Abstract
Neonatal foals respond poorly to conventional vaccines. These vaccines typically target T-helper (Th) cell dependent B-cell activation. However, Th2-cell immunity is impaired in foals during the first three months of life. In contrast, neonatal basophils are potent interleukin-4 (IL-4) producers. The purpose of this study was to develop a novel vaccine triggering the natural capacity of neonatal basophils to secrete IL-4 and to evaluate if vaccination resulted in B-cell activation and antibody production against EHV-1 glycoprotein C (gC). Neonatal vaccination was performed by oral biotinylated IgE (IgE-bio) treatment at birth followed by intramuscular injection of a single dose of streptavidin-conjugated gC/IL-4 fusion protein (Sav-gC/IL-4) for crosslinking of receptor-bound IgE-bio (group 1). Neonates in group 2 received the intramuscular Sav-gC/IL-4 vaccine only. Group 3 remained non-vaccinated at birth. After vaccination, gC antibody production was not detectable. The ability of the vaccine to induce protection was evaluated by an EHV-1 challenge infection after weaning at 7 months of age. Groups 1 and 2 responded to EHV-1 infection with an earlier onset and overall significantly increased anti-gC serum antibody responses compared to control group 3. In addition, group 1 weanlings had a decreased initial fever peak after infection indicating partial protection from EHV-1 infection. This suggested that the neonatal vaccination induced a memory B-cell response at birth that was recalled at weanling age after EHV-1 challenge. In conclusion, early stimulation of neonatal immunity via the innate arm of the immune system can induce partial protection and increased antibody responses against EHV-1.
Highlights
Equine herpesvirus type-1 (EHV-1) is member of the Varicellovirus genus in the Alphaherpesvirinae subfamily that is highly prevalent in most equine populations [1,2,3]
EHV-1 glycoprotein C (gC) and glycoprotein D (gD)-specific antibody values were measured in sera of all foals immediately after birth, before and after neonatal EHV-1 vaccination until foals were 3 months of age
While anti-immunoglobulin E (IgE) stimulated IL-4 production by basophils, as expected, Sav-gC/IL-4 fusion protein (gC/IL-4) stimulation did not result in detectable percentages of IgE+/IL-4+ cells (S2 Fig)
Summary
Equine herpesvirus type-1 (EHV-1) is member of the Varicellovirus genus in the Alphaherpesvirinae subfamily that is highly prevalent in most equine populations [1,2,3]. EHV-1 has a substantial impact on equine health and equine industries worldwide through respiratory disease, abortion, and encephalomyelopathy [3,4]. Most horses are first infected early in life and are believed to remain latently infected for life. Infected, lactating mares act as source of infection for their foals after birth, which in turn infect other foals and weanlings [1,2,5]. The virus is spread with respiratory secretions via direct nose-to-nose contact or contact with fomites. From here the virus spreads systemically via a cell-associated viremia, and latency is established in the trigeminal ganglion and possibly some long-lived immune cells [6,7]. EHV-1 is reactivated from the latent state and is shed again during times of stress, and all clinical manifestations may be seen during recrudescence [3]
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