Unidentified influenza virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281810 | ENA |
REPOSITORIES: ENA
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Project description:Influenza A virus infections are a major cause for respiratory disease in humans, which affects all age groups and contributes substantially to global morbidity and mortality. IAV have a large natural host reservoir in avian species. However, many avian IAV strains lack adaptation to other hosts and hardly propagate in humans. While seasonal or pandemic influenza A virus (IAV) strains replicate efficiently in permissive human cells, many avian IAV cause abortive non-productive infections in these hosts despite successful cell entry. However, the precise reasons for these differential outcomes are poorly defined. We hypothesized that the distinct course of an IAV infection with a given virus strain is determined by the differential interplay between specific host and viral factors. By using Spike-in SILAC mass spectrometry-based quantitative proteomics we characterized sets of cellular factors whose abundance is specifically up- or down-regulated in the course of permissive vs. non-permissive IAV infection, respectively. This approach allowed for the definition and quantitative comparison of about 3500 proteins in human lung epithelial cells in response to seasonal or low-pathogenic avian H3N2 IAV. Many identified proteins were similarly regulated by both virus strains, but also 16 candidates with distinct changes in permissive vs. non-permissive infection were found. RNAi-mediated knockdown of these differentially regulated host factors identified Vpr binding protein (VprBP) as pro-viral host factor since its down-regulation inhibited efficient propagation of seasonal IAV while over-expression increased viral replication of both seasonal and avian IAV. These results not only show that there are similar differences in the overall changes during permissive and non-permissive imfluenza virus infections, but also provide a basis to evaluate VprBP as novel anti-IAV drug target.
2017-03-14 | PXD005825 | Pride
Project description:To delineate specific patterns of signaling networks activated by H5N1 we used a comparative systems biology approach analyzing gene expression in endothelial cells infected with three different human and avian influenza strains of high and low pathogenicity. HUVECs were infected with either PR8, FPV or H5N1 virus. We used wildtype HUVEC or HUVEC transfected with a dominant negative mutant of IKK2 (block of the NF-kB signaling pathway).
2009-12-30 | E-GEOD-13637 | biostudies-arrayexpress
Project description:Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes. AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.
2025-07-28 | GSE296526 | GEO
Project description:To delineate specific patterns of signaling networks activated by H5N1 we used a comparative systems biology approach analyzing gene expression in endothelial cells infected with three different human and avian influenza strains of high and low pathogenicity.
2009-12-31 | GSE13637 | GEO
Project description:Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes (DE300 and DE256 were AT and DE558 and DE213 were not AT). AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.
2025-07-28 | GSE298058 | GEO
Project description:The purpose of this experiment was to understand the pathogenic role of individual 1918 genes on the host response to the 1918 pandemic influenza virus. We examined reassortant avian viruses nearly identical to the pandemic 1918 virus (1918-like avian virus) carrying either the 1918 HA or PB2 gene. Both genes enhanced 1918-like avian virus replication, but only the mammalian host adaptation of the 1918-like avian virus through reassortment of the 1918 PB2 led to increased lethality in mice. We demonstrate that 1918 PB2 enhances immune and inflammatory responses concomitant with increased cellular infiltration in the lung. We also show that 1918 PB2 expression results in the repression of both canonical and non-canonical Wnt signaling pathways which are crucial for inflammation mediated lung regeneration and repair.
2015-12-31 | GSE70502 | 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