Abstract
African horse sickness is a devastating disease that causes great suffering and many fatalities amongst horses in sub-Saharan Africa. It is caused by nine different serotypes of the orbivirus African horse sickness virus (AHSV) and it is spread by Culicoid midges. The disease has significant economic consequences for the equine industry both in southern Africa and increasingly further afield as the geographic distribution of the midge vector broadens with global warming and climate change. Live attenuated vaccines (LAV) have been used with relative success for many decades but carry the risk of reversion to virulence and/or genetic re-assortment between outbreak and vaccine strains. Furthermore, the vaccines lack DIVA capacity, the ability to distinguish between vaccine-induced immunity and that induced by natural infection. These concerns have motivated interest in the development of new, more favourable recombinant vaccines that utilize viral vectors or are based on reverse genetics or virus-like particle technologies. This review summarizes the current understanding of AHSV structure and the viral replication cycle and also evaluates existing and potential vaccine strategies that may be applied to prevent or control the disease.
Highlights
For several centuries, the devastating African horse sickness (AHS) has been a cruel scourge to horse owners in sub-Saharan Africa
The primary route of bluetongue virus (BTV) and African horse sickness virus (AHSV) host infection is believed to be initiated by the outer capsid proteins, there is evidence to suggest that BTV core-like particles (CLPs), i.e., particles that have lost the outer capsid proteins, are able to infect both insect and, to a lesser extent, mammalian cells [74]
Four months later, when the virus neutralizing antibody (VNAb) titres had decreased dramatically, vaccination with modified vaccinia Ankara (MVA)-VP2(5) representing a third AHSV serotype, elicited VNAb against AHSV 5, and induced an anamnestic response towards AHSV 4, 6 and 9 as well as the cross-reactive AHSV 8. These results demonstrate the suitability of MVA expressing AHSV VP2 (MVA-VP2) to be used as a polyvalent vaccine mixture providing protection against more than one AHSV serotype
Summary
The devastating African horse sickness (AHS) has been a cruel scourge to horse owners in sub-Saharan Africa. The primary route of BTV and AHSV host infection is believed to be initiated by the outer capsid proteins, there is evidence to suggest that BTV core-like particles (CLPs), i.e., particles that have lost the outer capsid proteins, are able to infect both insect and, to a lesser extent, mammalian cells [74]. In this regard, the upper domains of both BTV and AHSV VP7 trimers have characteristic Arg-Gly-Asp (RGD) motifs, albeit in slightly different locations [43]. The fact that there are holes in the surface of the outer capsid layer of both BTV and AHSV particles makes it tempting to speculate that these RGD sites on VP7 may play a role in the ability of viral CLPs to infect cells
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