Project description:In order to analysis the changes of protein expression and its influence on innate immune in mice lung after influenza virus infection,we detect protein expression profile by iTRAQ method
Project description:Small RNAs were profiled during influenza A virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response. Examination of microRNA abundance during influenza A virus infection.
Project description:A comparative gene expression analysis was performed using cDNA microarray technology in passage-2 normal human nasal epithelial cells to identify the differentially expressed genes between influenza A virus infected and uninfected cells. Two samples were analyzed. RNA was extracted from normal human nasal epithelial cells, which were further divided as H1N1 PI 0 day and H1N1 PI 2 day (influenza A virus infection for 48 hr).
Project description:The objective of this study was to examine the host transcriptional response to high and low pathogenecity viruses in mouse embryonic fibroblasts (MEFs) isolated from different mouse genetic backgrounds to further understand the contribution of interferon signaling pathways to host response to influenza. WT, IFNgR-/-, IFNabR-/-, or IFNabgR-/- MEFs were mock-infected or infected with the A/WSN/33 (WSN), reconstructed 1918 (r1918), or A/Vietnam/1203/2004 (VN1203) strains of influenza virus at an MOI of 2 PFU/cell. At 24 h p.i., total RNA was isolated from the cells and used for microarray hybridization. Experiments with VN1203 and r1918 were performed seperately (experiment a) from experiments with WSN (experiment b). Appropriate mock samples were harvested in each experiment. All gene expression profiles are compared to time-, experiment-, and genotype-matched mock-infected samples.
Project description:Whole-genome data was developed from influenza virus infected A549 cells to better characterize the effect of C646 on influenza virus infection A549 cells were treated with C646 or DMSO for 10 h, and then were infected with A/WSN/33 virus (WSN; H1N1) at a multiplicity of infection (MOI) 2. A549 cells for microarray studies were collected at different times. The gene expression in A549 cells was compared between C646-treated group and DMSO-treated group.
Project description:We found that a dose of influenza (5,000 pfu of recombinant influenza A/WSN/33 (rWSN) H1N1 virus strain) that resulted in 50% mortality in wildtype littermate control mice showed minimal mortality in Irgm1-/- mice, indicating that Irgm1 deficiency was protective during influenza infection. This protective effect was dependent on the Type I interferon receptor Ifnar. We performed transcriptional profiling to identify molecular mechanisms associated with protection from influenza infection in Irgm1-/- lung. Both male and female mice were used at 8-12 weeks of age. Lung gene expression was assessed by RNA-seq at the following times post-influenza infection: Day 3 (early time point, early histological damage present in control mice), Day 6 (intermediate time point, late histological damage present in control mice) and Day 10 (late time point, morbidity and mortality present in control mice).
Project description:Utilisation of RNA-binding proteins (RBPs) is an important aspect of post-transcriptional regulation of viral RNA. Viruses such as influenza A viruses (IAV) interact with RBPs to regulate processes including splicing, nuclear export and trafficking, while also encoding RBPs within their genomes, such as NP and NS1. But with almost 1000 RBPs encoded within the human genome it is still unclear what role, if any, many of these proteins play during viral replication. Using the RNA interactome capture (RIC) technique, we isolated RBPs from IAV infected cells to unravel the RBPome of mRNAs from IAV infected human cells. This led to the identification of one particular RBP, MKRN2, that associates with and positively regulates IAV mRNA. Through further validation, we determined that MKRN2 is involved in the nuclear-cytoplasmic trafficking of IAV mRNA likely through an association with the RNA export mediator GLE1. In the absence of MKRN2, IAV mRNAs accumulate in the nucleus of infected cells, which we suspect leads to their degradation by the nuclear RNA exosome complex. MKRN2, therefore, appears to be required for the efficient nuclear export of IAV mRNAs in human cells.
Project description:Mice were infected intranasally with 1.5x10E5 PFU and total RNA were extracted from mice lungs at day 3. RNA samples were extracted from mice lung infected or not by influenza virus.
Project description:A growing body of evidence suggests gene regulatory functions for the majority of non-protein-coding RNAs (ncRNAs). Besides small RNAs (sRNAs), the diverse class of long ncRNAs (lncRNAs) recently came into focus of research. So far, the relevance of lncRNAs in infection processes remains elusive. Here, we report the differential expression of several classes of lncRNAs during influenza A virus (IAV) infection in human lung epithelial cells. 2 biological replicates of each condition were hybridzed in an independent color-swap; A549 cells were washed with PBS and then infected with viruses at MOI 1 in infection buffer for for 60M-bM-^@M-^Imin at room temperature. Cells were incubated for the indicated time periods at 37M-bM-^@M-^IM-BM-0C in DMEM supplemented with 0.2% bovine serum albumin, 4M-bM-^@M-^ImM l-glutamine and antibiotics. Supernatants of A/WSN/33 (H1N1) virus infected A549 cells (MOI 5, 4hpi) were exposed to UV light for 5 min and then used to stimulate A549 cells for 4 h Supernatants of A/WSN/33 (H1N1) virus infected A549 cells (MOI 5, 8hpi) were exposed to UV light for 5 min and then used to stimulate A549 cells for 8 h
Project description:Influenza virus infection leads to global cardiac proteome remodeling during convalescence MTD project_description "Influenza virus infections lead to more than 500,000 hospitalizations in the U.S. every year. Patients with cardiovascular diseases have been shown to be at high risk of influenza mediated cardiac complications. Importantly, recent reports have provided clinical data supporting a direct link between laboratory-confirmed influenza virus infection and adverse cardiac events. However, the molecular mechanisms of how influenza virus infection induces detrimental cardiac changes, even after resolution of the pulmonary infection, is completely unknown.