ArticleThe American journal of pathology2014
HCV infection selectively impairs type I but not type III IFN signaling.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 63 citations in OpenAlex.
- Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.Pathogens (Basel, Switzerland) · 2024Review
- HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024Review
- CD81 suppresses NF-κB signaling and is downregulated in hepatitis C virus expressing cells.Frontiers in cellular and infection microbiology · 2024Article
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- Hepatitis C virus and intracellular antiviral response.Current opinion in virology · 2022Review
- Interactions of Autophagy and the Immune System in Health and Diseases.Autophagy reports · 2022Article
- Extracellular Vesicle Release Promotes Viral Replication during Persistent HCV Infection.Cells · 2021Article
- Article
- Advances in Hepatitis E Virus Biology and Pathogenesis.Viruses · 2021Review
- Review
- Integrated stress response in hepatitis C promotes Nrf2-related chaperone-mediated autophagy: A novel mechanism for host-microbe survival and HCC development in liver cirrhosis.Seminars in cell & developmental biology · 2020Review
- Regulation of Innate Immune Responses by Autophagy: A Goldmine for Viruses.Frontiers in immunology · 2020Review
- Regulation of Autophagy in Cells Infected With Oncogenic Human Viruses and Its Impact on Cancer Development.Frontiers in cell and developmental biology · 2020Review
- Type I interferons and endoplasmic reticulum stress in health and disease.International review of cell and molecular biology · 2020Review
- Review
- Polyphenylene carboxymethylene (PPCM) in vitro antiviral efficacy against Ebola virus in the context of a sexually transmitted infection.Antiviral research · 2019Article
- The IFN-λ4 Conundrum: When a Good Interferon Goes Bad.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019Review
- Hepatitis C virus infection increases autophagosome stability by suppressing lysosomal fusion through an Arl8b-dependent mechanism.The Journal of biological chemistry · 2019Article
- Article
- Crosstalk between Autophagy and Type I Interferon Responses in Innate Antiviral Immunity.Viruses · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
A stable and persistent Hepatitis C virus (HCV) replication cell culture model was developed to examine clearance of viral replication during long-term treatment using interferon-α (IFN-α), IFN-λ, and ribavirin (RBV). Persistently HCV-infected cell culture exhibited an impaired antiviral response to IFN-α+RBV combination treatment, whereas IFN-λ treatment produced a strong and sustained antiviral response that cleared HCV replication. HCV replication in persistently infected cells induced chronic endoplasmic reticulum (ER) stress and an autophagy response that selectively down-regulated the functional IFN-α receptor-1 chain of type I, but not type II (IFN-γ) or type III (IFN-λ) IFN receptors. Down-regulation of IFN-α receptor-1 resulted in defective JAK-STAT signaling, impaired STAT phosphorylation, and impaired nuclear translocation of STAT. Furthermore, HCV replication impaired RBV uptake, because of reduced expression of the nucleoside transporters ENT1 and CNT1. Silencing ER stress and the autophagy response using chemical inhibitors or siRNA additively inhibited HCV replication and induced viral clearance by the IFN-α+RBV combination treatment. These results indicate that HCV induces ER stress and that the autophagy response selectively impairs type I (but not type III) IFN signaling, which explains why IFN-λ (but not IFN-α) produced a sustained antiviral response against HCV. The results also indicate that inhibition of ER stress and of the autophagy response overcomes IFN-α+RBV resistance mechanisms associated with HCV infection.
Indexed as
Identifiers
What OpenQuestion holds
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.