Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA988813 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Seattle Flu Alliance Influenza-B genome sequencing and assembly
| PRJNA988156 | ENA
Project description:Seattle Flu Alliance RSV-B genome sequencing and assembly
| PRJNA988154 | ENA
Project description:Seattle Flu Alliance RSV-A genome sequencing and assembly
| PRJNA988152 | ENA
Project description:Using human umbilical vein endothelial cells (HUVECs) as cell models, the present study aims to explore the differential miRNAs in influenza virus-infected ECs and analyze their target genes involved in EC permeability regulation. As the results showed, permeability increased and F-actin cytoskeleton reorganized after HUVECs infected with influenza A virus (CA07 or PR8) at 30 MOI. most of these miRNAs were down-regulated after flu infection. It has been reported that PKC, Rho/ROCK, HRas/Raf/MEK/ERK, and Ca2+/CaM pathways are activated by flu infection and play important roles in permeability regulation.
2018-02-13 | GSE102866 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE29614: Time Course of Young Adults Vaccinated with Influenza TIV Vaccine during 2007/08 Flu Season GSE29615: Time Course of Young Adults Vaccinated with Influenza LAIV Vaccine during 2008/09 Flu Season GSE29617: Time Course of Young Adults Vaccinated with Influenza TIV Vaccine during 2008/09 Flu Season GSE29618: FACS-sorted cells from Young Adults Vaccinated with Influenza TIV or LAIV Vaccines during 2008/09 Flu Season Refer to individual Series
2011-07-10 | E-GEOD-29619 | biostudies-arrayexpress
Project description:influenza A virus and Influenza B virus Genome sequencing and assembly
| PRJNA932586 | ENA
Project description:Chronic obstructive pulmonary disease (COPD) collectively refers to chronic and progressive lung diseases causing not fully reversible limitations in airflow. COPD patients are at high risk for severe respiratory symptoms upon influenza virus infection. Airway epithelial cells provide the first-line antiviral defense, but whether their susceptibility and response to influenza virus infection changes in COPD has not been elucidated. Therefore, this study aimed to i) compare the susceptibility of COPD- and control-derived airway epithelium to influenza virus, and ii) assess protein changes during influenza virus infection by quantitative proteomics. Fluorescent stainings confirmed expression of human- and avian-type influenza virus receptors in primary human bronchial epithelial cells (phBECs) from COPD patients (n=4) and controls (n=3) differentiated at the air-liquid interface. Subjects were closely matched in age, sex, and smoking history and, for COPD-derived phBECs, included stage II (n=2), stage III (n=1) and stage IV (n=1). Proteomics of fully differentiated phBECs pre- and post-influenza A virus infection with A/Puerto Rico/8/34 (PR8) revealed no significant differences between GOLD stage II/ III COPD (n=3) and control phBECs in terms of flu receptor expression, cell type composition, virus replication, or protein profile pre- and post-infection. In contrast, COPD GOLD stage IV phBECs (n=1) showed a distinct pattern of flu receptor expression and a typical COPD phenotype as assessed by a literature-derived panel of 20 proteins and quantification of cell type composition. Independent of health state, proteomics showed a robust antiviral response to influenza virus infection, as well as upregulation of several novel influenza virus-regulated proteins.
2022-12-29 | PXD031461 | Pride
Project description:Human rhinovirus and influenza virus infections of the upper airway lead to colds and the flu and can trigger exacerbations of lower airway diseases including asthma and chronic obstructive pulmonary disease. Despite modest advances in the diagnosis and treatment of infections by these viruses, novel diagnostic and therapeutic targets are still needed to differentiate between the cold and the flu, since the clinical course of influenza can be severe while that of rhinovirus is usually more mild. In our investigation of influenza and rhinovirus infection of human respiratory epithelial cells, we used a systems approach to identify the temporally changing patterns of host gene expression from these viruses. After infection of human bronchial epithelial cells (BEAS-2B) with rhinovirus, influenza virus or co-infection with both viruses, we studied the time-course of host gene expression changes over three days. From these data, we constructed a transcriptional regulatory network model that revealed shared and unique host responses to these viral infections such that after a lag of 4-8 hours, most cell host responses were similar for both viruses, while divergent host cell responses appeared after 24-48 hours. The similarities and differences in gene expression after epithelial infection of rhinovirus, influenza virus, or both viruses together revealed qualitative and quantitative differences in innate immune activation and regulation. These differences help explain the generally mild outcome of rhinovirus infections compared to influenza infections which can be much more severe.
2015-12-21 | GSE71766 | GEO
Project description:The influenza A(H1N1)pdm09 virus caused a global flu pandemic in 2009 and contributes to seasonal epidemics. Different treatment and prevention options for influenza have been developed and applied with limited success. Here we report that an Akt inhibitor MK2206 possesses potent antiviral activity against influenza A(H1N1)pdm09 virus in vitro. We showed that MK2206 blocks the entry of different A(H1N1)pdm09 strains into cells. Moreover, MK2206 prevented A(H1N1)pdm09-mediated activation of cellular signaling pathways and the development of cellular immune responses. Importantly, A(H1N1)pdm09 virus was unable to develop resistance to MK2206. Thus, MK2206 is a potent anti-influenza A(H1N1)pdm09 agent.
2014-01-23 | GSE54293 | GEO
Project description:Human rhinovirus and influenza virus infections of the upper airway lead to colds and the flu and can trigger exacerbations of lower airway diseases including asthma and chronic obstructive pulmonary disease. Despite modest advances in the diagnosis and treatment of infections by these viruses, novel diagnostic and therapeutic targets are still needed to differentiate between the cold and the flu, since the clinical course of influenza can be severe while that of rhinovirus is usually more mild. In our investigation of influenza and rhinovirus infection of human respiratory epithelial cells, we used a systems approach to identify the temporally changing patterns of host gene expression from these viruses. After infection of human bronchial epithelial cells (BEAS-2B) with rhinovirus, influenza virus or co-infection with both viruses, we studied the time-course of host gene expression changes over three days. From these data, we constructed a transcriptional regulatory network model that revealed shared and unique host responses to these viral infections such that after a lag of 4-8 hours, most cell host responses were similar for both viruses, while divergent host cell responses appeared after 24-48 hours. The similarities and differences in gene expression after epithelial infection of rhinovirus, influenza virus, or both viruses together revealed qualitative and quantitative differences in innate immune activation and regulation. These differences help explain the generally mild outcome of rhinovirus infections compared to influenza infections which can be much more severe. Human bronchial epithelial cells (BEAS-2B) were infected with rhinovirus, influenza virus or both viruses and RNAs were then profiled at 10 time points (2, 4, 6, 8, 12, 24, 26, 48, 60 and 72hrs)
2015-12-21 | E-GEOD-71766 | biostudies-arrayexpress