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Expression profile of lungs from two fatal H5N1 influenza cases

ABSTRACT: The pathogenesis of avian influenza A H5N1 virus in human has not been clearly elucidated. There have been increasing evidence suggesting a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. However, the role of aberrant innate immune response in human lungs infected by avian influenza H5N1 virus has not been explored and direct evidence for inappropriate innate responses in lungs of avian influenza H5N1 virus infected patients is lacking.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22212 | GEO | 2010/06/09

SECONDARY ACCESSION(S): PRJNA128763

REPOSITORIES: GEO

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Expression profile of lungs from two fatal H5N1 influenza cases

Project description:The pathogenesis of avian influenza A H5N1 virus in human has not been clearly elucidated. There have been increasing evidence suggesting a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. However, the role of aberrant innate immune response in human lungs infected by avian influenza H5N1 virus has not been explored and direct evidence for inappropriate innate responses in lungs of avian influenza H5N1 virus infected patients is lacking. In order to obtain evidences for the proposed role of aberrant innate immune response in avian influenza H5N1 virus pathogenesis in human, we analyzed expression profile of lung tissues from two fatal cases of avian influenza H5N1 virus infected patients in comparison to normal human lung using an expression microarray.

2010-06-16 | E-GEOD-22212 | biostudies-arrayexpress

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

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Integrated Clinical, Pathologic, Virologic, and Transcriptomic Analysis of H5N1 Influenza Virus-Induced Viral Pneumonia in the Rhesus Macaque

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

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

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). Eight- to 10-week-old female wild-type and IFNR1-/- mice (on a 129S6/SvEv background) were anesthetized by intraperitoneal injection of 0.2 ml of 2,2,2-tribromoethanol in tert-amylalcohol (Avertin; Sigma-Aldrich, Milwaukee, WI). Ten times the 50% lethal dose (LD50), 3.2 × 10^4 PFU (1918) or 7 × 10^3 PFU (VN/1203), in 50 μl of infectious virus diluted in phosphate-buffered saline (PBS) was inoculated intranasally (i.n.). Lung tissue was harvested for microarray analysis from infected animals at 1, 3, and 4 days post-innoculation. For RNA isolation, lungs were frozen in individual tubes and stored in solution D (4 M guanidinium thiocyanate, 25 mM sodium citrate, 0.5% sarcosyl, 0.1 M β-mercaptoethanol). Separate microarrays were run for each infected mouse. This included 2 animals/time point for 1918 virus-infected mice (24 animals total) or 3 animals/time point for VN/1203-infected mice (36 animals total). Lung tissue from three uninfected wild type 129S6/SvEv mice was collected as a mock control. Equal masses of total RNA from the lung tissue of the three mice were pooled prior to being run on microarray. Two-channel microarrays were used to determine gene expression in the lungs. For each individual infected lung, gene expression from an infected lung was compared to gene expression from the pooled RNA from the mock control.

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Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

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Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

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

Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

2016-07-04 | E-GEOD-65231 | biostudies-arrayexpress

FluOMICS - Metabolomics analysis of mouse lungs infected with H5N1 (HALo) influenza virus

Project description:Metabolomics analysis of C57BL/6 mouse lungs infected with influenza A/Vietnam/1203/04 (H5N1) HALo virus, mock infected with PBS, or untreated.

2017-12-06 | MSV000081786 | MassIVE

Expression data from low- and high-pathogenicity avian influenza-infected chicken and duck cells

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

Next Generation Sequencing Facilitates Quantitative Analysis of H5N1 Wild Type and NS1-truncated Lung Transcriptomes in SPF chickens

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.

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