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The age of the chicken at the time of infection with infectious avian encephalomyelitis virus (IAEV) and the route of the administration of the virus had a marked effect on the development of the clinical disease. Chickens given the virus by intramuscular, intraperitoneal and oral routes exhibited a decreased susceptibility to development of clinical disease with increasing age. Irrespective of age, chickens were consistently susceptible to intracerebral inoculation of IAEV. Chickens infected with the virus at 1-, 7- and 14-days of age developed lower neutralising antibody titres to IAEV than chickens infected at 21 and 28 days. A relationship between the ability to produce specific neutralising antibody to IAEV and susceptibility to the development of clinical disease is discussed.

Normal chickens given infectious avian encephalomyelitis virus (IAEV) orally at 1, 7 or 14 days of age developed infectious avian encephalomyelitis (IAE), whereas those dosed with the virus at 21, 28 and 35 days of age did not. Chickens in all of these age groups that had been treated with cyclophosphamide or testosterone developed clinical IAE. Intraperitoneal inoculation of IAEV immunoglobulin at the time of dosing with the virus, or 48 hours later, protected normal and immunosuppressed chickens against the onset of clinical IAE. The titre of IAEV serum neutralising antibody was found to be lower in normal chickens given the virus at 1, 7 and 14 days of age in older chickens. These results suggest a significant role for the humoral immune system in the pathogenesis of IAE and in the development of immunity to the disease.

An immune response was induced in chickens vaccinated with the NSW-1 virus by the intramuscular, eye drop, wing web or oral methods. The oral procedure was the most sensitive in inducing an immune response with the lowest dose of virus. The wing web method was the least sensitive. Clinical IAE developed in 1 chicken following intramuscular vaccination. The virus was recovered from the faeces of chickens vaccinated orally with 700 CID50 of the virus from the third to the tenth day after vaccination.

An association was demonstrated between the development of clinical infectious avian encephalomyelitis (IAE), the persistence and titre of infectious avian encephalomyelitis virus (IAEV) in the brain of the chicken, the duration of detectable viraemia and the age of the chicken at the time of infection with the virus. The older the chicken at the time of infection the milder the disease, the lower the virus titre in the brain and the shorter the period of viraemia. IAEV serum neutralising antibody was produced earlier after infection in older chickens, and its detection was associated with decreasing virus titres in the brain and the cessation of detectable viraemia. Treatment of chickens with testosterone in ova, to inhibit the development of antibody synthesis, prevented the onset of age-associated resistance and testosterone treated birds were as susceptible to clinical IAE as baby chickens. The results suggested that the ability to produce IAEV serum neutralising antibody was an important component of age-associated resistance to IAE.

Infectious avian encephalomyelitis virus (IAEV) maternal antibody was detected in the serum of chickens for up to 21 days following hatching. This antibody protected chickens against clinical IAE after intracerebral inoculation with van Roekel strain or oral administration of the NSW-1 strain of IAEV. Maternal antibody to IAEV also protected testosterone bursectomised chickens against the development of clinical disease. IAEV maternal antibody also influeced the pattern of virus excretion in faeces and serological responsiveness. This influence on antibody responses persisted beyond the time that IAEV maternal antibody could be detected. The importance of IAEV maternal antibody on the strategy of vaccination against IAE is discussed.