Comparison of the efficacy of inactivated combination and modified-live virus vaccines against challenge infection with neuropathogenic equine herpesvirus type 1 (EHV-1).
ABSTRACT Equine herpesvirus type 1 (EHV-1) is a ubiquitous alphaherpesvirus of horses which causes rhinopneumonitis, abortion and myeloencephalopathy. To test the efficacy of commercial vaccines in protection against neurological EHV-1 challenge, groups of five horses were immunized with modified-live virus or an inactivated vaccine, or received placebo. Horses were challenged by aerosol with a recent virus isolate obtained from a case of paralytic EHV-1. The duration of fever decreased significantly in the modified-live virus vaccine group. Three animals in each of the inactivate and control groups showed alterations in neurological status. When compared to the inactivated vaccine, the modified-live virus vaccine induced significantly lower virus-neutralizing antibodies over the course of the study. The modified-live virus vaccine resulted in low EHV-1-specific IgG(T)/IgGa and IgG(T)/IgGb ratios, suggesting a bias towards a cytotoxic immune response. Virus shedding from the nasopharynx was almost undetectable in the modified-live virus group, and was significantly lower when compared to that in the other groups. Normalized lymphocyte viral genome copies were similar for the three groups, although animals vaccinated with the modified-live virus vaccine were qPCR-positive on fewer days when compared to those of the other groups. Based on data from neurological signs, rectal temperatures, virus isolation from nasal swabs and immune response specificity, we concluded that protection induced by the modified-live virus vaccine is superior to that induced by the inactivated combination vaccine.
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ABSTRACT: Equine herpesviruses type 1 (EHV-1) is a major cause of winter pyrexia in racehorses in two training centers (Ritto and Miho) in Japan. Until the epizootic period of 2008-2009, a vaccination program using a killed EHV-1 vaccine targeted only those of the 3-year-old susceptible horses with low antibody levels to EHV-1 antigens. However, because protective effect was not satisfactory, in 2009-2010 the vaccination program was altered to target all 3-year-old horses. To evaluate vaccine efficacy, we investigated the number of pyretic horses due to EHV-1 or equine herpesvirus type-4 (EHV-4) infection, or both, and examined the vaccination coverage in the 3-year-old population and in the whole population before and after changing the program. The mean estimated number of horses infected with EHV-1 or EHV-4, or both, among pyretic horses from 1999-2000 to 2008-2009 was 105±47 at Ritto and 66±44 at Miho. Although the estimated number of infected horses did not change greatly in the first period of the current program, it decreased from the second period, with means of 21±12 at Ritto and 14±15 at Miho from 2010-2011 to 2012-2013. Vaccination coverage in the 3-year-old population was 99.4% at Ritto and 99.8% at Miho in the first period, and similar values were maintained thereafter. Coverage in the whole population increased more gradually than that in the 3-year-old population. The results suggested that EHV-1 epizootics can be suppressed by maintaining high vaccination coverage, not only in the 3-year-old population but also in the whole population.Clinical and vaccine Immunology: CVI 05/2014; 21(8). DOI:10.1128/CVI.00258-14 · 2.37 Impact Factor
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ABSTRACT: The equine herpesvirus type 1 (EHV-1) open reading frame 34 (ORF34) is predicted to encode a polypeptide of 161 amino acids. We show that an ORF34 deletion mutant exhibited a significant growth defect in equine peripheral blood mononuclear cells taken directly ex vivo during early but not late times of infection. ORF34 protein (pORF34)-specific antibodies specifically reacted with a 28-kDa early polypeptide present in the cytosol of infected cells. From 10 h post infection, multiple smaller pORF34-specific protein moieties were detected indicating that expression of a late viral gene product(s) caused pORF34 degradation. Proteasome inhibitors blocked pORF34 degradation as did treatment of infected cells with a ubiquitin-activating enzyme (E1) inhibitor. Finally, kinetic studies showed that pORF34 is modified by addition of multiple copies of ubiquitin. Taken together, our findings suggest that the ubiquitin proteasome pathway is required for pORF34 degradation that may modulate protein activity in the course of infection.Virology 07/2014; s 460–461:11–22. DOI:10.1016/j.virol.2014.05.009 · 3.28 Impact Factor