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Altered pro-inflammatory cytokine mRNA levels in chickens infected with infectious bronchitis virus

Infectious bronchitis virus (IBV) replicates primarily in the respiratory tract and grows in various organs in chickens, with or without pathological effects. The diversity of this virus has been verified by sequence analysis of the S1 glycoprotein gene, but this method must be supplemented with fur...

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Detalles Bibliográficos
Autores principales: Jang, Hyesun, Koo, Bon-Sang, Jeon, Eun-Ok, Lee, Hae-Rim, Lee, Sang-Myeong, Mo, In-Pil
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Poultry Science Association Inc. Published by Elsevier Inc. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7194964/
https://www.ncbi.nlm.nih.gov/pubmed/23960111
http://dx.doi.org/10.3382/ps.2013-03116
Descripción
Sumario:Infectious bronchitis virus (IBV) replicates primarily in the respiratory tract and grows in various organs in chickens, with or without pathological effects. The diversity of this virus has been verified by sequence analysis of the S1 glycoprotein gene, but this method must be supplemented with further analysis for characterization of the agent. To increase our understanding of the pathogenesis of the disease caused by this virus, we investigated the response of chickens to 2 IBV with different genotypes, KIIa and ChVI. The clinical signs induced by the viruses were observed. In addition, the mRNA levels of the pro-inflammatory cytokines, IL-6, IL-1β, and lipopolysaccharide-induced tumor necrosis factor-α factor and the serum levels of α(1)-acid glycoprotein, which is a major acute phase protein, were measured. The KIIa genotype (Kr/ADL110002/2011) induced clinical signs accompanied by the excessive production of pro-inflammatory cytokines and a higher viral load. In chickens infected with this isolate, simultaneous peaks in the viral copy number and cytokine production were observed at 7 dpi in the trachea and 9 d postinoculation in the kidney. On the other hand, the chickens infected with the ChVI genotype (Kr/ADL120003/2012) did not show a response other than a mild upregulation of cytokines at 1 d postinoculation, which appears to indicate the invasion of the virus. In summary, we confirmed a differential innate response following infection with distinct IBV. We hypothesize that an excessive innate response contributes to the scale of the pathophysiologic effect in chickens.