Virological and serological investigation of Equid herpesvirus 1 infection in New Zealand

•Survey of EHV-1 infection among 52 slaughter horses in New Zealand is described.•32.7% horses tested positive for EHV-1 DNA in lymph nodes or trigeminal ganglia.•Our data comprise the first detection of EHV-1 with D752 genotype in New Zealand.•100% and 21.1% of horses were positive for EHV-4 and EHV-1 antibody, respectively.•The strength of agreement between results of EHV-1 PCR and EHV-1 serology was “fair”. Infection with equid herpesvirus 1 (EHV-1) may be asymptomatic, or may result in respiratory disease, abortion, neonatal death, or neurological disease. The aim of this study was to estimate the prevalence of EHV-1 infection, including differentiation between genotypes with aspartic acid (D) and asparagine (N) at position 752 of the DNA polymerase sequence, within a selected population of New Zealand horses. The second aim was to determine the predictive value of serology for detection of latently infected horses. Retropharyngeal lymph nodes (RLN) and trigeminal ganglia (TG) were dissected from 52 horses at slaughter and tested for the presence of EHV-1 DNA using magnetic bead, sequence-capture enrichment followed by nested PCR. Sera were tested for EHV-1 antibody using type-specific glycoprotein G ELISA. Overall, 17/52 horses tested positive for EHV-1 DNA. All but one positive PCR results were obtained from RLN samples. Fifteen of the EHV-1 positive horses harboured EHV-1 with N752 genotype, one of which was additionally infected with the D752 genotypes of the virus. Our data comprise the first detection of EHV-1 with D752 genotype in New Zealand and suggest that the “neurovirulent” variant of EHV-1 had been present in New Zealand for at least two years before the first reported outbreak of EHM. All sampled horses tested positive for EHV-4 antibody, and 11/52 tested positive for EHV-1 antibody. The strength of agreement between results of EHV-1 PCR and EHV-1 serology was “fair” (Kappa 0.259, 95% CI: −0.022–0.539), which was likely a reflection of low levels of both EHV-1 antibody in sera and EHV-1 DNA in tissues tested.