Project description:We used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1)) The Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells were harvested at 2, 4, 6, 8 and 10 hpi and RNA extraction was performed using standard protocol as described by Affymetrix. The aim of this experiment is to analyze host response to Influenza A virus (A/Singapore/478/2009 (pH1N1)) infection.
Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5
Project description:We used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1))
Project description:Virus-host interactions are complicated processes, and multiple cellular proteins have been reported to promote or inhibit viral replication through different mechanisms. Recent progress has implicated circular RNAs (circRNA) in cancer biology and progression; however, the role of circRNAs in viral infection remains largely unclear. Here, we detected 11,620 circRNAs in A549 cells and found that 411 of them were differentially expressed in influenza virus-infected A549 cells. We characterized a novel intronic circRNA, AIVR, that was upregulated in influenza virus-infected A549 cells, and found that silencing of AIVR significantly promoted influenza virus replication in A549 cells. We further found that AIVR predominantly localizes in the cytoplasm and works as a microRNA (miRNA) sponge. One of the miRNAs absorbed by AIVR binds the mRNA of CREBBP, which is an important component of the large nucleoprotein complex IFN-β enhanceosome that accelerates IFN-β production. AIVR-overexpression significantly increased the mRNA and protein levels of INF-β in the influenza virus-infected A549 cells. Therefore, the upregulation of AIVR is a cellular antiviral strategy, with AIVR exerting its antiviral effect by absorbing miRNA and promoting the expression of CREBBP to facilitate IFN-β production. Our study provides new insights into the roles of circRNAs in the cellular innate antiviral response.
Project description:Epithelial cells are the first line of defense within the lung. Disruption of the epithelial barrier by pathogens enables the systematic dissemination of bacteria or viruses within the host, leading to severe diseases with fatal outcomes. Thus, the lung epithelium can be damaged by seasonal and pandemic influenza A viruses. Influenza A virus infection induced dysregulation of the immune system is beneficial for the dissemination of bacteria to the lower respiratory tract, causing bacterial and viral co-infection. Host cells regulate protein homeostasis and the response to different stimuli, for instance pathogen infections, by post translational modification of proteins. Aside from protein phosphorylation, ubiquitination of proteins is an essential regulatory tool in virtually every cellular process, such as protein homeostasis, the host immune response, cell morphology, and in clearing of cytosolic pathogens. Here, we analyzed the proteome and ubiquitinome of A549 cells in response to Streptococcus pneumoniae D39 Δcps and influenza A virus H1N1 as well as bacterial and viral co-infection. Pneumococcal infection induced alterations in the ubiquitination of proteins involved in the organization of the actin cytoskeleton and Rho GTPases, but had minor effects on the abundance of host proteins. H1N1 infection is reflected by an anti-viral state of A549 cells. Finally, co infection resembled the imprints of both infecting pathogens with a minor increase in the observed alterations in protein and ubiquitination abundance.
Project description:The “Spanish influenza” of 1918 claimed an unprecedented number of lives, yet the determinants of virulence for this virus are still not fully understood. Here, we used functional genomics and an in vitro human lung epithelial cell infection model to define the global host transcriptional response to the eight-gene 1918 virus. To better understand the role of the 1918 virus NS1 gene, we also evaluated the host response to fully reconstructed 1918 and reassortant 1918 virus containing the NS1 gene from A/Texas/36/91 (a seasonal isolate of human influenza virus). A549 cells were infected with either recombinant 1918 influenza, a chimeric virus that contained seven genes from recombinant 1918 and the NS1 from A/Texas/36/91 (Tx/91), or mock. Cells were harvested for microarray analysis at 2, 6, and 24hr following infection.
Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5 A four chip study using total RNA extracted from SGC-7901 cells transfected with siRNA negative control and SGC-7901 cells knock down of MTA2 with siRNA. Each chip measures the expression level of 45033 genes collected from the authoritative data source including NCBI
