ArticleJournal of virology2011
Analysis of interferon signaling by infectious hepatitis C virus clones with substitutions of core amino acids 70 and 91.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Trial
- Global distribution and temporal analysis of R70Q/H oncogenic mutations in hepatitis C virus subtype 1b core protein.Frontiers in cellular and infection microbiology · 2025Article
- Crosstalk between RNA Metabolism and Cellular Stress Responses during Zika Virus Replication.Pathogens (Basel, Switzerland) · 2020Review
- Frequency of Interferon-Resistance Conferring Substitutions in Amino Acid Positions 70 and 91 of Core Protein of the Russian HCV 1b Isolates Analyzed in the T-Cell Epitopic Context.Journal of immunology research · 2018Article
- Hepatitis C virus induces a prediabetic state by directly impairing hepatic glucose metabolism in mice.The Journal of biological chemistry · 2017Article
- Impact of hepatitis C virus core mutations on the response to interferon-based treatment in chronic hepatitis C.World journal of gastroenterology · 2016Observational
- Evaluation of Interferon Resistance in Newly Established Genotype 1b Hepatitis C Virus Cell Culture System.Journal of clinical and translational hepatology · 2016Article
- Chaperones in hepatitis C virus infection.World journal of hepatology · 2016Review
- Emerging roles of interferon-stimulated genes in the innate immune response to hepatitis C virus infection.Cellular & molecular immunology · 2016Review
- SOCS3 mRNA expression and polymorphisms as pretreatment predictor of response to HCV genotype 3a IFN-based treatment.SpringerPlus · 2016Article
- Kinetic response of wild and mutant core codon 70 strains of HCV genotype 1b to pegylated interferon-α and ribavirin therapy.Virology journal · 2015Article
- The role of HCV proteins on treatment outcomes.Virology journal · 2015Review
- Amino Acid Polymorphisms in Hepatitis C Virus Core Affect Infectious Virus Production and Major Histocompatibility Complex Class I Molecule Expression.Scientific reports · 2015Article
- Substitution in Amino Acid 70 of Hepatitis C Virus Core Protein Changes the Adipokine Profile via Toll-Like Receptor 2/4 Signaling.PloS one · 2015Article
- Impact of hepatitis C virus heterogeneity on interferon sensitivity: an overview.World journal of gastroenterology · 2014Review
- Production and pathogenicity of hepatitis C virus core gene products.World journal of gastroenterology · 2014Review
- Unfolded protein response in hepatitis C virus infection.Frontiers in microbiology · 2014Review
- SOCS3, a Major Regulator of Infection and Inflammation.Frontiers in immunology · 2014Review
- Identification of alpha interferon-induced envelope mutations of hepatitis C virus in vitro associated with increased viral fitness and interferon resistance.Journal of virology · 2013Article
- Impact of host and virus genome variability on HCV replication and response to interferon.Current opinion in virology · 2013Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substitution of amino acids 70 and 91 in the hepatitis C virus (HCV) core region is a significant predictor of poor responses to peginterferon-plus-ribavirin therapy, while their molecular mechanisms remain unclear. Here we investigated these differences in the response to alpha interferon (IFN) by using HCV cell culture with R70Q, R70H, and L91M substitutions. IFN treatment of cells transfected or infected with the wild type or the mutant HCV clones showed that the R70Q, R70H, and L91M core mutants were significantly more resistant than the wild type. Among HCV-transfected cells, intracellular HCV RNA levels were significantly higher for the core mutants than for the wild type, while HCV RNA in culture supernatant was significantly lower for these mutants than for the wild type. IFN-induced phosphorylation of STAT1 and STAT2 and expression of the interferon-inducible genes were significantly lower for the core mutants than for the wild type, suggesting cellular unresponsiveness to IFN. The expression level of an interferon signal attenuator, SOCS3, was significantly higher for the R70Q, R70H, and L91M mutants than for the wild type. Interleukin 6 (IL-6), which upregulates SOCS3, was significantly higher for the R70Q, R70H, and L91M mutants than for the wild type, suggesting interferon resistance, possibly through IL-6-induced, SOCS3-mediated suppression of interferon signaling. Expression levels of endoplasmic reticulum (ER) stress proteins were significantly higher in cells transfected with a core mutant than in those transfected with the wild type. In conclusion, HCV R70 and L91 core mutants were resistant to interferon in vitro, and the resistance may be induced by IL-6-induced upregulation of SOCS3. Those mechanisms may explain clinical interferon resistance of HCV core mutants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.