ArticleJournal of virology2012
Hepatitis C virus-mediated inhibition of cathepsin S increases invariant-chain expression on hepatocyte surface.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Cathepsin S: molecular mechanisms in inflammatory and immunological processes.Frontiers in immunology · 2025Review
- Key role of interferon regulatory factor 1 (IRF-1) in regulating liver disease: progress and outlook.Journal of Zhejiang University. Science. B · 2024Review
- The Key Role of Lysosomal Protease Cathepsins in Viral Infections.International journal of molecular sciences · 2022Review
- ZIKV Infection Induces DNA Damage Response and Alters the Proteome of Gastrointestinal Cells.Viruses · 2020Article
- Ectromelia virus suppresses expression of cathepsins and cystatins in conventional dendritic cells to efficiently execute the replication process.BMC microbiology · 2019Article
- Depletion of MicroRNA-373 Represses the Replication of Hepatitis C Virus via Activation of Type 1 Interferon Response by Targeting IRF5.Yonsei medical journal · 2018Article
- Interferon regulatory factor 5 (IRF5) suppresses hepatitis C virus (HCV) replication and HCV-associated hepatocellular carcinoma.The Journal of biological chemistry · 2017Article
- Giving CD4+ T cells the slip: viral interference with MHC class II-restricted antigen processing and presentation.Current opinion in immunology · 2016Review
- Contribution of autophagy to antiviral immunity.FEBS letters · 2015Review
- Influence of host resistance on viral adaptation: hepatitis C virus as a case study.Infection and drug resistance · 2015Review
- Production and pathogenicity of hepatitis C virus core gene products.World journal of gastroenterology · 2014Review
- Hepatitis C virus infection: establishment of chronicity and liver disease progression.EXCLI journal · 2014Review
- Influence of HIV and HCV on T cell antigen presentation and challenges in the development of vaccines.Frontiers in microbiology · 2014Review
- Viral proteome size and CD8+ T cell epitope density are correlated: the effect of complexity on selection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocytes are the main source of hepatitis C virus (HCV) replication and contain the maximum viral load in an infected person. Chronic HCV infection is characterized by weak cellular immune responses to viral proteins. Cathepsin S is a lysosomal cysteine protease and controls HLA-DR-antigen complex presentation through the degradation of the invariant chain. In this study, we examined the effect of HCV proteins on cathepsin S expression and found it to be markedly decreased in dendritic cells (DCs) exposed to HCV or in hepatocytes expressing HCV proteins. The downregulation of cathepsin S was mediated by HCV core and NS5A proteins involving inhibition of the transcription factors interferon regulatory factor 1 (IRF-1) and upstream stimulatory factor 1 (USF-1) in gamma interferon (IFN-γ)-treated hepatocytes. Inhibition of cathepsin S by HCV proteins increased cell surface expression of the invariant chain. In addition, hepatocytes stably transfected with HCV core or NS5A inhibited HLA-DR expression. Together, these results suggested that HCV has an inhibitory role on cathepsin S-mediated major histocompatibility complex (MHC) class II maturation, which may contribute to weak immunogenicity of viral antigens in chronically infected humans.
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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.