Influenza A virus strain:H5N1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248762 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Influenza A virus strain:H5N1 Genome sequencing and assembly
| PRJNA342929 | ENA
Project description:The cellular transcriptome of C57BL/6 mouse lungs was profiled by mRNA-Seq analysis at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53. A/Wyoming/03/03 (H3N2) influenza virus replicates poorly in mice and lung tissue collected from mice inoculated with this virus did not carry viral loads detectable by plaque assay.
2017-05-05 | GSE98527 | GEO
Project description:H5N1 Influenza A virus Raw sequence reads
| PRJNA381590 | ENA
Project description:Human tracheobronchial epithelial (HTBE) cells are considered to serve as a good correlate of influenza virus infection in the human respiratory tract. mRNA-Seq analysis was used to profile the cellular transcriptome of HTBE cells at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53.
2016-10-27 | GSE89008 | GEO
Project description:Analysis of lung samples from mice infected with a severe H5N1 influenza virus (VN/1203/04/H5N1) or a mild H1N1 influenza virus (NYMC-X-179A) on day 3 and day 5 post-infection. Uninfected controls were used for comparison.
2016-12-20 | GSE70882 | GEO
Project description:Human tracheobronchial epithelial (HTBE) cells are considered to serve as a good correlate of influenza virus infection in the human respiratory tract. ChIP-Seq analysis was used to profile histone acetylation (H3K27ac) in HTBE cells at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53.
2018-12-14 | GSE113702 | GEO
Project description:Human monocyte-derived macrophages (MDM) serve as a model for resident alveolar macrophages (AM) in the human respiratory tract. mRNA-Seq analysis was used to profile the cellular transcriptome of MDM cells at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53.
2017-05-05 | GSE97672 | GEO
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.
2010-06-09 | GSE22212 | GEO
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
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