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Title: Variable regulation of chicken embryo fibroblasts gene expression by H5N1 avian influenza viruses

Author
item Sarmento, Luciana
item Pantin Jackwood, Mary
item Afonso, Claudio
item Wasilenko, Jamie
item Estevez, Carlos

Submitted to: International Poultry Forum Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 10/29/2007
Publication Date: 1/21/2008
Citation: Sarmento, L., Pantin Jackwood, M.J., Afonso, C.L., Wasilenko, J.L., Estevez, C. 2008. Variable regulation of chicken embryo fibroblasts gene expression by H5N1 avian influenza viruses [abstract]. International Poultry Scientific Forum, January 21-22, 2008, Atlanta, Georgia. p. 33.

Interpretive Summary:

Technical Abstract: Highly pathogenic avian influenza viruses (HPAIVs) cause severe clinical disease associated with high mortality in chickens and other gallinaceous species. However, the mechanism by which different strains of AIV overcome host response is still not clear. In the present study, differences in early transcriptional host responses were evaluated by infecting chicken embryo fibroblasts (CEF) with two highly pathogenic H5N1 avian influenza viruses, CK/HK/220/97 and Egret/HK/757.2/02. A complete chicken genome microarray was used to assess differences in gene expression between cells infected with either virus. A total of 191 genes showed differential expression by two-fold or more at 4 hpi when comparing the two viruses. Gene ontology revealed that the differentially expressed genes are involved in many vital functional classes including immunity/cytokinesis, apoptosis, transcription, cell cycle and proliferation and development. Semi-quantitive RT-PCR was used to validate the differential expression of selected genes from different categories and to investigate whether these genes and/or other genes were induced or suppressed later in the infection. It was found that CK/HK/220/97 is a stronger inducer of the innate immune response in CEF than Egret/HK/757.2/02, particularly IFN-a and the Mx gene. Our data suggest that avian influenza viruses may use different mechanisms and multiple strategies to evade host response.