Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA258395 | ENA |
REPOSITORIES: ENA
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Project description:Cyclophilin binding drugs, NIM811 and cyclosporin A (CsA), inhibit the replication of HCV replicon. We investigated the mode of action of these drugs and identified host factors essential for HCV replication in a subgenomic replicon model. Experiment Overall Design: Cultured Huh7 cell were treated with CsA or NIM811 at different concentrations. Cells were harvested after 12, 24 or 48 hours. The extracted mRNA were hybridized on Affymetrix U133 Plus 2 microarrays.
2009-05-11 | E-GEOD-15935 | biostudies-arrayexpress
Project description:Hepatitis C virus (HCV) RNA synthesis and protein expression affect cell homeostasis by modulation of gene expression. The impact of HCV replication on global cell transcription has not been fully evaluated. Thus, we analysed the expression profiles of different clones of human hepatoma-derived Huh7 cells carrying a self-replicating HCV RNA which express all viral proteins (HCV replicon system).<br><br>First, we compared the expression profile of HCV replicon clone 21-5 with both the Huh-7 parental cells and the 21-5 cured (21-5c) cells. In these latter, the HCV RNA has been eliminated by IFN-? treatment. To confirm data, we also analyzed microarray results from both the 21-5 and two other HCV replicon clones, 22-6 and 21-7, compared to the Huh-7 cells. The study was carried out by using the Applied Biosystems (AB) Human Genome Survey Microarray v1.0 which provides 31,700 probes that correspond to 27,868 human genes. A total of 15 hybridization were performed, allowing to compare transcription profiles among the following groups of cell lines:<br><br>- HCV replicon clone: 21-5 (4 hybs)<br><br>- cured HCV replicon clone: 21-5c (4 hybs)<br><br>- parental cell line: Huh-7 (4 hybs)<br><br>- other HCV replicon clones: 21-7 (2 hybs); 22-6 (1 hyb)
2008-06-27 | E-MEXP-1686 | biostudies-arrayexpress
Project description:Hepatitis C Virus (HCV) has a extremely narrow host cell tropism and robustly infects only very few cell lines, most importantly the human hepatoma cell line Huh7. This cell line was isolated from a 57-year old Japanese male with fulminant hepatitis. Different subclones and passages of the Huh7 cell line show up to 1000-fold differences in HCV replication efficiency (permissiveness). In this experiment, we sought to identify factors responsible for these differences by correlating gene expression from eight different uninfected Huh7 variants with their respective HCV permissiveness. HCV replication efficiency was determined using electroporation of a subgenomic luciferase reporter replicon (genotype 1b, "con1/ET") and measuring luciferase activity at 48h post transfection normalized to the input value at 4h p.t.. "Relative permissiveness" of cell lines corresponds to their replication efficiency, normalized to the efficiency in the lowest permissive cells (Huh7 p13 and p28).
2019-11-08 | GSE140114 | GEO
Project description:OSM increases the antiviral effect of IFNα in Huh7 cells infected with hepatitis A virus (HAV) or HCV replicon and synergizes with IFNα in the induction of antiviral genes
2009-01-21 | GSE13046 | GEO
Project description:Tp80 is a novel antiviral compound. Antiviral mechanism of Tp80 is the inhibition of the viral genome replication through the recoverly of GPx2 expression downregulated by HCV infection. We used microarrays to evaluated the effect of Tp80 on the transcriptome of HCV replicon cells, compared with Non-infected host cells or non-treated HCV replicon cells.
2016-12-20 | GSE60488 | GEO
Project description:Expression data from 'naïve' and HVC-replicon containing Huh7 cells (Clone A cells)
| PRJNA116979 | ENA
Project description:OSM increases the antiviral effect of IFNα in Huh7 cells infected with hepatitis A virus (HAV) or HCV replicon and synergizes with IFNα in the induction of antiviral genes 16 samples. Four replicates for each experimental condition. 72 hours of treatment in DMEM supplemented with 2% FBS.
2009-01-20 | E-GEOD-13046 | biostudies-arrayexpress
Project description:The main goal of this study is to characterize the transcriptional modulations induced by antiviral compounds derived from chloroquine on Huh7 cells infected with HCV. And thus to identify among the genes modulated by infection, those who are regulated by chloroquine and potentially involved in the antiviral activity of the compound.Two HCV cell models were used: a non-infectious HCV replicon and the infectious HCV cell culture (HCVcc). In addition, this study aimed to highlight the characteristics of derivatives of antiviral chloroquine, compared with chloroquine itself. Abstract from the associated publication: Autophagy is a process of self-degradation of cellular components in which double-membrane autophagosomes sequester organelles or portion of cytosol and fuse with lysosomes or vacuoles for breakdown by resident hydrolases. Autophagy is upregulated in response to extra- or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection. Indeed, infection with hepatitis C virus (HCV) was shown to induce autophagy through ER stress signaling and subsequent Unfolded Protein Response (UPR) activation. Moreover, a role of autophagy in promoting HCV infection has been suggested and chloroquine (CQ), a lysosomal protease inhibitor, has been seen blocking autophagy as well as inhibiting HCV replication. In the present report, mechanisms accounting for these inhibitory effects were investigated. Gene expression profiling was performed on CQ treated JFH-1-infected Huh7 cells to identify the host cellular genes that are transcriptionally regulated by infection, and silenced by CQ-based treatment. Herein, we demonstrate that CQ reduces the expression of genes induced by the viral infection such as those encoding autophagic key factors triggering the turn-off of mTOR activity as well as factors involved in p53 and NF-KappaB activities. However, we present several lines of evidence demonstrating that the CQ repressive effect observed on the HCV-induced pathways results from a decrease of ER stress due to the upstream pH-dependent inhibitory effect of CQ on viral replication. Gene expression modulations were measured in Huh7 harboring replicon cells stimulated with a 10M-BM-5M of a Chloroquine derivative compound called CQd, during 6h, 12h and 24h. Two independent experiments were performed at each time. An untreated control condition was performed in each experiment, expression was measured at the 24h time point. For the HCVcc model, gene expression analysis was analyzed in two conditions: infection and treatment of infected cells. To characterize modulations in time course of infection, Huh7 naM-CM-/ve cells were infected with JFH1/CS-N6-A4 viral stock and gene expression was measured at 6h, 24h and 48h postinfection. For each kinetic time point, an uninfected condition was performed and gene expression was measured. An additional control testing the interferon (IFN) induced modulations on infected cells was included and gene expression was measured after a 48h stimulation with 100 IU of IFN (alpha 2 b). To characterize the antiviral modulations resulting from treatment with Chloroquine (CQ) or a derivative compound (CQd), gene expression was measured in JFH1/CS-N6-A4 infected Huh7 cells treated with 40M-BM-5M of CQ or CQd during 12h or 48h post-treatment and infection. For each kinetic time point 12h and 48h, an untreated infected control was also performed and gene expression measured.
2012-06-30 | E-GEOD-30351 | biostudies-arrayexpress
Project description:Time series data of HCV (JC1) infection of Huh7 cells
| PRJNA168577 | ENA
Project description:Short hairpin RNA (shRNA) expression strategies that allow safe and persistent target mRNA knockdown are key to the success of many in vitro or in vivo RNAi applications. Here, we propose a novel solution which is expression of a promoterless miRNA-adapted shRNA (shmiRNA) from an engineered genomic miRNA locus. For proof-of-concept, we genetically “vaccinated” liver cells against a human pathogen, by using TALEns or CRISPR to integrate an anti-hepatitis C virus (HCV) shmiRNA into the liver-specific miR-122/hcr gene. Reporter assays and qRT-PCR confirmed anti-HCV shmiRNA expression as well as miR-122 integrity and functionality. Specificity and safety of shmiRNA integration were validated via PCR, cDNA and miRNA profiling, and whole genome sequencing. A subgenomic HCV replicon and a full-length reporter virus, but not a Dengue virus control, were significantly impaired in the modified cells. Our original combination of DNA engineering and RNA expression technologies should benefit numerous applications, from basic miRNA research, to human cell and gene therapy Four Huh7 cells lines at 3 different passages were analyzed. The reference cell line was Huh7 wild type cells (WT). The other three cell lines had an integration of an anti-HCV shmiRNA in the hcr locus and miR-122 intact (T2 31.3) or mutated (TS 30.20 and U6 20.16). RNA was extracted from three different passages.
2015-05-07 | E-GEOD-68620 | biostudies-arrayexpress