Abstract

Background: The molecular pathogenesis of avian influenza viruses vary greatly with individual bird species and virus strain. The molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or the low pathogenic avian influenza virus (LPAIV) in avian species remains poorly understood. Methods & Materials: Thus, global immune response of chickens infected with HPAI H5N1 (A/duck/India/02CA10/2011) and LPAI H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. Results: HPAI H5N1 virus induced excessive mRNA expression of type I IFNs (IFNA and IFNG), cytokines (IL1B, IL18, IL22, IL13, and IL12B), chemokines (CCL4, CCL19, CCL10, and CX3CL1) and IFN stimulated genes (OASL, MX1, RSAD2, IFITM5, IFIT5, GBP 1, and EIF2AK) in lung tissues. This dysregulation of host innate antiviral genes may be the critical determinant of the severity and the outcome of the influenza infection in chickens. In contrast, the expression levels of most of these genes remained unchanged in the lungs of LPAI H9N2 virus infected chickens. Conclusion: This study indicated the relationship between host antiviral genes and their roles in pathogenesis of HPAIV infection in chickens.

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