H1N1 Influenza project
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA70953 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 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:An influenza A microarray was used to type influenza A H1N1 specimens collected in Washington State and the results compared with identification by both culture and real time RT PCR. The microarray was more sensitive than conventional influenza testing. Cluster analysis of the microarray data discriminated specimens into distinct clades. Specimens from two pediatric decedents formed a unique clade upon H1 analysis. Keywords: Comparative genome study; Influenza A strains; Subtype H1N1
2008-11-01 | GSE12226 | GEO
Project description:To determine whether differential expression of cellular microRNAs plays a role in the host response to Influenza A (H1N1) infection, we have employed the Agilent miRNA microarray (V3) as a discovery platform to identify microRNAs between the critically ill Patients with Influenza A (H1N1) and the healthy controls.
2012-12-28 | GSE24956 | 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:Differential expression was determined in Calu-3 cells between mock infected and infected with H1N1 influenza virus A/Netherlands/602/2009 at nine time points post-infection. As a comparison, cells were also infected with A/CA/04/2009 H1N1 influenza virus at 4 time points post-infection.
2012-09-13 | GSE40844 | GEO
Project description:Influenza A virus is a kind of single negative-stranded RNA virus which belongs to the Orthomyxoviridae family. It can cause localized outbreak or worldwide epidemic in a short time for its great contagiosity, fast spread speed and a wide range of host, and H1N1 influenza virus is a strong pathogenic subtype of influenza A virus. Influenza A virus infection has been shown to alter miRNA expression both in cultured cells and in animal models. We used microRNA microarrays to detail the programme of microRNA expression and identified distinct classes of differentially regulated microRNAs during this process.
2014-10-21 | GSE62495 | GEO
Project description:An influenza A microarray was used to type influenza A H1N1 specimens collected in Washington State and the results compared with identification by both culture and real time RT PCR. The microarray was more sensitive than conventional influenza testing. Cluster analysis of the microarray data discriminated specimens into distinct clades. Specimens from two pediatric decedents formed a unique clade upon H1 analysis. Keywords: Comparative genome study; Influenza A strains; Subtype H1N1 23 influenza A H1N1 specimens collected in Washington State were subtyped by microarray and data was compared with identification by both culture and real time RT PCR.
2008-10-31 | E-GEOD-12226 | biostudies-arrayexpress
Project description:Background: Pandemic H1N1 influenza A is a newly emerging strain of human influenza that is easily transmitted between people and has spread globally to over 116 countries. Human infection leads to symptoms ranging from mild to severe with lower respiratory complications observed in a small but significant number of infected individuals. Little is currently known about host immunity and Pandemic H1N1 influenza infections. Methods: We examined the pathogenic potential of the pandemic influenza A vaccine strain, A/California/07/2009 (H1N1), in ferrets, and characterized the host immune responses using microarray analysis. Gene expression profiles in lung tissue were compared with those from ferrets infected with A/Brisbane/59/2007. Results: Chemokines CCL2, CCL8, CXCL7 and CXCL10 along with the majority of ISGs were expressed early, correlated to lung pathology, and abruptly decreased expression in 5 days. Interestingly, the drop in innate immune gene expression was replaced by a significant increase in the expression of the adaptive immune genes for granzymes and immunoglobulins. Serum anti-pandemic influenza H1N1 antibodies were also observed on day 7, commensurate with the elimination of viral load. Conclusions: We propose that the innate phase of host immunity causes lung pathology and a delay or failure to effectively switch to the adaptive phase contributes to morbidity and mortality during severe human pandemic H1N1 influenza A infections. Keywords: influenza, immune response, cytokines, chemokines, lung infection, time course
2010-03-31 | GSE17079 | GEO