In the past, the disease has also spread to Europe, specifically to Spain in 1969 and Spain and Portugal in 1987 [1] and [2]. The latest outbreak in Western Mediterranean countries lasted 5 years [3] and [4]. To date no effective treatment exists for AHS and consequently control of the disease relies on preventive vaccination. AHS vaccines, based on attenuated AHS viruses, have been in use in South Africa for almost 100 years and permitted

the subsistence of horses in that part of the world. There are nine different serotypes of AHS virus (AHSV) and protective immunity is long-lived against homologous serotypes. Thus, vaccination in endemic countries is normally CHIR-99021 chemical structure performed by administration of combinations of representative attenuated strains of each of the virus serotypes. Serotypes 5 and 9 are normally excluded from vaccine formulations. Serotype 5 is difficult to attenuate and partially cross-reacts with serotype 8; and serotype 9 does not normally occur in South Africa (the main AHSV vaccine manufacturing country) and partially cross-reacts with serotype 6 [3], [5] and [6]. Despite their apparent efficacy, live AHSV vaccines have a number of disadvantages [4]. These include: (a) the risk of reversion

to virulence; (b) the risk of gene segment re-assortment between field and vaccine strains; (c) the risk of introducing foreign topotypes into a new geographical region, since vaccines are based on South African strains; (d) the absence of DIVA (Differentiating Infected from Vaccinated Animals) capacity, that is the check details inability to serologically differentiate vaccine-induced immunity from that induced by natural infection; and (e) the contra-indications for use in pregnant mares because of their teratogenicity. In addition to these science-based shortcomings of the live vaccines it is also important to consider the potential logistical delays between the first detection of an outbreak and the deployment of sufficient vaccine doses to where they would be needed. The recognised shortcomings of

Ketanserin existing live AHSV vaccines has meant that alternative vaccination strategies have been pursued over the years. These have included the use of killed vaccines [7], [8] and [9], vaccines based on baculovirus-expressed AHSV capsid proteins [10], DNA vaccines [11] and those based on the use of poxvirus expression vectors [12], [13] and [14]. The latter appear to be a particularly promising strategy, which has started to produce encouraging results. We have demonstrated recently that recombinant MVA viruses expressing VP2 from AHSV serotype 4 (MVA-VP2), the major capsid protein of AHSV and main target of virus neutralising antibodies (VNAb), induced VNAb in horses and complete protection against virulent challenge in a mouse model [12] and [13].