Small RNA sequencing of HCV infected hepatoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA657046 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12450051.fastq.gz | Fastqsanger.gz | |||
| SRR12450052.fastq.gz | Fastqsanger.gz | |||
| SRR12450053.fastq.gz | Fastqsanger.gz | |||
| SRR12450054.fastq.gz | Fastqsanger.gz | |||
| SRR12450055.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:HCV infection requires both virus and host factors, including endogenous genes, a large proportion of which are noncoding RNAs (ncRNAs). The identification and mechanistic elucidation of these stably and conservatively expressed RNAs will shed light on HCV gene diagnosis and therapy. Nevertheless, most studied ncRNAs in HCV are microRNAs, with numerous other types of ncRNAs being neglected, such as long noncoding RNAs (lncRNAs) or small nucleolar RNAs (snoRNAs). Here, using two different hepatoma cell lines, we performed small RNA sequencing and analyzed the differential expression of microRNAs and snoRNAs, which provide data for further functional validation of snoRNAs and microRNAs during HCV infection.
2020-08-18 | GSE156205 | GEO
Project description:expression profiling of HCV infected human hepatoma cells
2010-12-31 | E-MEXP-2548 | biostudies-arrayexpress
Project description:Transcriptional profiling of human hepatoma cell lines comparing control uninfected Huh7.5 cells with Huh7.5 cells persistently infected with HCV (HPI cell). The latter maintains and produces HCV.
2014-12-01 | GSE52321 | GEO
Project description:Characterization of PPAR-α regulated miRNAs in HCV infected hepatoma cells
| PRJNA423012 | ENA
Project description:Hepatitis C virus (HCV) is a global problem. To better understand HCV infection researchers employ in vitro HCV cell-culture (HCVcc) systems that use Huh-7 derived hepatoma cells that are particularly permissive to HCV infection. A variety of hyper-permissive cells have been subcloned for this purpose. In addition, subclones of Huh-7 which have evolved resistance to HCV are available. However, the mechanisms of susceptibility or resistance to infection among these cells have not been fully determined. In order to elucidate mechanisms by which hepatoma cells are susceptible or resistant to HCV infection we performed genome-wide expression analyses of six Huh-7 derived cell cultures (Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1) R that have different levels of permissiveness to infection. A great number of genes, representing a wide spectrum of functions are differentially expressed between cells. To focus our investigation, we identify host proteins from HCV replicase complexes, perform gene expression analysis of three HCV infected cells (infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2) and conduct a detailed analysis of differentially expressed host factors by integrating a variety of data sources. Our results demonstrate that changes relating to susceptibility to HCV infection in hepatoma cells are linked to the innate immune response, secreted signal peptides and host factors that have a role in virus entry and replication. This work identifies both known and novel host factors that may influence HCV infection. Our findings build upon current knowledge of the complex interplay between HCV and the host cell, which could aid development of new antiviral strategies. Six Huh-7 derived hepatoma cell types that have different levels of susceptibility to HCV infection in cell culture are used: Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1. Of these the first three (label starting Huh are susceptible to HCV infection and the latter three (label starting R are resistant to HCV infection. All cell types are derived from Huh-7. Huh-7.5.1 is a subclone of Huh-7.5 that in turn is a subclone of Huh-7. Huh-7.5.1c2 is a subclone of Huh-7.5.1. R1.09 and R1.10 are subclones of R1 that is inturn a sublone of Huh-7.5,1. R2.1 is a subclone of Huh-7.5.1.
2011-06-11 | GSE29889 | GEO
Project description:Expression data from HCV infected hepatoma carcinoma cell line Huh7-MAVSR cells
| PRJNA433419 | ENA
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:Hepatitis C virus (HCV) is a global problem. To better understand HCV infection researchers employ in vitro HCV cell-culture (HCVcc) systems that use Huh-7 derived hepatoma cells that are particularly permissive to HCV infection. A variety of hyper-permissive cells have been subcloned for this purpose. In addition, subclones of Huh-7 which have evolved resistance to HCV are available. However, the mechanisms of susceptibility or resistance to infection among these cells have not been fully determined. In order to elucidate mechanisms by which hepatoma cells are susceptible or resistant to HCV infection we performed genome-wide expression analyses of six Huh-7 derived cell cultures (Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1) R that have different levels of permissiveness to infection. A great number of genes, representing a wide spectrum of functions are differentially expressed between cells. To focus our investigation, we identify host proteins from HCV replicase complexes, perform gene expression analysis of three HCV infected cells (infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2) and conduct a detailed analysis of differentially expressed host factors by integrating a variety of data sources. Our results demonstrate that changes relating to susceptibility to HCV infection in hepatoma cells are linked to the innate immune response, secreted signal peptides and host factors that have a role in virus entry and replication. This work identifies both known and novel host factors that may influence HCV infection. Our findings build upon current knowledge of the complex interplay between HCV and the host cell, which could aid development of new antiviral strategies. Six Huh-7 derived hepatoma cell types that have different levels of susceptibility to HCV infection in cell culture are used: Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1. Of these the first three (label starting Huh are susceptible to HCV infection and the latter three (label starting R are resistant to HCV infection. All cell types are derived from Huh-7. Huh-7.5.1 is a subclone of Huh-7.5 that in turn is a subclone of Huh-7. Huh-7.5.1c2 is a subclone of Huh-7.5.1. R1.09 and R1.10 are subclones of R1 that is inturn a sublone of Huh-7.5,1. R2.1 is a subclone of Huh-7.5.1. 39 samples are used. In every case there are 3 biological replicates, i.e., there are 13 unique conditions (39/3=13). These samples are subdivided between two studies: (1) A comparison of HCV infection resistant cells R1.09, R1.10 and R2 against HCV susceptible Huh-7.5.1. (2) A comparison of JFH1 HCV infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2 cells versus their uninfected counterparts. In each case there are two uninfected counterparts, cells that were harvested after being in culture for 20 hours and cells that were harvested at the same time point as the infected cells, that is, at the peak time of infection. Peak times for infection vary between cells, depending on their susceptibility to infection: 168 hours for Huh-7, 120 hours for Huh-7.5.1 and 96 hours for Huh-7.5.1c2.
2011-06-11 | E-GEOD-29889 | biostudies-arrayexpress
Project description:A total of 52 patients were analyzed: 21 of them monoinfected with HCV and 31 coinfected with HIV (HCV/HIV). HCV patients were recruited from Hospital Italiano and Hospital José María Ramos Mejía from Buenos Aires, Argentina, and HCV/HIV patients from Hospital Universitario La Paz, Hospital Infanta Leonor, Hospital Universitario La Princesa, Hospital Puerta de Hierro, from Madrid, Spain. All samples were processed at the National Center for Microbiology (Madrid). Patients were naıve of treatment for HCV. CHC infection was defined by the presence of anti-HCV antibodies in serum and detectable HCV RNA in plasma samples in at least 2 separate occasions. All HIV+ patients had HIV antibodies, CD4+ T-cells counts ≥ 500 cel/mm3 for at least one year before sample collection, and undetectable HIV viral load since they received suppressive antiretroviral treatment (ART) for at least one year. Plasma extracellular vesicles isolation and RNA purification was performed using the ExoRNeasy Serum/Plasma Midi kit (QIAGEN, Cat #77044). EVs were phenol-lysed and total RNA was purified by ethanol-based membrane binding into spin columns. Quality and integrity were evaluated by the Bioanalyzer 2100 with Agilent RNA 6000 Nano kit (Agilent). Small RNA library synthesis and sequencing were performed at Centre for Genomic Regulation (CRG) at Barcelona (Spain). Small RNA libraries were constructed with Illumina’s TruSeq Small RNA kit v.4 (Illumina) and 50nts (1x50) were sequenced in an Illumina HiSeq2500, with a single read approach.
2023-02-27 | E-MTAB-11811 | biostudies-arrayexpress
Project description:Small RNA sequencing of plasma extracellular vesicles from HCV and HIV/HCV coinfected patients
| PRJEB53428 | ENA