Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168577 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Huh7/5-2 cells (Binder et al., Hepatology 2007) were mock infected (DMEM) (time points 4 and 48 h) or infected with the chimeric HCV virus Jc1 (Pietschmann et al., PNAS 2006) (all time points). Multiplicity of infection was 15 (TCID50). Cells were lysed after 4, 12, 24, 48 and 72 hours post infection and total cellular RNA was prepared.
2012-06-15 | GSE38720 | GEO
Project description:Huh7/5-2 cells (Binder et al., Hepatology 2007) were mock infected (DMEM) (time points 4 and 48 h) or infected with the chimeric HCV virus Jc1 (Pietschmann et al., PNAS 2006) (all time points). Multiplicity of infection was 15 (TCID50). Cells were lysed after 4, 12, 24, 48 and 72 hours post infection and total cellular RNA was prepared. Mock infected cells serve as controls for the infected samples. The whole experiment was repeated on independent days (2 biological replicates). The dataset was also submitted to GEO (GSE38720).
2012-06-30 | E-MTAB-1148 | biostudies-arrayexpress
Project description:Cytosolic lipid droplets (LDs) are vital to Hepatitis C Virus (HCV) infection as the putative sites of virion assembly. To identify novel regulators of HCV particle production, we performed quantitative LD proteome analysis. Huh7.5 cells were labeled by stable isotope labeling with heavy amino acids in cell culture (SILAC) and subsequently infected with an HCV Jc1 reporter virus. After selection for HCV-infected cells, equal amounts of HCV-infected and uninfected control cells were mixed, LDs were isolated and analyzed by LC-ESI-MS/MS.
2016-09-26 | PXD004707 | Pride
Project description:Hepatitis C virus (HCV) infection is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. HCV can be sensed by host innate immunity to induce expression of interferons (IFNs) and a number of antiviral effectors. HCV-encoded NS3/4 serine protease can subvert host innate immune responses by cleaving MAVS, a critical adaptor protein in the RLR-mediated IFN signaling. To study innate immunity in the context of HCV infection, we constructed Huh7-MAVSR cells which express a mutant MAVS resistant to NS3/4A cleavage. HCV infection induces robust IFN response in Huh7-MAVSR cells, providing a cellular system to study antiviral innate immune response against HCV infection. To analyze host innate antiviral effectors against HCV infection, we performed an mRNA microarray analysis in the HCV-infected Huh7-MAVSR cells.
2018-02-08 | GSE110312 | GEO
Project description:Gene expression profiles of differentiated Huh7.5.1 cells infected with HCV Jc1 clone
| PRJNA278074 | ENA
Project description:Expression data from Tp80-Treated HCV replicon cell, Huh7/RepFeo.
| PRJNA258395 | ENA
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:To facilitate accurate measurement of the relative expression levels in Hepatitis C virus infection, we carried out in four human cancer cell lines derived from Hepatic (Hec3B; human hepatoma and Huh7; human hepatocellular carcinoma) or nonhepatic (Hec1B; human endometrial and 293T;human embryonic kidney) cells. These experiments identified several genes , expression of which was altered in the same direction among them with real time PCR analysis. Hepatic (Hec3B and Huh7) or nonhepatic (Hec1B and 293T) cells were examined after HCV infection and after mock-treatment. Each cell line was run in singlet.
2012-05-20 | E-GEOD-32886 | biostudies-arrayexpress
Project description:Long term cell culture adaptation of hepatitis C virus resulted in increased replication fitness in various human liver cell lines but in a moderate decrease in virus particle production upon infection of primary human hepatocytes (PHH). In order to identify molecular mechanisms conferring phenotypic differences in replicative fitness of the cell culture adapted virus strain p100pop, we infected PHH and Huh-7 cells with HCV, using the cell culture adapted strain p100pop or a Jc1 strain with similar genome organisation (Jc1-SP). Total RNA was extracted at 28 hours post inoculation and used for RNA sequencing. Transcriptome analyses, gene ontology enrichment analyses and KEGG pathway analyses revealed strong differences in the transcriptional signature of infected hepatoma cells and primary hepatocytes and the two virus strains used in this study. Wheras an innate immune response was induced in primary cells regardless of the infecting virus strain, this was not detectable in Huh-7 cells. Even though both viruses induce a similar host response in primary cells, the data indicate that the presence of cell culture adaptive mutations results in an increased expression of genes involved in the defense response to viral infection. In Huh-7 cells, differentially expressed genes associated with ER stress and apoptosis were solely enhanced upon p100pop infection but not upon Jc1-SP infection.
2024-01-19 | GSE246981 | GEO
Project description:Expression data in human hepatocytes with HCV infection
| PRJNA163091 | ENA