Transcription profiling by array of H5N1 avian influenza virus in chicken cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Gallus gallus
DISEASE(S): normal
SUBMITTER: Tamsyn Crowley
PROVIDER: E-MEXP-3432 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This study is planned to characterize the proteome profile of HPAI H5N1 virus infected chicken lung tissues to identify the molecular pathogenesis and proteomic determinant associate with disease progression in susceptible host.
2022-03-02 | PXD010358 | Pride
Project description:The H5N1 avian influenza virus clade 2.3.4.4b outbreak represents a major pandemic threat for humans, with some reported cases of severe and fatal respiratory illness. A key unanswered question is the pathogenesis of severe H5N1 disease following respiratory infection. In this study, we explored mechanisms of pathogenesis of severe H5N1 disease in cynomolgus and rhesus macaques following infection with the H5N1 isolate A/Texas/37/2024 (huTX37-H5N1). Cynomolgus macaques developed severe pneumonia that was lethal in 100% of macaques by 7 days post-infection. By contrast, rhesus macaques demonstrated dose-dependent mortality, and surviving animals showed protective immunity against high-dose re-challenge. A multi-omics analysis demonstrated that H5N1 infection was characterized by robust induction of proinflammatory cytokines, innate immune cells, complement, coagulation, apoptosis, and immune exhaustion pathways. Taken together, our data indicate inflammation and immune dysregulation as key mechanisms of H5N1 pathogenesis in nonhuman primates.
2025-08-01 | GSE287709 | 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:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from chickens infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.
2015-01-19 | E-MTAB-2908 | biostudies-arrayexpress
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: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: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:Background Clade 2.3.4.4b highly pathogenic avian influenza (HPAI) H5N1 viruses are widely circulating in North America with unprecedented transmission into novel host species. A high incidence of neurologic disease is observed in carnivores infected with clade 2.3.4.4b HPAI H5N1 viruses and historical outbreaks of HPAI H5N1 in humans are also associated with neurologic complications, raising concerns about neurotropism and neurovirulence of clade 2.3.4.4b HPAI H5N1 viruses. Methods We analyzed virus replication kinetics, cellular tropism, and host responses to infection in human cerebral organoids (hCOs) inoculated with clade 2.3.4.4b HPAI H5N1 viruses compared to a historical clade 1 HPAI H5N1 virus and a seasonal influenza A virus. Results HPAI H5N1 viruses replicated to high titers in hCOs, but replication of the seasonal influenza A virus was not detected. Viral antigen and RNA were detected primarily in neuron- and astrocyte-like cells. Interferon responses to infection with HPAI H5N1 viruses were observed in a small population of bystander cells. Higher levels of cell death and proinflammatory cytokines and chemokines were observed in organoids inoculated with the historical HPAI H5N1 isolate. Conclusions Clade 2.3.4.4b HPAI H5N1 viruses exhibit similar neurotropism compared to a historical clade 1 HPAI H5N1 virus. Lower levels of cell death and inflammatory cytokine production induced by clade 2.3.4.4b viruses may indicate reduced neuropathogenic potential of these viruses in humans.
2025-12-31 | GSE301348 | GEO
Project description:HPAI H5N1 Genomes from Punta San Juan, Peru
| PRJNA1359009 | ENA
Project description:Susceptible (DBA/2J, 129/SvImJ, A/J) and Resistant (SM/J, C57BL/6J, Balb/cJ) mouse strain were inoculated with a highly pathogenic H5N1 influenza A virus (A/Hong Kong/213/2003) for 24 and 168 hours. Uninfected control animals were included. Differences in expression were analyzed and used to identify candidate genes and pathways that contributed to the difference in H5N1 pathogenesis in these two groups of mice.
2015-01-09 | GSE64798 | GEO