Gallus gallus
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ABSTRACT:
PROVIDER: PRJNA145915 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:H5N1 subtype highly pathogenic avian influenza virus has been spreading to Asia, Eurasia and African coutries. An original or six of recombinant H5N1 subtype influenza viruses with varying survivability were infected to chickens for elucidating genes correlated with pathogenicity.
2012-03-31 | GSE32378 | GEO
Project description:H5N1 subtype highly pathogenic avian influenza virus has been spreading to Asia, Eurasia and African coutries. An original or six of recombinant H5N1 subtype influenza viruses with varying survivability were infected to chickens for elucidating genes correlated with pathogenicity. Two chickens were infected with each 10^6EID50/ head virus intranasally, and their lung was collected from infected chicken at 24 hours after infection.
2012-03-30 | E-GEOD-32378 | biostudies-arrayexpress
Project description:While infection of chickens with highly pathogenic avian influenza (HPAI) H5N1 subtypes often leads to complete mortality within 24 to 48 h, infection of ducks in contrast causes mild or no clinical signs. Rapid onsets of fatal disease in chickens, but with no evidence of severe clinical symptoms in ducks, suggest underlying differences in their innate immune mechanisms. To understand the molecular basis for such difference, chicken and duck primary lung cells, infected with a low-pathogenicity avian influenza (LPAI) and two HPAI H5N1 viruses, were subjected to RNA expression profiling using Affymetrix Chicken GeneChip arrays. We used microarrays to analyze the gene expression profiles of primary chicken and duck lung cells infected with H2N3 LPAI and two H5N1 influenza virus subtypes to understand the molecular basis of host susceptibility and resistance. We have identified a set of key genes and pathways that could play an important role in mediating innate host resistance to avian influenza in chickens and ducks.
2014-12-04 | GSE33389 | GEO
Project description:While infection of chickens with highly pathogenic avian influenza (HPAI) H5N1 subtypes often leads to complete mortality within 24 to 48 h, infection of ducks in contrast causes mild or no clinical signs. Rapid onsets of fatal disease in chickens, but with no evidence of severe clinical symptoms in ducks, suggest underlying differences in their innate immune mechanisms. To understand the molecular basis for such difference, chicken and duck primary lung cells, infected with a low-pathogenicity avian influenza (LPAI) and two HPAI H5N1 viruses, were subjected to RNA expression profiling using Affymetrix Chicken GeneChip arrays. We used microarrays to analyze the gene expression profiles of primary chicken and duck lung cells infected with H2N3 LPAI and two H5N1 influenza virus subtypes to understand the molecular basis of host susceptibility and resistance. We have identified a set of key genes and pathways that could play an important role in mediating innate host resistance to avian influenza in chickens and ducks. 24 hours following infection, total RNA from cells was extracted. Replicate RNA samples from each of the virus-infected (H2N3, H5N1 50-92, or H5N1 ty-Ty) or mock-infected chicken and duck cells (4 treatment groups for each species) were used for microarray analysis. Each of the RNA samples was hybridized to one GeneChipM-BM-. Chicken Genome Array (Affymetrix), and a total of 16 array chips were used.
2014-12-04 | E-GEOD-33389 | biostudies-arrayexpress
Project description:Spleen transcriptome response to infection with avian pathogenic Escherichia coli in broiler chickens
| PRJNA133759 | ENA
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs.
2016-01-02 | GSE65231 | GEO
Project description:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from chickens infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.
2015-01-19 | E-MTAB-2908 | biostudies-arrayexpress
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs. Agilent Custom Chicken Gene Expression 8X60k (AMADID: G4102A_059389) designed by Genotypic Technology Private Limited , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2016-07-04 | E-GEOD-65231 | biostudies-arrayexpress
Project description:H5N1 highly pathogenic avian influenza (HPAI) has raised global concern for causing huge economic losses in poultry industry. By using reversal genetic technical, we have rescued a H5 wild-type virus rS and its NS1-truncated virus S-NS99, harboring only 99 amino acids in the amino terminus of NS1. We then used a high-throughput RNA-seq method to analyze host and pathogen transcriptomes in the lungs of chickens infected with rS and S-NS99. Sequenced numbers of viral transcripts and expression levels of host immune-related genes at 1 day post infection (dpi) were higher in rS-infected than S-NS99-infected chickens. The numbers of immune response of rS-infected chickens by Gene Ontology (GO) enrichment were higher than S-NS99-infected chickens. KEGG pathway analysis revealed rS infection could provoke significantly stronger immune response than S-NS99. Collectively, our data provide new insight into the underlying mechanisms of the differential length NS1 of avian influenza viruses.
2018-05-25 | GSE114880 | GEO
Project description:Relative expression levels of mRNAs in chicken cecal epithelia experimentally infected with Eimeria tenella were measured at 4.5 days post-infection. Two weeks old chickens were uninfected (negative control) or were orally inoculated with sporulated oocysts of Eimeria tenella. Cecal epithelia samples were collected from >12 birds in infected or uninfected group at 4.5 d following infections, in which samples from 4 birds were pooled together to form a total 3 biological replicates in each group. Parasite merozoites were also collected from four infected chickens at 5 d after infections. Uninfected control samples, merozoites and infection group samples were selected for RNA extraction and hybridization on Affymetrix microarrays. We used Affymetrix GeneChip chicken genome arrays to detail the chicken cecal epithelia gene expression in the control and E. tenella-infected birds.
2012-12-10 | GSE39602 | GEO