Transcriptional profiles of chicken embryo cell cultures following infection with infectious bursal disease virus

Infectious bursal disease virus (IBDV) is the causative agent of infectious bursal disease in chickens and causes a significant economic loss for the poultry industry. Little is understood about the mechanism involved in the host responses to IBDV infection. For better understanding the IBDV-host in...

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Bibliographic Details
Published in:Archives of virology Vol. 152; no. 3; pp. 463 - 478
Main Authors: Li, Y. P, Handberg, K. J, Juul-Madsen, H. R, Zhang, M. F, Jørgensen, P. H
Format: Journal Article
Language:English
Published: Wien Vienna : Springer-Verlag 01-03-2007
New York, NY Springer
Springer Nature B.V
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Summary:Infectious bursal disease virus (IBDV) is the causative agent of infectious bursal disease in chickens and causes a significant economic loss for the poultry industry. Little is understood about the mechanism involved in the host responses to IBDV infection. For better understanding the IBDV-host interaction, we measured steady-state levels of transcripts from 28 cellular genes of chicken embryo (CE) cell cultures infected with IBDV vaccine stain Bursine-2 during a 7-day infection course by use of the quantitative real-time RT-PCR SYBR green method. Of the genes tested, 21 genes (IRF-1, IFN 1-2 promoter, IFNAR-1, IRF-10, IFN-γ, 2',5'-OAS, IAP-1, caspase 8, TRAIL-like, STAT-3, IL-6, IL-8, MIP-3α, MHC-I, MHC-II, TVB, GLVR-1, OTF, IL-13Rα, ST3GAL-VI and PGK) showed an increased expression. The remaining seven genes (IFNAR-2, IFN-α, NF-κB subunit p65, BLRcp38, DDX1, G6PDH and UB) showed a constant expression or only slight alteration. Apparently, the host genes involved in pro-inflammatory response and apoptosis, interferon-regulated proteins, and the cellular immune response were affected by IBDV infection, indicating involvement in the complex signaling pathways of host responses to the infection. This study thus contributes to the understanding of the pathogenesis of IBD and provides an insight into the virus-host interaction.
Bibliography:http://dx.doi.org/10.1007/s00705-006-0878-9
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ISSN:0304-8608
1432-8798
DOI:10.1007/s00705-006-0878-9