Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq for splenic gene expression in response to Newcastle disease virus challenge in Hy-Line Brown chickens

ABSTRACT: In order to have a better understanding about genetic regulation of response to NDV challenge, and also to identify the candidate genes regulating disease resistance in combination with GWAS, gene expression in spleen of Hy-Line Brown chickens was investigated. The chickens were divided into two groups (8 chickens/group) that are respectively treated by NDV(200 ul of 108 EID50%) and Phosphate-buffered saline (PBS) through nasal and ocular inoculation routes at 21 days post hatch. Gene expression in spleen was then detected by RNA-seq at 2 and 6 day post inoculation (dpi).

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Gallus gallus

SUBMITTER: Jibin Zhang

PROVIDER: E-MTAB-8350 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Highly pathogenic avian influenza virus (HPAIV) is a permanent threat due to its capacity to cross species barriers and generate severe infections and high mortality in humans. Recent findings have highlighted the potential role of PB1-F2, a small accessory influenza protein, in the pathogenesis process mediated by HPAIV in mammals. In this study, using a recombinant H5N1 HPAIV (wt) and its PB1-F2-deleted mutant (M-NM-^TF2), we studied the effects of PB1-F2 in a chicken model. Unexpectedly, when using low inoculation dose we observed that the wt-infected chickens had a higher survival rate than the M-NM-^TF2-infected chickens, a feature that contrasts with what is usually observed in mammals. High inoculation dose had similar mortality rate for both viruses, and comparison of the bio-distribution of the two viruses indicated that the expression of PB1-F2 allows a better spreading of the virus within chicken embryos. Transcriptomic profiles of lungs and blood cells were characterized at two days post-infection in chickens inoculated with the wild type (wt) or the M-NM-^TF2 mutant viruses. In lungs, the expression of PB1-F2 during the infection induced pathways related to calcium signaling and repressed a large panel of immunological functions. In blood cells, PB1-F2 was associated to a gene signature specific for mitochondrial dysfunction and down-modulated leucocytes activation. Finally we compared the effect of PB1-F2 in lungs of chickens and mice. We identified that gene signature associated to tissue damages is a PB1-F2 feature shared by the two species; by contrast, the early inhibition of immune response mediated by PB1-F2 observed in chickens is not seen in mice. In summary, our data suggest that PB1-F2 expression deeply affect the immune host response in chickens in a way that may attenuate pathogenicity, a feature differing from what was previously observed in mammal species. Three-condition experiment, virus-infected (wt or M-NM-^TF2) vs. Mock-infected chickens. Biological replicates: 2x5 control replicates, 5 wt replicates, 5 M-NM-^TF2 replicates.

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RNA-seq for splenic gene expression in response to Newcastle disease virus challenge in Hy-Line Brown chickens

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