E-MEXP-714
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-714 | ExpressionAtlas | 2025-01-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-714-analysis-methods.tsv | Tabular | |||
| E-MEXP-714-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-714-configuration.xml | Xml | |||
| E-MEXP-714-percentile-ranks.tsv | Tabular | |||
| E-MEXP-714.condensed-sdrf.tsv | Tabular |
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Project description:NK cells are believed to contribute to the control of hepatitis C virus infection and pathogenesis of liver disease. Standard treatment of both acute and chronic hepatitis C is based on the administration of interferon alpha, however, the effects of type I interferons on human NK cells have not been studied in the context of hepatitis C. We therefore first performed a microarray screen for genes differentially regulated in human NK cells after stimulation of PBMC with recombinant interferon alpha-2b. One of the genes upregulated was TRAIL which was confirmed in vitro on the protein level. Keywords: Interferon alpha; human NK cells; stimulation for 6 hours; cells sorted after stimulation of whole PBMC
2010-08-18 | GSE15743 | GEO
Project description:NK cells are believed to contribute to the control of hepatitis C virus infection and pathogenesis of liver disease. Standard treatment of both acute and chronic hepatitis C is based on the administration of interferon alpha, however, the effects of type I interferons on human NK cells have not been studied in the context of hepatitis C. We therefore first performed a microarray screen for genes differentially regulated in human NK cells after stimulation of PBMC with recombinant interferon alpha-2b. One of the genes upregulated was TRAIL which was confirmed in vitro on the protein level. Keywords: Interferon alpha; human NK cells; stimulation for 6 hours; cells sorted after stimulation of whole PBMC NK cells of PBMC of five healthy controls have been either isolated directly or after culturing for 6h in media containing 10% human AB serum supplemented with 1 and 100 ng/ml recombinant IFNa-2b. RNA of NK cells of the healthy controls was isolated and RNA was pooled for the hybridization.
2010-08-18 | E-GEOD-15743 | biostudies-arrayexpress
Project description:Temporal analysis of genes regulated by Interferon-alpha 2a in a HCV (Hepatitis C Virus) Replicon Cell line
2011-11-08 | E-MEXP-714 | biostudies-arrayexpress
Project description:Approximately 50% of patients with chronic hepatitis C (CHC) have a sustained virologic response (SVR) to treatment with pegylated interferon (pegINF)-α and ribavirin. Non-response to treatment is associated with constitutively increased expression of IFN-stimulated genes (ISGs) in the liver. Treatment of patients with acute hepatitis C (AHC) is more effective, with SVR rates >90%. We investigated mechanisms of the different responses of patients with CHC and AHC to pegIFN-α therapy. We analyzed IFN signaling and ISG expression in liver samples from patients with acute hepatitis C (AHC), patients with chronic hepatitis (CHC), and individuals without hepatitis C (controls) using microarray, immunohistochemical, and protein analyses. Findings were compared with those from primary human hepatocytes stimulated with IFN-α or IFN-γ, as reference sets. Expression levels of 100s of genes, primarily those regulated by IFN-γ, were altered in liver samples from patients with AHC compared with controls. Expression of IFN-γ–stimulated genes was induced in liver samples from patients with AHC, whereas expression of IFN-α–stimulated genes was induced in samples from patients with CHC. In an expression analysis of negative regulators of IFN-α signaling, we did not observe differences in expression of SOCS1 or SOCS3 between liver samples from patients with AHC and those with CHC. However, USP18 (another negative regulator of IFN-α signaling), was upregulated in liver samples of patients with CHC that did not respond to therapy, but not in AHC. In conclusion, differences in expression of ISGs might account for the greater response of patients with AHC, compared to those with CHC, to treatment with pegINF-α and ribavirin. Specifically, USP18 is upregulated in liver samples of patients with CHC that do not respond to therapy, but not in patients with AHC. (Interferon-γ Stimulated Genes, but not USP18, are Expressed in Livers of Patients with Acute Hepatitis C; Dill MT, Makowska Z et al, Gastroenterology 2012 (in press)) Primary human hepatocytes from 2 donors were analyzed. From each donor there are 5 samples: untreated cells, cells treated with interferon alpha (1000 IU/ml) for 6 and 24 hours and cells treated with interferon gamma (1000 IU/ml) for 6 and 24 hours.
2012-06-08 | E-GEOD-38147 | biostudies-arrayexpress
Project description:Patients chronically co-infected by Hepatitis B Virus (HBV) and Hepatitis D Virus (HDV) suffer from the most aggressive form of viral hepatitis leading to severe liver disease such as cirrhosis, hepatocellular carcinoma and liver decompensation. Treatments options are very limited with only two drugs used in clinic (IFN-α and Bulevertide) that rarely allow viral clearance. The molecular mechanisms leading to inhibition of HDV by IFN-α (in patients but also in vitro) are not known and mechanisms behind treatment failures in patients also remain elusive. Here we aimed at the identification of interferon stimulated genes (ISGs) that can specifically inhibit intracellular HDV replication. IFN-α was able to inhibit HDV in both co-infected differentiated HuH7.5-NTCP- and HepaRG cells (dHuH7.5-NTCP and dHepaRG, respectively). We hypothesized that ISGs responsible for the antiviral effect of HDV should be upregulated in both dHepaRG and dHuH7.5-NTCP cells upon treatment with IFN-α. To identify these ISGs, dHuh7.5-NTCP and dHepaRG cells were stimulated with IFN-α for 8h, total RNAs were extracted and gene expression was analyzed by RNAseq.
2025-04-23 | GSE288203 | GEO
Project description:Hepatitis C virus (HCV) infection is primarily treated with a pegylated interferon alpha based therapy, a regime that induces antiviral effects through the upregulation of many interferon-stimulated genes (ISGs). Whilst a number of anti-HCV ISGs have previously been identified, others may also be involved. Micorarrays were used to validate the presence of ISGs within subtracted libraries generated using the related techniques of suppression subtractive hybridisation and mirror orientation selection, which had initally been impllemented to isolate clones of ISGs following the interferon-alpha treatment of Huh-7 cells. Microarray data was generated for both untreated and interferon-alpha treated Huh-7 cells. No replicates were performed, however the microarray data was verified via the use of non-parametric (spearman) correlation analysis with RT-PCR data that had been generated using the same Huh-7 cell total RNA samples as the microarray experiments earlier.
2011-11-30 | E-GEOD-34022 | biostudies-arrayexpress
Project description:Hepatitis C virus (HCV) infection is primarily treated with a pegylated interferon alpha based therapy, a regime that induces antiviral effects through the upregulation of many interferon-stimulated genes (ISGs). Whilst a number of anti-HCV ISGs have previously been identified, others may also be involved. Micorarrays were used to validate the presence of ISGs within subtracted libraries generated using the related techniques of suppression subtractive hybridisation and mirror orientation selection, which had initally been impllemented to isolate clones of ISGs following the interferon-alpha treatment of Huh-7 cells.
2011-11-30 | GSE34022 | GEO
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
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
2024-09-02 | BIOMD0000000892 | BioModels
Project description:Transcriptional response to hepatitis C virus infection and interferon alpha treatment in the human liver
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