Hepatitis C virus subtype 1b
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REPOSITORIES: ENA
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Project description:Hepatitis C virus subtype 1b Targeted Locus (Loci)
| PRJNA275480 | ENA
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
2019-12-13 | BIOMD0000000892 | BioModels
Project description:Ultra-deep sequencing of hepatitis B virus quasispecies in association with clinical status and nucleos(t)ide analogue treatment
| PRJDB2174 | ENA
Project description:The purpose of this study is to determine if there is an association between hepatitis C infection and kidney cancer. All patients who are diagnosed with kidney cancer and who will either have a biopsy or surgery will be offered to be tested for hepatitis C. The control group will be colon cancer patients. Both groups would be of recent diagnosis (6 months).
| 2110600 | ecrin-mdr-crc
Project description:The aim of this deep sequencing project is to determine whether treatment of chronically Hepatitis C infected chimpanzees with an antiviral compound leads to accumulation of viral mutants. The liver-expressed microRNA-122 (miR-122) is essential for hepatitis C virus (HCV) RNA accumulation in cultured liver cells, but its potential as a target for antiviral intervention has not been assessed. Here, we show that treatment of chronically infected chimpanzees with a locked nucleic acid (LNA)-modified oligonucleotide (SPC3649) complementary to miR-122 leads to long-lasting suppression of HCV viremia with no evidence for viral resistance or side effects in the treated animals. Furthermore, transcriptome and histological analyses of liver biopsies demonstrated derepression of target mRNAs with miR-122 seed sites, down-regulation of interferon-regulated genes (IRGs) and improvement of HCV-induced liver pathology. The prolonged virological response to SPC3649 treatment without HCV rebound holds promise of a new antiviral therapy with a high barrier to resistance.
2009-12-03 | GSE18919 | GEO
Project description:Hepatitis B virus (HBV) can integrate into the chromosomes of infected hepatocytes, contributing to the production of hepatitis B surface antigen (HBsAg) and to hepatocarcinogenesis. We performed spatial transcriptomics to investigate the intrahepatic cell heterogeneity and the spatial distribution of transcriptionally active HBV integration events in different phases of chronic HBV infection. Our analysis revealed that transcriptionally active HBV integration occurred in chronically HBV-infected patients in different phases, including those patients with HBsAg loss, and antiviral treatment was associated with a decreased number and extent of viral integrations.
2023-09-30 | GSE243367 | GEO
Project description:Hepatitis C virus (HCV) infection can result in viral chronicity or clearance. Although host genetics and particularly genetic variation in the interferon lambda (IFNL) locus are associated with spontaneous HCV clearance and treatment success, the mechanisms guiding these clinical outcomes remain unknown. Using a laser capture microdissection-driven unbiased systems virology approach, we isolated and transcriptionally profiled HCV-infected and adjacent primary human hepatocytes (PHH) approaching single cell resolution. An innate antiviral immune signature dominated the transcriptional response, but differed in magnitude and diversity between HCV-infected and adjacent cells. Molecular signatures associated with more effective antiviral control were determined by comparing donors with high and low infection frequencies. Cells from donors with clinically unfavorable IFNL genotypes were infected at a greater frequency and exhibited dampened antiviral and cell death responses. These data suggest that early virus-host interactions, particularly host genetics and induction of innate immunity, critically determine the outcome of HCV infection.
2014-02-12 | GSE54648 | GEO
Project description:Chronic hepatitis B (CHB) is a global health care challenge and a major cause of liver disease. Existing therapies do not result in a functional cure in most individuals, necessitating new antiviral strategies against Hepatitis B virus (HBV). To identify additional therapeutic avenues, we performed a focused screen of epigenetic modifiers to identify inhibitors of HBV replication. From this work we identified small molecule inhibitors of the histone lysine demethylase 5 (KDM5) with antiviral activity against HBV. To enhance the cellular permeability and liver accumulation of the most potent KDM5 inhibitor identified (GS-080) a prodrug was developed (GS-5801) that resulted in improved bioavailability and liver exposure as well as increased accumulation of the H3K4me3:H3 ratio on chromatin. GS-5801 treatment of HBV-infected primary human hepatocytes inhibited HBV replication and antigen levels. Evaluation of GS 5801 antiviral activity in a humanized mouse model of HBV infection, however, did not result in antiviral efficacy, despite achieving pharmacodynamic levels of H3K4me3:H3 predicted to be efficacious. Together these data highlight discordance between the antiviral effects of GS 5801 observed in HBV-infected primary human hepatocytes.
2021-02-24 | GSE165727 | GEO