Abstract
Influenza viruses cause severe respiratory infections in humans and birds, triggering global health concerns and economic burden. Influenza infection is a dynamic process involving complex biological host responses. The objective of this study was to illustrate global biological processes in ileum and cecal tonsils at early time points after chickens were infected with low pathogenic avian influenza virus (LPAIV) H9N2 through transcriptome analysis. Total RNA isolated from ileum and cecal tonsils of non-infected and infected layers at 12-, 24- and 72-h post-infection (hpi) was used for mRNA sequencing analyses to characterize differentially expressed genes and overrepresented pathways. Statistical analysis highlighted transcriptomic signatures significantly occurring 24 and 72 hpi, but not earlier at 12 hpi. Interferon (IFN)-inducible and IFN-stimulated gene (ISG) expression was increased, followed by continued expression of various heat-shock proteins (HSP), including HSP60, HSP70, HSP90 and HSP110. Some upregulated genes involved in innate antiviral responses included DDX60, MX1, RSAD2 and CMPK2. The ISG15 antiviral mechanism pathway was highly enriched in ileum and cecal tonsils at 24 hpi. Overall, most affected pathways were related to interferon production and the heat-shock response. Research on these candidate genes and pathways is warranted to decipher underlying mechanisms of immunity against LPAIV in chickens.
Highlights
Influenza viruses cause severe respiratory infections in humans and birds, triggering global health concerns and economic burden
Global profiles of differentially expressed (DE) genes in chicken infected with low pathogenic Avian influenza viruses (AIVs) subtype H9N2
Transcriptomic changes were detectable in cecal tonsils and peaked at 24 hpi
Summary
Influenza viruses cause severe respiratory infections in humans and birds, triggering global health concerns and economic burden. The objective of this study was to illustrate global biological processes in ileum and cecal tonsils at early time points after chickens were infected with low pathogenic avian influenza virus (LPAIV) H9N2 through transcriptome analysis. Several studies have interrogated transcriptomics of host responses to LPAIV and highly pathogenic A IV24–26 These studies have revealed a complex network of immune responses initiated by avian influenza viruses, at cellular and tissue levels, in the respiratory tract24,27–30, ileum[8,31], dendritic cells[25] and chicken embryonic fibroblasts[32]. Pattern-recognition receptors (PRRs) are the host’s innate immune sensors, and at least three distinct classes of PRRs recognize influenza virus infection[33,34] This recognition leads to secretion of cytokines, chemokines and antimicrobial peptides by cells, including dendritic cells and macrophages. Viral NS1 targets melanoma differentiation-associated protein 5 (MDA5) and directly interferes with the function of different I SGs37,38
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