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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Exotic & Emerging Avian Viral Diseases Research » Research » Publications at this Location » Publication #307304

Title: Assessment of NDV neuropathogenesis through the ICPI model

item MOURA, VERIDIANA - US Department Of Agriculture (USDA)
item Susta, Leonardo
item BROWN, CORRIE - University Of Georgia
item Miller, Patti
item CARDENAS GARCIA, STIVALIS - University Of Georgia
item Afonso, Claudio

Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 9/11/2014
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Newcastle disease (ND) is caused by virulent strains of Newcastle disease virus (NDV). The intracerebral pathogenicity index (ICPI) is the internationally recognized system used to assess the virulence of NDV strains, and because of the direct inoculation of the virus in the brain, here it was used to assess the neurovirulence and neurotropism of different NDV strains. Seven NDV strains (4 velogenic, 2 mesogenic, 1 lentogenic) were evaluated for lesion-inducing ability (HE) and viral replication (immunohistochemistry, IHC) in the nervous tissue of chicks inoculated through the ICPI method. Velogenic strains induced death of all infected birds, accompanied by severe lesions (edema, inflammation of ependyma and choroid plexus) and extensive replication in the nervous tissue by day 2 post-infection (pi). Pathogenesis of mesogenic strains was slightly delayed compared to velogenic strains, with a similar pattern of lesions and virus replication at day 3 and 4 pi, when all birds died. The lentogenic NDV strain did not cause death of infected birds, and minimal virus replication was observed only in the epithelium of the ependyma and choroid plexus. By day 3 pi, the lentogenic strain caused lymphoid proliferaton within the chorioid plexus and in scattered subependymal areas, suggesting a reaction to local virus replication. Results show that extensive NDV replication in the brain is typical of both velogenic and mesogenic strains, but not lentogenic NDV strains. In addition, this study suggests that differences in the rate of progression of neurovirulence, but not differences in neurotropism, differentiate mesogenic from velogenic NDV strains. Lastly, our data suggest that the ICPI method might be used as a model to investigate NDV neuropathogenesis.