Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA139513 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Periodic outbreaks of highly pathogenic avian H5N1 influenza viruses and the current H1N1 pandemic highlight the need for a more detailed understanding of influenza virus pathogenesis. To investigate the host transcriptional response induced by pathogenic influenza viruses, we used a functional-genomics approach to compare gene expression profiles in lungs from wild-type 129S6/SvEv and interferon receptor (IFNR) knockout mice infected with either the fully reconstructed H1N1 1918 pandemic virus (1918) or the highly pathogenic avian H5N1 virus Vietnam/1203/04 (VN/1203).
2013-07-16 | GSE48890 | GEO
Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease. Calu-3 cells were infected with VN1203 influenza virus and profiled at 0, 3, 7, 12, 18, and 24 hours post infection. There are 3 mock and infected replicates for each time point.
2011-09-01 | E-GEOD-28166 | biostudies-arrayexpress
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.
2022-08-22 | PXD002719 | Pride
Project description:To study miRNA expression profiles during highly pathogenic avian influenza virus infection, we conducted global miRNA expression profiling in human lung epithelial cells (A549) with or without H5N1 IAV infection. .
2014-09-25 | GSE61701 | GEO
Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease.
2011-09-02 | GSE28166 | 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. 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: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: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: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