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Maternal antibody inhibition of recombinant Newcastle disease virus vectored vaccine in a primary or booster avian influenza vaccination program of broiler chickens

Kateri Bertran, Dong-Hun Lee, Miria F. Criado, Charles L. Balzli, Lindsay F. Killmaster, Darrell R. Kapczynski, David E. Swayne
Vaccine 2018 v.36 no.43 pp. 6361-6372
broiler chickens, Meleagrid alphaherpesvirus 1, antibodies, Influenza A virus, influenza vaccination, vaccines, Avian orthoavulavirus 1, avian influenza, immune response, active immunity, progeny, viral shedding, chicks, mortality
Maternally-derived antibodies (MDA) provide early protection from disease, but may interfere with active immunity in young chicks. In highly pathogenic avian influenza virus (HPAIV)-enzootic countries, broiler chickens typically have MDA to Newcastle disease virus (NDV) and H5 HPAIV, and their impact on active immunity from recombinant vectored vaccines is unclear. We assessed the effectiveness of a spray-applied recombinant NDV vaccine with H5 AIV insert (rNDV-H5) and a recombinant turkey herpesvirus (HVT) vaccine with H5 AIV insert (rHVT-H5) in commercial broilers with MDA to NDV alone (MDA:AIV−NDV+) or to NDV plus AIV (MDA:AIV+NDV+) to provide protection against homologous HPAIV challenge. In Experiment 1, chicks were spray-vaccinated with rNDV-H5 at 3 weeks (3w) and challenged at 5 weeks (5w). All sham-vaccinated progeny lacked AIV antibodies and died following challenge. In rNDV-H5 vaccine groups, AIV and NDV MDA had completely declined to non-detectable levels by vaccination, enabling rNDV-H5 spray vaccine to elicit a protective AIV antibody response by 5w, with 70–78% survival and significant reduction of virus shedding compared to shams. In Experiment 2, progeny were vaccinated with rHVT-H5 and rNDV-H5 at 1 day (1d) or 3w and challenged at 5w. All sham-vaccinated progeny lacked AIV antibodies and died following challenge. In rHVT-H5(1d) vaccine groups, irrespective of rNDV-H5(3w) boost, AIV antibodies reached protective levels pre-challenge, as all progeny survived and virus shedding significantly decreased compared to shams. In contrast, rNDV-H5-vaccinated progeny had AIV and/or NDV MDA at the time of vaccination (1d and/or 3w) and failed to develop a protective immune response by 5w, resulting in 100% mortality after challenge. Our results demonstrate that MDA to AIV had minimal impact on the effectiveness of rHVT-H5, but MDA to AIV and/or NDV at the time of vaccination can prevent development of protective immunity from a primary or booster rNDV-H5 vaccine.