Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA470650 | ENA |
REPOSITORIES: ENA
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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: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. Total RNA obtained from NCI-H1666 cells, which are non-small cell lung cancer cell line. NCI-H1666 cells were non- or MK2206-treated (10 μM) and mock- or virus-infected (A/Helsinki/p14/2009) at moi of 3.
2014-01-23 | E-GEOD-54293 | biostudies-arrayexpress
Project description:The biological basis for the increased severity of influenza A viruses during the 2009 influenza pandemic remains unclear. Intra-host evolution of quasispecies and strong inflammation were identified as important hallmarks of severe pandemic H1N1 influenza A virus 2009 (A(H1N1)pdm09) infection. HA-222D/G quasispecies of A(H1N1)pdm09 were shown to undergo fast evolution and to cause severe influenza in human and mice. Here, we analysed the whole genome transcriptional response of mice infected with the A/Jena/5258/09 (mpJena/5258) virus over a period of 12 days to gain insights into the pathogenesis of A(H1N1)pdm09 HA-222D/G quasispecies on a molecular level. Remarkably, the transcriptional response to severe mpJena/5258 showed biphasic expression profile for the majority of genes which was never shown before. The gene expression analysis shows first peak with 968 differentially expressed genes at day 2 post infection (p.i.), followed by a stagnant recovery phase with 359 differentially expressed genes at day 4 p.i., and a second peak with 1001 differentially expressed genes at day 7 p.i., finally followed by a recovery phase. Using a reverse engineering strategy, a regulatory network was inferred to identify key interactions leading to severe pathogenesis of mpJena/5258. Known regulatory interactions were extracted by Pathway Studio 9.0 and softly integrated during network inference. The results demonstrate a hyper-responsive action and a positive feedback loop of IFN gamma (Ifng), Stat1 and Tlr3 signalling during mpJena/5258 infection. In conclusion, mpJena/5258 infection is associated with biphasic gene expression profile and a positive feedback mechanism of Ifng which correlates with the evolution of HA-222D/G quasispecies and leads to overwhelming immune response. A significant correlation were found between the co-expression action of three genes (Ifng, Stat1 and Tlr3) with a phenomenological clinical symptom score.
2017-02-10 | GSE67241 | GEO
Project description:Himanshu Manchanda, Nora Seidel, Andi Krumbholz, Andreas Sauerbrei, Michaela Schmidtke & Reinhard Guthke. Within-host influenza dynamics: a small-scale mathematical modeling approach. Biosystems 118 (2014).
The emergence of new influenza viruses like the pandemic H1N1 influenza A virus in 2009 (A(H1N1)pdm09) with unpredictable difficulties in vaccine coverage and established antiviral treatment protocols emphasizes the need of new murine models to prove the activity of novel antiviral compounds in vivo. The aim of the present study was to develop a small-scale mathematical model based on easily attainable experimental data to explain differences in influenza kinetics induced by different virus strains in mice. To develop a three-dimensional ordinary differential equation model of influenza dynamics, the following variables were included: (i) viral pathogenicity (P), (ii) antiviral immune defense (D), and (iii) inflammation due to pro-inflammatory response (I). Influenza virus-induced symptoms (clinical score S) in mice provided the basis for calculations of P and I. Both, mono- and biphasic course of mild to severe influenza induced by three clinical A(H1N1)pdm09 strains and one European swine H1N2 virus were comparatively and quantitatively studied by fitting the mathematical model to the experimental data. The model hypothesizes reasons for mild and severe influenza with mono- as well as biphasic course of disease. According to modeling results, the second peak of the biphasic course of infection is caused by inflammation. The parameters (i) maximum primary pathogenicity, (ii) viral infection rate, and (iii) rate of activation of the immune system represent most important parameters that quantitatively characterize the different pattern of virus-specific influenza kinetics.
2024-09-02 | BIOMD0000000712 | BioModels
Project description:The differences of clinical characteristics in complex seizures induced by influenza A(H1N1)pdm09 and rotavirus gastroenteritis are well known, but the pathogenic mechanisms remain unclear. We analyzed the gene expression profiles in the peripheral whole blood cells isolated from pediatric patients using an Affymetrix oligonucleotide microarray. Results provide insights into the difference of the pathogenesis in the patients with complex seizures induced by influenza A(H1N1)pdm09 and rotavirus infections.
2013-09-05 | GSE50628 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE36461: MiRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009) GSE36462: MiRNA profiling during infection with H7N7 influenza A virus (A/Ck/Germany/R28/H7N7/2003) GSE36553: mRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009) Refer to individual Series
2012-04-09 | E-GEOD-36555 | biostudies-arrayexpress
Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison.
2013-04-17 | GSE46087 | GEO
Project description:The differences of clinical characteristics in complex seizures induced by influenza A(H1N1)pdm09 and rotavirus gastroenteritis are well known, but the pathogenic mechanisms remain unclear. We analyzed the gene expression profiles in the peripheral whole blood cells isolated from pediatric patients using an Affymetrix oligonucleotide microarray. Results provide insights into the difference of the pathogenesis in the patients with complex seizures induced by influenza A(H1N1)pdm09 and rotavirus infections. The gene expression profiles in the peripheral whole blood of ten patients (n=5; complex seizures, n=5; control) with influenza A(H1N1)pdm09 and six patients (n=3; complex seizures, n=3; control) with rotavirus gastroenteritis were examined. Whole blood samples were collected from patients in the acute phase of the disease and in the recovery phase.
2013-09-05 | E-GEOD-50628 | biostudies-arrayexpress
Project description:To further understand the roles of miRNA during influenza A virus infection, we performed miRNA profiling in human alveolar adenocarcinoma cell lines, A549 cells, infected with influenza A virus A/Beijing/501/2009(H1N1) and A/goose/Jilin/hb/2003(H5N1).
2017-03-22 | GSE96857 | GEO