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ABSTRACT:
PROVIDER: PRJNA380165 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5367444.fastq.gz | Fastqsanger.gz |
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Project description:With the purpose to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus at 24 hours post-infection(hpi) and fowl adenovirus-4 at 48 dpi. The spleens of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 2426 differentially expressed genes were obtained in the duck-origin H7N9 subtype avian influenza virus group, including 913 up-regulated genes and 1513 down-regulated genes, and there were 1534 differentially expressed genes were obtained in the fowl adenovirus-4 group, including 632 up-regulated genes and 902 down-regulated genes.
2020-06-03 | GSE151662 | GEO
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: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: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: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.
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Project description:Ducks and wild aquatic birds are the natural reservoirs of avian influenza viruses. However, the host proteome response that causes disease in vivo during infection by the highly pathogenic avian influenza (HPAI) H5N1 virus is still not well understood. In the present study, we compared the proteome response in Muscovy duck lung tissue during 3 day of infection with either a highly virulent or an avirulent H5N1 virus. During infection, proteins involved in immune response of neutrophils and size of cells were increased markedly in the lung by the virulent strain, while the avirulent strain evoked a distinct response, characterized by an increase in proteins involved in cell movement, maturation of dendritic cells, adhesion of phagocytes, and immune response of macrophages.
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Project description:In order to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus. The lungs of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus were collected and high throughout sequenced. Compared with the control group, there were 740 differentially expressed genes were obtained in infection group, including 602 up-regulated genes and 138 down-regulated genes. The analysis of the GO items showed that the differentially expressed genes were involved in immune responses and inflammatory responses. The results of KEGG analysis showed that 7 pathways were enriched significantly, in those the Toll-like pathway had 11 up-regulated genes, namely IL-6, TLR4, Pik3, IRF7, MD-2, IRF5, MYD88, CD86, STAT1, TLR2, and CCL4. There were 7 up-regulated genes in NOD-like receptor signaling pathway, which were IRF7, CTSB, P2RX7, CYBB, PSTPIP1, HSP90AA1, and NAMPT. In Toll-like signaling pathway，TLR4 was activated by MD-2 after viral infection, and then activated downstream IRF5. At the same time, the NLRP3 inflammasome also played an important role in the process of H7N9 virus infection.
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Project description:Transcriptional profiling of chicken embryonic fibroblasts (DF-1 cells) comparing the effects of chicken cells transfected with duck RIG-I compared to empty-vector transfected cells following with low or highly pathogenic avian influenza. Goal was to determine the effects of duck RIG-I on influenza-induced immune gene expression.
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