepartment of Companion Animal Clinical Studies, Faculty of Veterinary Medicine, University of Pretoria, Onderstepoort, South Africa.ORCID https://orcid.org/0000-0003-3763-8203
Emma H HooijbergDepartment of Companion Animal Clinical Studies, Faculty of Veterinary Medicine, University of Pretoria, Onderstepoort, South Africa.ORCID https://orcid.org/0000-0002-4367-799X
Amelia GoddardDepartment of Companion Animal Clinical Studies, Faculty of Veterinary Medicine, University of Pretoria, Onderstepoort, South Africa.ORCID https://orcid.org/0000-0002-8415-4802

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAfrican horse sickness (AHS), caused by the vector-borne African horse sickness virus (AHSV), is endemic to sub-Saharan Africa and infection results in high mortality in naïve equine populations. Clinical signs include submucosal petechiae and prolonged bleeding post venepuncture indicative of hypocoagulation. Pathological activation of haemostasis may result from tissue factor expression as a result of vascular endothelial damage or dysfunction, the proposed pathologic mechanism in AHS, potentially resulting in disseminated intravascular coagulation (DIC).

objectivesTo describe haemostatic changes during experimental AHSV infection and to characterise DIC using plasma-based and viscoelastic assays. STUDY

designIn vivo experiments.

methodsFour horses were experimentally infected with AHSV. Blood samples were obtained before infection, then every 24 h until humane euthanasia. Haematology and thromboelastography (TEG) were performed and prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen and D-dimer concentrations, as well as activities of antithrombin (AT) and coagulation factors II, VII, VIII, X, and XII were measured.

resultsOver the disease course, TEG variables showed increased clot initiation time (R) and decreased α-angle, maximum amplitude (MA), and clot strength (G). The velocity curve showed decreased maximum rate of thrombus generation (MRTG) and thrombus generation (TG), and increased time to maximum rate of thrombus generation (TMRTG). Prothrombin time, aPTT and D-dimer concentration increased while AT activity decreased. All horses developed severe thrombocytopenia.

conclusionsHorses experimentally infected with AHSV developed a consumptive coagulopathy with a bleeding phenotype. These findings fulfil the criteria of overt DIC characterised by procoagulant activation, inhibitor consumption and increased fibrinolytic activity.

Indexed as

African Horse SicknessAfrican Horse Sickness VirusDisseminated Intravascular CoagulationAnimalsFemaleHorsesMaleemerging diseasehorseinfectious diseaseOrbivirusvector‐borne disease

Identifiers

PMID41572601
PMCPMC12892386

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.