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Title:   Author  item
                                            Lillehoj, Hyunitem
                                            KIM, CHUL-HONG - VIS SCI ANRI,ARSitem
                                            KAPCZYNSKI, DARREL - USDA,ARS ATHENS,GAitem
                                            KEELER, CALVIN - UNIV DE NEWARK,DE
  Submitted to: Avian Immunology Group Meeting
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 7/23/2008
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: In this study, we applied functional genomics tools to investigate the early immunological  response of chickens to highly pathogenic (HP) avian influenza virus (AIV). Infection with HPAIV usually results in the rapid death of  poultry. The aim of this study was to identify host immune genes which are associated with local immune response to HPAIV H5N1 isolated from Southeast Asia. Gene mRNA expression profiles isolated from spleen and Peyer’s patch, from naïve and vaccinated chickens, were examined after infection with HPAI using a newly developed 10K chicken intestinal-intraepithelial lymphocyte cDNA microarray. Two groups (naïve or H5N9-vaccinated) of 4 week-old chickens were infected with H5N1 viruses.  Comparative gene expression in the spleen and Peyer’s patches were compared to that of mock challenged birds at 24 hr following AI infection using Volcano plot methods with p<0.05 false discovery rate. Differential expression analysis revealed that the immune response genes, especially those associated with inflammation and apoptosis including Ah221, CCL4, CXCR4, FCGBP1, DDX47, IL1R1, TNFSF10, TFNSF15, and XCL1 were significantly downregulated in the Peyer’s patches of vaccinated chickens challenged with H5N1, compared to naïve-challenged birds. These results suggest that the  vaccination reduces the viral pathogenicity induced by highly pathogenic H5N1 mostly via the dampening of “cytokine storm” phenomenon.


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