Subcutaneous Administration of Low-Molecular-Weight Heparin to Horses Inhibits Ex Vivo Equine Herpesvirus Type 1-Induced Platelet Activation.
Authors: Stokol Tracy, Serpa Priscila B S, Brooks Marjory B, Divers Thomas, Ness Sally
Journal: Frontiers in veterinary science
Summary
# Editorial Summary Equine herpesvirus type 1 (EHV-1) causes significant morbidity and mortality through thrombotic complications in the placenta and spinal cord; this research investigated whether anticoagulant therapy could mitigate virus-induced platelet dysfunction in vivo. Nine healthy horses received subcutaneous injections of either unfractionated heparin (UFH), low-molecular-weight heparin (LMWH—enoxaparin), or saline in a blinded crossover design, with blood samples analysed at multiple timepoints to measure platelet activation (P-selectin expression) when exposed to two EHV-1 strains ex vivo. LMWH, but not UFH, successfully inhibited EHV-1-induced platelet activation 40 hours post-treatment when anti-Xa activity exceeded 0.1 U/ml, though this protection was lost by 60 hours as drug levels declined; notably, neither anticoagulant prevented activation at high viral concentrations. Substantial individual variation in platelet response was observed between horses, and minor injection site reactions occurred with both heparin protocols. These findings suggest that LMWH therapy could represent a rational adjunctive treatment for EHV-1-associated thrombosis, particularly in neurological cases, though practitioners should recognise the time-dependent nature of protection, the virus load-dependent response, and the need for optimised dosing schedules before implementing this approach clinically.
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Practical Takeaways
- •LMWH (enoxaparin) may help prevent blood clots in horses with EHV-1 infection by reducing platelet activation, particularly in early infection stages
- •Dosing timing matters: anti-Xa activity and platelet protection peaked at 40 hours but diminished by 60 hours, suggesting frequent dosing intervals or dose optimization may be necessary
- •Effectiveness is limited to lower viral loads; at high viral concentrations neither heparin prevented platelet activation, so LMWH is not a complete solution for severe EHV-1 disease
Key Findings
- •Low-molecular-weight heparin (LMWH) inhibited platelet activation induced by low-concentration EHV-1 at 40 hours post-treatment, while unfractionated heparin (UFH) did not
- •LMWH maintained anti-Xa activity above 0.1 U/ml at 40 hours (range 0.15-0.48) compared to UFH which did not achieve this threshold
- •Platelet inhibitory effect of LMWH was no longer detectable by 60 hours when anti-Xa activity had decreased to 0.03-0.07 U/ml
- •Neither heparin inhibited platelet activation induced by high viral concentrations (5 × 10⁶ plaque forming units/mL)