Avian adenoviruses were isolated from two pigeons affected with inclusion body hepatitis (IBH) by using chicken embryo liver cell cultures. One of the isolates, designated strain S-PL1, replicated in the cell nuclei forming intranuclear inclusion bodies, showed adenovirus-like morphology by electron microscopy, and cross-reacted serologically with strain SR-48 known as serotype 2 of fowl adenovirus. The strain S-PL1 killed day-old chicks by subcutaneous inoculation, and its 50% chicken lethal dose was 10(3.8) plaque forming units per bird. Severe lesions characterized with IBH and pancreatitis, were produced in chicks inoculated with the virus. Intranuclear inclusion bodies were also recognized in the liver, pancreas, kidney, proventriculus, small intestine, and caecum. By indirect immunofluorescence test, intranuclear viral antigens were detected in the liver, pancreas and other tissues.

SUMMARYHigh virus-neutralizing antibodies were induced in specific-pathogen-free breeding hens by administration of live and killed avian nephritis virus (ANV), strain M-8, antigens. Ten-day-old embryos from immune hens survived challenge by ANV which was administered by the yolk sac or allantoic cavity route. When the progeny chicks from immune dams were infected with ANV orally or by contact challenge, the virus replicated in the intestine. However, they were protected against pathological damage and virus replication in the kidney. The chicks without maternal antibodies showed apparent renal lesions and virus replication to high titre in the kidneys.

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The pathogenicities of three cytopathic avian enteroviruses, strains AAF7, M-8, and G-4260 which were classified as avian nephritis viruses, were compared following inoculation into chicken kidney cell (CKC) cultures, embryonating eggs, and 1-day-old chicks. Strain M-8 produced the largest plaques, highest yields in CKC cultures, highest pathogenicity for embryonating eggs, and severest lesions in the kidney of experimentally-infected chicks. In contrast, strain AAF7 was the least pathogenic. All strains caused growth retardation and nephritis in experimentally-infected chicks.