Authors: Stokol Tracy, Serpa Priscila Beatriz da Silva, Zahid Muhammad N, Brooks Marjory B
Journal: Frontiers in veterinary science
Summary
# Editorial Summary: EHV-1-Induced Thrombosis and Potential Therapeutic Targets Equid herpes virus type-1 causes significant morbidity and mortality in horses partly through thrombotic complications in the placenta and spinal cord, yet the precise mechanisms driving clot formation remain poorly understood. Stokol and colleagues investigated whether anticoagulants and antiplatelet agents could suppress virus-induced platelet activation by exposing equine platelet-rich plasma to two pathogenic EHV-1 strains and measuring P-selectin expression as a marker of platelet activation. Both unfractionated heparin (0.05 U/mL) and low-molecular-weight heparin (2.5 µg/mL) demonstrated superior dose-dependent inhibition of platelet activation compared with phosphodiesterase inhibitors, though all four drugs tested successfully blocked virus-induced platelet responses in vitro. These findings suggest that heparin anticoagulants warrant investigation as adjunctive therapies during EHV-1 infection, potentially mitigating abortion storms and neurological complications; however, clinical efficacy trials are essential before practitioners can confidently incorporate these agents into treatment protocols for naturally infected horses.
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Practical Takeaways
- •Heparin and PDE inhibitors warrant clinical trial evaluation as adjunctive therapies to reduce life-threatening thrombotic complications in EHV-1-infected horses, particularly those presenting with myeloencephalopathy or abortion
- •UFH and LMWH demonstrate promising ex vivo efficacy at clinically achievable concentrations and represent the most potent antiplatelet option among drugs tested
- •Current findings support development of treatment protocols combining anticoagulants with standard EHV-1 management to mitigate ischemic injury from vessel thrombosis
Key Findings
- •Unfractionated heparin (UFH) at 0.05 U/mL and low-molecular-weight heparin (LMWH) at 2.5 μg/mL maximally inhibited EHV-1-induced platelet activation ex vivo
- •Phosphodiesterase inhibitors IBMX and cilostazol blocked EHV-1-induced platelet activation in dose-dependent manner, though with lower efficacy than heparins
- •All tested inhibitors suppressed both EHV-1 and thrombin-induced platelet activation, suggesting potential to reduce thrombotic complications
- •Heparin anticoagulants showed superior platelet inhibition compared to PDE antagonists at tested concentrations