Project description:To analyse differential expression genes(LncRNA and mRNA) in ATG7 knockdown cells and control cells upon influenza virus infection, transcriptome RNA sequencing was performed
Project description:Eosinophils are terminally differentiated granulocytes that participate in innate immunity against Influenza A Virus (IAV). Here, we investigate transcriptional changes that occur in IAV-infected human A549 aveolar epithelial carcinoma cells with and without direct or indirect exposure to mouse bone marrow-derived eosinophils (BMdEos). Global changes in the transcriptome of A549 cells due to Influenza A virus-infection and/or direct and indirect eosinophil exposure were assessed using ThermoFisher/Affymetrix Clariom™ S Human microarrays.
Project description:Purpose: To explore the roles of host lncRNAs during IAV infection Methods:profiling whole transcriptional alterations using RNA-seq in neutrophil samples from 3 patients infected with IAV in the acute stage and their matched recovery-stage samples Results:We identified a total of 404 differentially expressed genes (FC>2, p<0.05), including 234 up-regulated and 170 down-regulated genes,in each patient sample Conclusion:Our study is the first profile of the transcriptome of IAV-infected patients' neutrophils
Project description:Analysis of gene expression in A549 cells infected with influenza A virus or Mock and treated with Itaconic acid (IA), or Dimethyl itaconate (DI) to investigate the effects itaconate have on transcriptional response in A549 cells. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.
Project description:To identify miRNAs that are affected by IAV infection, we adopted a systematic approach, and performed a miRNA microarray analysis using a human alveolar adenocarcinoma cell line, A549, which was infected with a common laboratory strain of influenza A/WSN/33(H1N1) virus (WSN). We compared miRNA expression profiles in A549 cells infected with WSN for 2, 6, and 10 hours at a multiplicity of infection (MOI) of 2. Among 955 miRNAs on the microarray, 209 miRNAs were detected in all three infected A549 samples, but when compared with analysis results from mock-infected A549 cells, most expression changes were less than 1.5-fold , which was consistent with a previous report (Buggele et al., 2013). Therefore, we established 1.5-fold expression change as a threshold to select for miRNAs potentially affected by WSN infection. Further screening revealed 116 miRNAs that underwent 1.5-fold or greater expression changes at any timepoint following WSN infection.
Project description:RNAseq analysis of A549-TRIM28 KO cells that were infected with low pathogenic laboratory strain PR8 (H1N1) Differentially expressed genes in infected vs. non-infected cells Project: A549_TRIM28_KO
Project description:Although accumulating evidence has shown that long non-coding RNAs (lncRNAs) are involved in multiple biological processes, considerably less is known regarding their functions in influenza A virus (IAV) replication. Here, lncRNA expression profiles were determined by RNA sequencing in three pairs of influenza virus A/Puerto Rico/8/34 (H1N1)-infected or uninfected A549 cells.
Project description:Influenza A Virus (IAV) is a recurring respiratory virus with antiviral therapies of limited use. Understanding host proteins essential for IAV infection can identify targets for alternative host-directed therapies (HDTs). Using affinity purification-mass spectrometry and global phosphoproteomic and protein abundance analyses with three IAV strains (pH1N1, H3N2, H5N1) in three human cell types (A549, NHBE, THP-1), we mapped 332 IAV-human protein-protein interactions and identified 13 IAV-modulated kinases. Whole exome sequencing of patients who experienced severe influenza revealed several genes, including the structural scaffold protein AHNAK, with predicted loss-of-function variants that were also identified in our proteomic analyses. Of our identified host factors, 54 significantly altered IAV infection upon siRNA knockdown, and two factors, COPB1 and AHNAK, were also essential for productive infection by SARS-CoV-2. Finally, 16 compounds targeting our identified host factors suppressed IAV replication, with three targeting ATP6V1A, CDK2 and FLT3 showing pan-antiviral activity across influenza and coronavirus families. This study provides a comprehensive network model of IAV infection in human cells, identifying functional host targets for pan-viral HDT. This project includes the global proteomic data (abundance and phosphorylation), the AP-MS data has been submitted separately as its own dataset and has its own dataset identifier.