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ABSTRACT:
PROVIDER: PRJNA717395 | ENA |
REPOSITORIES: ENA
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Project description:We attempted to identify potential miRNAs that can regulate viral replication by screening host miRNAs in EV71-infected RD cells. To compare the differential expression of miRNAs in EV71-infected cells at different time points, miRNA expression profiles were analyzed using Agilent Human MicroRNA Array chips. At 5 h p.i., the expression levels of most miRNAs in EV71-infected cells were not different from those of mock-infected cells. However, five miRNAs (miR-574-3p, miR-574-5p, miR-181d, miR-197, and miR-939) showed a miRNAs (miR-193a-3p and miR-324-5p) exhibited a increase in expression level in response to EV71 infection at 10 h p.i.
2016-01-01 | GSE75455 | GEO
Project description:We attempted to identify potential miRNAs that can regulate viral replication by screening host miRNAs in EV71-infected RD cells. To compare the differential expression of miRNAs in EV71-infected cells at different time points, miRNA expression profiles were analyzed using Agilent Human MicroRNA Array chips. At 5 h p.i., the expression levels of most miRNAs in EV71-infected cells were not different from those of mock-infected cells. However, five miRNAs (miR-574-3p, miR-574-5p, miR-181d, miR-197, and miR-939) showed a miRNAs (miR-193a-3p and miR-324-5p) exhibited a increase in expression level in response to EV71 infection at 10 h p.i. RD cells were seeded (2*106 cells) in 10 cm dishes and incubated overnight. The cells were infected with EV71 (strain 2231) on ice at an M.O.I. of 10. After adsorption for 1 h, the virus suspension was replaced with DMEM containing 2% FBS, and the cells were harvested at the indicated times. Total cellular RNA extraction and miRNA microarray analyses were performed using the Agilent Human MicroRNA Array V2 chip, which contains 723 human and 76 viral miRNAs, each with 16 duplicates. Total gene signals were detected and analyzed using the GeneSpring 7.3.1 software and were normalized to the 75th percentile.
2016-07-03 | E-GEOD-75455 | biostudies-arrayexpress
Project description:Enterovirus 71 (EV71) is one of the leading causes of hand, foot and mouth disease with neurological complications in some cases. To study the pathogenesis of EV71 infection, large scale analyses of EV71 infected cells have been performed. However, most of these studies employed rhabdomyosarcoma (RD) cells or used transcriptomic strategy. Here, we performed SILAC-based quantitative proteomic analysis of EV71-infected U251 cells, a human glioma cell line. A total of 3,125 host proteins were quantified, 451 of which were differentially regulated as a result of EV71 infection at 8 hpi or 20 hpi or both.
2015-09-15 | PXD002454 | Pride
Project description:Ribosome profiling (Ribo-Seq) (maps positions of translating ribosomes on the transcriptome) analysis of human (RD) cells infected with enterovirus strains EV7, EV71, and PV1.
2018-10-19 | E-MTAB-6180 | biostudies-arrayexpress
Project description:During the life cycle of Enterovirus 71 (EV71), N6-methyladenosine (m6A) modification has an important impact on viral replication and the cellular response to viral infection, but the effect of m6A modification on cellular RNAs and pathways during infection is still unknown. The purpose of this research was to investigate the role of m6A in regulating host cell inflammatory response and disease progression during EV71 infection. Methylation RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) results show the m6A methylation modification map of control and EV71-infected groups of RD cells. And multilevel validation showed that decreased expression of demethylase FTO (fat mass and obesity-associated protein) was responsible for the elevated total m6A levels in EV71-infected RD cells and that TXNIP may be a target gene for demethylase FTO action. Further functional experiments showed that demethylase FTO silencing promoted TXNIP expression, activation of NLRP3 inflammasome and promoted the release of pro-inflammatory factors in vitro, and demethylase FTO overexpression showed the opposite result. Further tested in an animal model of severe EV71 infection, with results consistent with in vitro. In conclusion, our findings suggested that depletion of demethylase FTO in the presence of EV71 infection increased the m6A level of TXNIP mRNA 3ʹ UTR, increased mRNA stability, and promoted TXNIP expression, which activated the NLRP3 inflammasome and led to the release of pro-inflammatory factors, ultimately promoted HFMD progression. This could help with the development and prevention of m6A modification inhibitor-based drugs for viral-related inflammation and disease.
2023-06-13 | GSE234534 | GEO
Project description:Hand, foot and mouth disease (HFMD), caused by enterovirus 71 (EV71), presents mild to severe disease, and sometimes fatal neurological and respiratory manifestations. However, reasons for the severe pathogenesis remain undefined. To investigate this, infection and viral kinetics of EV71 isolates from clinical disease (mild, moderate and severe) from Sarawak, Malaysia, were characterized in human rhabdomyosarcoma (RD), neuroblastoma (SH-SY5Y) and peripheral blood mononuclear cells (PBMCs). High resolution transcriptomics was used to decipher EV71-host interactions in PBMCs. Ingenuity analyses revealed similar pathways triggered by all EV71 isolates, although the extent of activation varied. Importantly, several pathways were found to be specific to the severe isolate, including triggering receptor expressed on myeloid cells 1 (TREM-1) signaling. Depletion of TREM-1 in EV71-infected PBMCs with peptide LP17 resulted in decreased levels of pro-inflammatory genes, and reduced viral loads for the moderate and severe isolates. Mechanistically, this is the first report describing the transcriptome profiles during EV71 infections in primary human cells, and the involvement of TREM-1 in the severe disease pathogenesis, thus providing new insights for future treatment targets.
2020-03-16 | GSE135964 | GEO
Project description:HT29 cells was infected with EV71 at MOI 1 or nil respectively and harvested at 36hpi We use miRNA microarray to profile and identify miRNA which are up or down regulated due to EV71 infection
2014-05-08 | GSE57372 | GEO
Project description:Enterovirus 71 (EV71) and Coxsackievirus A16 (CA16) are the predominant etiological agents of hand, foot, and mouth disease (HFMD) and both belong to the human enterovirus A species of the Picornaviridae family. These viruses share similar genetic homology, although the clinical manifestations of HFMD caused by the two viruses have some discrepancies. Furthermore, the underlying mechanisms leading to these differences remain unclear. microRNAs (miRNAs) participate in numerous biological or pathological processes, including host responses to viral infections, by targeting messenger RNAs (mRNAs) for translational repression or degradation. Here, we focused on differences in miRNA expression patterns in peripheral blood mononuclear cells (PBMCs) of rhesus monkeys infected with EV71 or CA16 at different time points using high-throughput sequencing technology. For the first time, this study demonstrated that EV71 and CA16 infection result in specific miRNA expression patterns in PBMCs.
2016-08-19 | GSE85820 | GEO
Project description:We performed comprehensive miRNA profiling in EV71- and CA16-infected human umbilical vein endothelial cells (HUVECs) at multiple time points using high-throughput sequencing. The results showed that 135 known miRNAs exhibited remarkable differences in expression. Of these, 30differentially expressed miRNAs presented opposite trends in EV71- and CA16-infected samples. Subsequently, we mainly focused on the 30 key differentially expressed miRNAs through further screening to predict targets.Gene ontology (GO) and pathway analysis of the predicted targets showed the enrichment of 14 biological processes, 9 molecular functions, 8 cellular components, and 85 pathways. The regulatory networks of these miRNAs with predicted targets, GOs, pathways, and coexpression genes were determined, suggesting that miRNAs display intricate regulatory mechanisms during the infection phase. Consequently, we specifically analyzed the hierarchical GO categories of the predicted targets involved in biological adhesion. The results indicated that the distinct changes induced by EV71 and CA16 infection may be partly linked to the function of the blood-brain barrier. Taken together, this is the first report describing miRNA expression profiles in HUVECs with EV71 and CA16 infections using high-throughput sequencing. Our data provide useful insights that may help to elucidate the different host-pathogen interactions following EV71 and CA16 infection and offer novel therapeutic targets for these infections.
2017-02-07 | GSE94551 | GEO
Project description:We have previously shown that Heparin (Hep) significantly inhibited Enterovirus 71 (EV71) infection and binding in both Vero and a human neural cell line, SK-N-SH, in vitro. Therefore, in this study we intended to gain insight into the cellular and molecular mechanisms of action of Hep against clinical EV71 infection in SK-N-SH cells. Instead of stating a long list of gene functions and pathways, we tried to select for EV71-induced genes that were exclusively affected by antiviral activity of Hep through a multi-level comparison and characterization. Overall, our microarray analysis may suggest that Hep might exert its anti-EV71 activity in SK-N-SH cells, at least in part, through the following mechanisms: i. Reduction of the down-regulation effect of EV71 on TOX that would lead to an increased population of effective, mature T-cells and NK-cells; ii. Reduction of the up-regulation effect of EV71 on GIP, that in turn, would reduce recruiting different GPCRs, leading to a reduced viral infection in host cells; iii. Partially neutralization of the EV71-mediated apoptosis through expression of CARP2 that acts as an anti-apoptosis ubiquitin protein ligase (E3). EV71 is a neurovirological virus that can sometimes cause severe and fatal CNS complications in infected patients. Since still there is no approved drug for prophylaxis of EV71-casued disease, discovering a molecular drug target(s) for EV71 infection would be crucial. This was the first study to report direct assessment of mechanisms of action of antivirals against EV71 infection. SK-N-SH cells were infected with a clinical EV71 isolate followed by treatment with 125 µg/mL of Hep. At 72 hours post infection, antiviral activity and cytotoxicity of Hep at 125 µg/mL in 12-well plates were carried out at the same time as RNA extraction. This way, we could ensure that we would assess transcript profiles of the host cells under the same condition and time as assessment of antiviral activity and cytotoxicity for the same replicates. Changes in expression profiles of the host cells were comparatively assessed under four conditions: cell control (neither infection nor treatment, designated CC), treated only with Hep (compound control, designated Cyto), EV71-infected cells treated with Hep (treatment, designated H), and infected with EV71 without treatment with Hep (virus control, designated V). All experiments were applied in triplicate, and totally twelve GeneChip® Human Gene 1.0 ST arrays were purchased from Affymetrix and processed. Then, the following five contrasts were made: Hep vs. CC; VC vs. CC; Cyto vs CC; Hep vs. VC; and Hep vs. Cyto. For each contrast, only samples from the two target groups were included. The statistical parameters of ANOVAs, p values, multiple test corrections, and fold changes were calculated within each contrast. Then, a multi-level selection and analysis procedure was employed in order to attribute changes in the gene transcription level to antiviral activity of Hep.
2011-12-10 | E-GEOD-34234 | biostudies-arrayexpress