Chicken Infections
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45365 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5985340.fastq.gz | Fastqsanger.gz | |||
| ERR5985590.fastq.gz | Fastqsanger.gz | |||
| ERR5985600.fastq.gz | Fastqsanger.gz | |||
| ERR5985790.fastq.gz | Fastqsanger.gz | |||
| ERR5985601.fastq.gz | Fastqsanger.gz |
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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: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: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:Viral pneumonia has been frequently reported during early stages of influenza virus pandemics and in many human cases of highly pathogenic avian influenza (HPAI) H5N1 virus infection. To better understand the pathogenesis of this disease, we produced non-lethal viral pneumonia in rhesus macaques by using an HPAI H5N1 virus (A/Anhui/2/2005; referred to as Anhui/2). Infected macaques were monitored for 14 days, and tissue samples were collected at 6 time points for virologic, histopathologic and transcriptomic analyses.
2012-04-11 | GSE37149 | GEO
Project description:Current prophylactic and therapeutic strategies targeting human influenza viruses include vaccines and antivirals. Given variable rates of vaccine efficacy and antiviral resistance, alternative strategies are urgently required to improve disease outcomes. Here we describe the use of HiSeq deep sequencing to analyze host gene expression in primary human alveolar epithelial type II (ATII) cells infected with highly pathogenic avian influenza H5N1 virus. We employed primary human ATII cells isolated from normal human lung tissue donated by patients that underwent lung resection. Human host gene expression following HPAI H5N1 virus (A/Chicken/Vietnam/0008/04) infection of primary ATII cells was analyzed using Illumina HiSeq deep sequencing.
2018-10-09 | GSE119767 | GEO
Project description:The highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in nature and threaten public health. Although several viral determinants and host factors that influence the virulence of HPAI H5N1 viruses in mammals have been identified, the detailed molecular mechanism remains poorly defined and requires further clarification. In our previous studies, we characterized two naturally isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethality in mice. Here, we explored the molecular determinants and potential mechanism for this difference in virulence. By using reverse genetics, we found that a single amino acid at position 158 of the hemagglutinin (HA) protein substantially affected the systemic replication and pathogenicity of these H5N1 influenza viruses in mice. We further found that the G158N mutation introduced an N-linked glycosylation at sites 158–160 of the HA protein and that this N-linked glycosylation enhanced viral productivity in infected mammalian cells and induced stronger host immune and inflammatory responses to viral infection. These findings further our understanding of the determinants of pathogenicity of H5N1 viruses in mammals.
2016-12-22 | GSE89246 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamburger Hamilton stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: cross-species comparison
2009-12-03 | GSE11028 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamilton Hamburger stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: cross-species comparison
2009-12-03 | GSE11027 | GEO
Project description:The chicken LSCC-HD3 cell line (HD3) generated from erythroid precursors is an established avian model for erythroid differentiation and lineage-specific gene expression. We obtained Hi-C maps of genomic interactions for HD3 cell line and revealed A/B compartments and topologically-associating domains. By analysis of contact patterns in the Hi-C maps of HD3 cells we identified more than 25 interchromosomal translocations of regions ≥200 Kb on both micro- and macrochromosomes. Intrachromosomal inversions, deletions and duplications were also detected in HD3 cells. Hi-C data obtained for HD3 chicken cell line demonstrate that it has a highly rearranged karyotype, with most of the chromosomes involved in unbalanced translocations.
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