Pathogenesis, tissue tropism, and biochemical characterization of pneumotropic, nephrotropic, and vaccine strains of the infectious bronchitis virus

Abstract

The experiments were performed to determine the pathogenesis, tissue tropism, and persistence of Australian T, Arkansas 99, and Holland 52 infectious bronchitis viruses (IBV), and to compare protein and nucleic acid profiles of pneumotropic and nephrotropic IBV using SDS-PAGE, immunoblotting and oligonucleotide fingerprinting techniques. Tracheal lesions caused by each isolate were similar in chickens inoculated by the eyedrop or intracardiac routes, differing only in severity. Eyedrop administration with Arkansas 99 produced most severe lesions. Lesions included desquamation of ciliated and glandular epithelium at two days postinfection. Later, basal cell proliferation and inflammatory cell infiltration were seen. Epithelial maturation followed. Renal lesions in chickens inoculated with Australian T or Holland 52-IBV were degeneration and necrosis of cortical tubules, and interstitial lymphocytic infiltration on day 4 postinfection. Cystic dilation, necrosis and sloughing of tubular epithelium, and diffuse interstitial lymphocytic infiltration were present on day 8, especially in the medulla. Regeneration of tubules followed and was advanced on day 11. Glomeruli were not affected. No renal lesions were present in the Arkansas 99-infected chickens. Lesions were absent in the bursae of Fabricius. Virus isolation studies demonstrated that IBV could be recovered from trachea through day 14 postinfection and from cecal tonsils and kidney through day 29. The eye was not a reliable source at any time. Electron microscopy studies demonstrated that Arkansas 99 and Australian T-IBV replicated in the tracheal epithelium, and Australian T-IBV replicated in renal tubular epithelium. The spike and matrix proteins of the IBV isolates had similar electrophoretic mobility. The nucleocapsid protein of the Arkansas vaccine virus migrated slower than the nucleocapsid proteins of the other isolates. The nucleocapsid protein of the Arkansas-field virus was not detected. Immunoblot studies indicated common antigens were present in the proteins of Massachusetts 41, Holland 52, Gray, and Australian T-IB viruses, although antisera to the Australian T-IBV reacted only with the matrix proteins of Australian T-IBV. Regardless of their antigenic similarities, fingerprint analysis of the genomes of Australian T, Massachusetts 41, and Arkansas DPI-IB viruses indicated these viruses were genetically distinct. The patterns of the T1 ribonuclease generated oligonucleotides were dissimilar.