Abstract
Vaccination is one of the most effective tools for limiting the impact of equine influenza (EI). The humoral immunity established following a primary vaccination course can decrease significantly between the second (V2) and third immunisations (V3), leaving some horses insufficiently protected for several weeks. This so-called “immunity gap” poses a challenge to all EI vaccines. During this period, the EI infection of vaccinated animals may be followed by marked clinical signs and virus shedding. However, several EI vaccines have been shown to stimulate equine influenza virus (EIV)-specific cell-mediated immunity, which is likely to play a role in protection against EIV infection and/or mitigate the clinical and virological signs of EI. Reducing the interval between V2 and V3 has been shown to be counterproductive to longer-term immunity. Further research is needed to define and address the “immunity gap” in horses. This study aimed to measure the level of protection induced by a whole inactivated, ISCOMatrix adjuvanted, EI and tetanus vaccine (Equilis Prequenza-Te) when challenged during the immunity gap (i.e., immediately before the recommended boost immunisation, more than 5 months after V2) using infection with a recent heterologous Florida Clade 2 (FC2) equine influenza virus (EIV) strain. This vaccine was tested in a Welsh mountain pony model. A group of seven ponies was vaccinated twice, 4 weeks apart. The protective antibody response was measured and ponies were challenged, along with 5 unvaccinated control ponies, by experimental infection with the FC2 A/eq/Northamptonshire/1/13 EIV strain, 158 days (around 5.2 months) after V2 and their clinical signs and virus shedding were monitored. EI serology was measured by single radial haemolysis (SRH) and haemagglutination inhibition (HI). Clinical signs and virus shedding (measured by qRT-PCR and hen’s egg titration) were compared with controls. All vaccinates had detectable, low SRH antibody titres and most had detectable, low HI titres. Significant clinical and virological protection was observed in vaccinates (p < 0.05), supporting the good performance of this vaccine against a recent EIV strain. In this study, the impact of the immunity gap in ponies was limited after primary vaccination with this whole inactivated, ISCOMatrix adjuvanted EI and tetanus vaccine (Equilis Prequenza-Te) when infected several months after V2 with a recent FC2 strain, which is representative of EIV circulating in the EU.
Highlights
Equine influenza (EI) is a major viral respiratory disease in horses associated with high morbidity and potential catastrophic economic consequences [1]
The impact of the immunity gap in ponies was limited after primary vaccination with this whole inactivated, ISCOMatrix adjuvanted EI and tetanus vaccine (Equilis Prequenza-Te) when infected several months after V2 with a recent Florida Clade 2 (FC2) strain, which is representative of equine influenza virus (EIV) circulating in the EU
It is important to note that most EI vaccines have been shown to stimulate EIV-specific cell-mediated immunity [2], which is likely to play a role in protection against EIV infection and/or in the mitigation of clinical signs and virus shedding following EIV infection
Summary
Equine influenza (EI) is a major viral respiratory disease in horses associated with high morbidity and potential catastrophic economic consequences [1]. The EI vaccines available commercially reduce the clinical signs and virus shedding following EIV infection and do not generally produce long-lasting sterilising immunity (i.e., protection against infection beyond what is demonstrated at or around onset of immunity (2–3 weeks after V2)) Such protection is primarily correlated with the level of circulating antibodies to EIV, with the single radial haemolysis (SRH) and haemagglutination inhibition (HI) assays being suitable for measuring EIV haemagglutinin (HA)-specific antibody titres in horses [8]. Thresholds have been defined previously for SRH antibody titres that correlate positively with a reduction in clinical signs of EI (titres > 85 mm2 ) and virus shedding (titres > 120–154 mm2 ) after infection with an EIV strain that is homologous to the virus strain contained in the vaccine [9,10] This is supported by more recent experimental EI vaccine studies and field data [2,6]
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