Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of genome-length HCV RNA-replicating OL8(3.5Y) cells and OL8(3.5Y)-derived ribavirin-resistant cells

ABSTRACT: Ribavirin (RBV) is a potential partner of interferon-based therapy and recently approved therapy using direct acting antivirals for patients with chronic hepatitis C, However, the precise mechanisms undelying RBV action against hepatitis C virus (HCV) replication are not yet understood. To clarify this point, we established RBV-resistant cell lines from RBV-sensitive HCV RNA-replicating cell line, OL8(3.5Y), and characterized their features. We used microarrays to compare the gene expression pattern between OL8(3.5Y) cells and three RBV-resistant cells and identified genes commonly altered by more than four-fold among RBV-resistant cells compared with the OL8(3.5Y) cells. Growing cells from RBV-sensitive OL8(3.5Y) and three RBV-resistant cell lines were used for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Shinya Satoh

PROVIDER: E-GEOD-60948 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data of genome-length HCV RNA-replicating OL8(3.5Y) cells and OL8(3.5Y)-derived ribavirin-resistant cells

Project description:Ribavirin (RBV) is a potential partner of interferon-based therapy and recently approved therapy using direct acting antivirals for patients with chronic hepatitis C, However, the precise mechanisms undelying RBV action against hepatitis C virus (HCV) replication are not yet understood. To clarify this point, we established RBV-resistant cell lines from RBV-sensitive HCV RNA-replicating cell line, OL8(3.5Y), and characterized their features. We used microarrays to compare the gene expression pattern between OL8(3.5Y) cells and three RBV-resistant cells and identified genes commonly altered by more than four-fold among RBV-resistant cells compared with the OL8(3.5Y) cells.

2014-08-30 | GSE60948 | GEO

Virus genotype-dependent gene expression in progressive liver disease prior to the development of advanced cirrhosis

Project description:Despite advances in antiviral therapy, molecular drivers of Hepatitis C Virus (HCV)-related liver disease remain poorly characterised. Chronic infection with HCV genotypes (1 and 3) differ in presentation of liver steatosis and virological response to therapies, both to interferon and direct acting antivirals. Using whole transcriptome microarrays, we analysed gene expression profiles of liver tissue obtained from individuals infected with either HCV G1 or G3 in progressive and advanced liver disease and identified key altered cellular pathways.

2019-06-01 | E-MTAB-7751 | biostudies-arrayexpress

Ribavirin Treated Huh7.5.1 Cells

Project description:The combination of peginterferon and ribavirin is the standard treatment for chronic hepatitis C. Our recent clinical study suggests that ribavirin augments the induction of interferon stimulated genes (ISGs) in patients treated for HCV infection [1]. In order to further characterize the mechanisms of action of ribavirin, we examined the effect of ribavirin treatment on ISG induction in cell culture. In addition, the effect of ribavirin on infectious HCV cell culture systems was also studied. Similar to interferon-alpha, ribavirin potently inhibits JFH-1 infection of Huh7.5.1 cells in a dose-dependent manner, which spans the physiological concentration of ribavirin in vivo. Microarray analysis and subsequent quantitative PCR assays demonstrated that ribavirin treatment resulted in the induction of a distinct set of ISGs. These ISGs, including IRF7 and IRF9 are known to play an important role in anti-HCV responses. When ribavirin is used in conjunction with interferon, induction of specific ISGs is synergistic when compared to either drug applied separately. Direct up-regulation of these antiviral genes by ribavirin is mediated by a novel mechanism different from those associated with interferon signaling and intracellular double stranded RNA sensing pathways such as RIG-I and MDA5. RNA interference studies excluded the activation of the Toll-like receptor and NF-KappaB pathways in the action of ribavirin. In conclusion, our study suggests that ribavirin, acting via a novel innate mechanism, potentiates the anti-HCV effect of interferon. Understanding the mechanism of action of ribavirin would be valuable in identifying novel antivirals. RNA from three samples were treated with Ribavirin and compared to three PBS treated samples

2012-01-01 | E-GEOD-23031 | biostudies-arrayexpress

Ribavirin Treated Huh7.5.1 Cells

2012-01-01 | GSE23031 | GEO

Sandip2013 - Modeling the dynamics of hepatitis C virus with combined antiviral drug therapy: interferon and ribavirin.

Project description:Modeling the dynamics of hepatitis C virus with combined antiviral drug therapy: interferon and ribavirin. Banerjee S1, Keval R, Gakkhar S. Author information 1 Department of Mathematics, Indian Institute of Technology Roorkee (IITR), Roorkee 247667, Uttaranchal, India. Electronic address: sandofma@iitr.ernet.in. Abstract A mathematical modeling of hepatitis C virus (HCV) dynamics and antiviral therapy has been presented in this paper. The proposed model, which involves four coupled ordinary differential equations, describes the interaction of target cells (hepatocytes), infected cells, infectious virions and non-infectious virions. The model takes into consideration the addition of ribavirin to interferon therapy and explains the dynamics regarding a biphasic and triphasic decline of viral load in the model. A critical drug efficacy parameter has been defined and it is shown that for an efficacy above this critical value, HCV is eradicated whereas for efficacy lower this critical value, a new steady state for infectious virions is reached, which is lower than the previous steady state value. Copyright © 2013 Elsevier Inc. All rights reserved. KEYWORDS: Hepatitis C virus (HCV); Infected cells; Infectious virions; Interferon; Noninfectious virions; Ribavirin; Target cells

2020-01-09 | MODEL1912120002 | BioModels

Sandip2013 - Modeling the dynamics of hepatitis C virus with combined antiviral drug therapy: interferon and ribavirin.

2024-09-02 | BIOMD0000000892 | BioModels

Baseline Intrahepatic and Peripheral Innate Immune Responses are Associated with Hepatitis C Virus Eradication in Patients Receiving Direct Acting Antivirals

Project description:Hepatitis C virus (HCV) infection induces interferon stimulated genes (ISGs) and downstream innate immune responses. This study investigated whether baseline and on-treatment differences in these responses predict response versus virological breakthrough during therapy with direct acting antivirals (DAA). Microarray and nanostring analyses were performed on paired liver biopsies and analyzed using linear mixed models. As biomarkers for peripheral IFN responses, peripheral blood natural killer cells were assessed for pSTAT1 and TRAIL expression and for cytotoxicity.

2018-12-14 | GSE109278 | GEO

Antiviral HCV Treatment Induces Rapid Proteomic and Phospho-proteomic Changes in Hepatic Interferon and ERK1/2 Signaling Pathways

Project description:Although treatment of chronic hepatitis C virus (HCV) infection with direct acting antivirals (DAAs) results in high rates of cure, liver fibrosis does not resolve immediately after HCV eradication. Resolution of fibrosis occurs in some, but not all patients, after HCV cure, and hepatic decompensation and hepatocellular carcinoma can still occur in patients with pre-existing cirrhosis. We hypothesized that evaluation of the host liver proteome in the context of HCV treatment would provide insight into how inflammatory and fibrinogenic pathways change upon HCV eradication. We evaluated the whole liver proteome and phosphoproteome using paired liver biopsies from 8 HCV-infected patients collected before or immediately after treatment with DAAs in clinical trials. We identify interferon stimulated proteins as the predominant pathways that decrease with HCV treatment, which is consistent with previous analyses of the liver transcriptome during DAA therapy. While there was no change in the proteome of pathways associated with liver fibrosis, we identified a decrease in the phosphoproteome signature for ERK1/ERK2 as a result of HCV treatment. Conclusion: There is a reduction in the endogenous interferon-mediated antiviral response and alterations in the phosphoproteome that may precede resolution of fibrosis in the liver immediately after treatment of HCV with DAAs.

2023-03-11 | PXD024846 | Pride

Small Molecule Degraders of the Hepatitis C Virus Protease Reduce Susceptibility to Resistance Mutations

Project description:Targeted protein degradation (TPD) has emerged as a promising new drug development paradigm. We leveraged this strategy to develop a new class of small molecule antivirals that induce proteasomal degradation of viral proteins. Telaprevir, a ‘reversible-covalent’ inhibitor that binds to the hepatitis C virus (HCV) protease active site was conjugated to ligands that recruit the CRL4CRBN ligase complex, yielding compounds that can both inhibit and induce the degradation of the HCV NS3/4A protease. We developed an optimized degrader, DGY-08-097, that potently inhibits HCV in a cellular infection model and demonstrate that protein degradation contributes to its antiviral activity. Finally, we show that this new class of antiviral agents can overcome viral variants that confer resistance to traditional enzymatic inhibitors such as telaprevir. Overall, our work provides proof-of-concept that targeted protein degradation may provide a new paradigm for the development of antivirals with superior resistance profiles.

2019-07-03 | PXD014346 | Pride

Hepatic gene expression before and during interferon and ribavirin combination therapy

Project description:Patients who cleared HCV viremia early during therapy tended to show favorable outcomes, whereas patients who needed a longer period to clear HCV had poorer outcomes. We explored the mechanisms of treatment resistance by comparing hepatic gene expression before and during treatment

2009-12-31 | GSE17183 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data