Therapy of allergic rhinitis using ribavirin spray to clear nasal commensal viruses
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE271863 | GEO | 2024/08/21
REPOSITORIES: GEO
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Project description:To explore the impact of nasal commensal viruses on the onset and progression of allergic rhinitis, We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of CD45+ cells in the nasal mucosa of mice treated with Vehicle, Ribavirin, Vehicle-OVA, or Ribavirin-OVA.
2024-08-21 | GSE266238 | GEO
Project description:For analyzing the exploratory nasal commensal viruses, we performed the metatranscriptomic analysis of the nose swabs from the enrolled AR patients both before and after treatments, as well as sequenced the nose swabs from a set of healthy volunteers without AR history.Simultaneously, to assess the expression of interferon-stimulated genes in patients with allergic rhinitis, we analyzed the gene expression of host reads.
2024-08-21 | GSE275114 | GEO
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.
2012-01-01 | GSE23031 | GEO
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
Project description:The cutaneous T-cell lymphoma Hut78 was treated with ribavirin for 120 h, and the gene expression of the treated cells was compared with respect to the expression of the cells without treatment. We evaluated the effect of treatment with ribavirin upon gene expression in a cutaneous T-cell lymphoma model, Hut78. Ribavirin treatment decreased approximately 90% of the viability of Hut78 cells. A complete genomic analysis of transcriptomic status after treatment with ribavirin of cutaneous T cell lymphoma Hut78 revealed an impact on the overall expression of transcripts.
2020-08-02 | GSE118066 | GEO
Project description:Background/Aims: Ribavirin improves treatment response to pegylated-interferon (PEG-IFN) in chronic hepatitis C but the mechanism remains controversial. We studied correlates of response and mechanism of action of ribavirin in treatment of hepatitis C. Methods: 70 treatment-naïve patients were randomized to 4 weeks of ribavirin (1000-1200 mg/d) or none, followed by PEG-IFN alfa-2a and ribavirin at standard doses and durations. Patients were randomized to undergo a liver biopsy either 24 hours before, or 6 hours after starting PEG-IFN. Hepatic gene expression was assessed by microarray and interferon-stimulated gene (ISG) expression quantified by the nCounter platform. Temporal changes in ISG expression were assessed by qPCR in peripheral-blood mononuclear cells (PBMC) and by serum levels of IP-10. Results: After four weeks of ribavirin monotherapy, HCV levels decreased by 0.5±0.5 log10 (p=0.009 vs. controls) and ALT by 33% (p<0.001). Ribavirin pretreatment, while modestly augmenting the induction of ISGs by PEG-IFN, did not modify the virological response to subsequent PEG-IFN and ribavirin treatment. However, biochemical, but not virological response to ribavirin monotherapy predicted response to subsequent combination treatment (rapid virological response, 71% in biochemical responders vs. 22% non-responders, p=0.01; early virological response, 100% vs. 68%, p=0.03, sustained virological response 83% vs. 41%, p=0.053). Ribavirin monotherapy lowered serum IP-10 levels but had no effect on ISG expression in PBMC. Conclusion: Ribavirin is a weak antiviral but its clinical effect in combination with PEG-IFN seems to be mediated by a separate, indirect mechanism, which may act to reset the interferon responsiveness in HCV-infected liver. Ribavirin pretreatment does not alter the clinical outcome of subsequent combination therapy.
2013-03-08 | GSE38663 | GEO
Project description:Predicting Treatment response to Hepatitis C, PEG-IFN/Ribavirin
2010-01-04 | PRD000181 | Pride
Project description:Live-attenuated viral vaccines have been successfully used to combat infectious disease for decades but due to their empirical derivation, little is known about their mechanisms of attenuation. This lack of understanding makes the development of next generation live attenuated vaccines difficult. The success of the 17D vaccine and availability of the parent virus, Asibi, makes it an excellent model to understand the molecular basis of attenuation of a live attenuated vaccine and the effects of viral diversity on vaccine function. Due to the differences in genetic diversity between WT Asibi virus and its 17D vaccine derivative, we investigated the changes in genetic diversity of 17D and Asibi viruses following treatment with ribavirin.
2020-01-01 | E-MTAB-8504 | biostudies-arrayexpress
Project description:Background/Aims: Ribavirin improves treatment response to pegylated-interferon (PEG-IFN) in chronic hepatitis C but the mechanism remains controversial. We studied correlates of response and mechanism of action of ribavirin in treatment of hepatitis C. Methods: 70 treatment-naïve patients were randomized to 4 weeks of ribavirin (1000-1200 mg/d) or none, followed by PEG-IFN alfa-2a and ribavirin at standard doses and durations. Patients were randomized to undergo a liver biopsy either 24 hours before, or 6 hours after starting PEG-IFN. Hepatic gene expression was assessed by microarray and interferon-stimulated gene (ISG) expression quantified by the nCounter platform. Temporal changes in ISG expression were assessed by qPCR in peripheral-blood mononuclear cells (PBMC) and by serum levels of IP-10. Results: After four weeks of ribavirin monotherapy, HCV levels decreased by 0.5±0.5 log10 (p=0.009 vs. controls) and ALT by 33% (p<0.001). Ribavirin pretreatment, while modestly augmenting the induction of ISGs by PEG-IFN, did not modify the virological response to subsequent PEG-IFN and ribavirin treatment. However, biochemical, but not virological response to ribavirin monotherapy predicted response to subsequent combination treatment (rapid virological response, 71% in biochemical responders vs. 22% non-responders, p=0.01; early virological response, 100% vs. 68%, p=0.03, sustained virological response 83% vs. 41%, p=0.053). Ribavirin monotherapy lowered serum IP-10 levels but had no effect on ISG expression in PBMC. Conclusion: Ribavirin is a weak antiviral but its clinical effect in combination with PEG-IFN seems to be mediated by a separate, indirect mechanism, which may act to reset the interferon responsiveness in HCV-infected liver. Ribavirin pretreatment does not alter the clinical outcome of subsequent combination therapy. Analysis of liver biopsy samples from 52 patients under 4 different treatment conditions.
2013-03-08 | E-GEOD-38663 | biostudies-arrayexpress
Project description:Study of PBMC gene expression during the first 10 weeks of therapy with Pegylated-interferon-alfa2b (PegIntronTM) and ribavirin (administered by weight) in HCV patients. This study compared the kinetics of gene expression during the first 10 weeks of therapy with Pegylated-interferon-alfa2b (PegIntronTM) and ribavirin (administered by weight) in HCV patients with the recently completed Virahep C study (9999) in which Peginterferon-alfa2a and ribavirin was administered. RNA was isolated from peripheral blood monocytes from twenty treatment-naïve patients just before treatment (day 0,) and at days 3, 6, 10, 13, 27, 42 and 70 days after treatment. Gene expression at each time was compared to that of day 0 using Affymetrix DNA-micro-arrays. Focusing upon genes that changed at least 1.5-fold and p<0.001, the numbers were high at day 3 (300 probes) and 10 (255) but dropped at days 6 (128) and 13 (142) but were steady at later time points. A large number of genes continued to be up regulated throughout the trial period. A second group of genes, including CXCL10, chemokine receptor 1, TRAIL, IL1 R and genes associated with complement and lipid metabolism, were transiently induced. CDKN1C (cyclin kinase inhibitor 1) was induced early but repressed at later times. Genes induced at later times were mostly related to blood chemistry and oxygen transport. Genes down regulated were related to ribosomal proteins and eukaryotic translation complexes. By week 10, 50% of the patients demonstrated a positive response to therapy. Conclusions: The response to pegintron/ribavirin was similar to that reported for Pegasys/ribavirin, although the extent of gene induction was less. No differences were found between patients responding to treatment or non-responders during this period. Our data suggest that more than once a week dosing might be desirable early on during treatment. Keywords: Time Course, gene expression
2009-04-21 | GSE11342 | GEO