Senior Lecturer in Equine Medicine University of Pretoria Onderstepoort, Gauteng, South Africa
Abstract: Background - African Horse Sickness (AHS) is caused by the African Horse Sickness Virus (AHSV). Infection results in high morbidity and mortality in naïve horses. The nature and role of the immune system and inflammatory cascade has only been investigated in vitro, in limited studies. Hypothesis – Experimental AHSV infection results in an inflammatory response. Animals - Four AHSV-negative horses Methods – Prospective, longitudinal, experimental study. Following infection with AHSV, blood was obtained q12h until humane euthanasia. Complete white blood cell count (WBC), serum amyloid A (SAA), iron concentration, and cytokines IL-1α, IL-2, IL-6, IL-8, IL-10, IL-12, IL-17, IFN-γ, TNF-α, and MCP-1 were measured. Results - All horses developed severe clinical signs typical of AHS, necessitating humane euthanasia. Statistically significant changes were observed in WBC (p=0.026); however, these were not deemed clinically relevant. Changes in acute phase reactants SAA (p < 0.001) and iron (p=0.001) were significant but unexpectedly mild and delayed. Substantial changes in cytokine concentration were observed in TNF-α (up to 30-fold) and IL-10 (up to 150-fold) towards the final disease stages. All other cytokines remained under the detection limit or only displayed minor increases inconsistent over time and between horses. Conclusions and clinical importance - Despite severe clinical signs, no horses mounted an effective inflammatory response indicated by the lack of an inflammatory leukogram and the subtle changes in acute phase reactants. The lack of a proinflammatory cytokine response is unexpected. These findings suggest viral interference with the host innate immune system resulting in a muted inflammatory response.