ArticleProceedings of the National Academy of Sciences of the United States of America2010
Plasmacytoid dendritic cells sense hepatitis C virus-infected cells, produce interferon, and inhibit infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
169 citing papers in PubMed, 1 synthesis or guideline pooled it, 258 citations in OpenAlex.
- Sexually transmitted hepatitis C virus infections: current trends, and recent advances in understanding the spread in men who have sex with men.Journal of the International AIDS Society · 2019Pooled it
- High prevalence of autoantibodies neutralizing type I IFNs in Japanese patients with hepatitis C.Journal of human immunity · 2026Article
- Hepatitis C in the Direct-Acting Antiviral Era: Immunopathogenesis, Dendritic Cells and Modern Clinical Management.Biomedicines · 2026Review
- Sensing of SARS-CoV-2-infected cells by plasmacytoid dendritic cells is modulated via an interplay between CD54/ICAM-1 and CD11a/LFA-1 αJournal of virology · 2025Article
- Metabolic deficiencies underlie reduced plasmacytoid dendritic cell IFN-I production following viral infection.Nature communications · 2025Article
- A State-of-the-Art Review on the Recent Advances in Exosomes in Oncogenic Virus.Health science reports · 2024Article
- Viral Hepatitis: Host Immune Interaction, Pathogenesis and New Therapeutic Strategies.Pathogens (Basel, Switzerland) · 2024Review
- Macrophage phagocytosis of SARS-CoV-2-infected cells mediates potent plasmacytoid dendritic cell activation.Cellular & molecular immunology · 2023Article
- 3D engineered tissue models for studying human-specific infectious viral diseases.Bioactive materials · 2023Review
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- Human dendritic cell subsets: An updated view of their ontogeny and functional specialization.European journal of immunology · 2022Review
- CD169eLife · 2022Article
- Dendritic Cell-Based Immunotherapy in Hot and Cold Tumors.International journal of molecular sciences · 2022Review
- Toll-like Receptor Response to Hepatitis C Virus Infection: A Recent Overview.International journal of molecular sciences · 2022Review
- Hepatitis C Virus Alters Macrophage Cholesterol Metabolism Through Interaction with Scavenger Receptors.Viral immunology · 2022Article
- Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma.Cancers · 2022Review
- Peripheral blood iNKT cell activation correlates with liver damage during acute hepatitis C.JCI insight · 2022Article
- Antigen transfer and its effect on vaccine-induced immune amplification and tolerance.Theranostics · 2022Review
- A TLR7 antagonist restricts interferon-dependent and -independent immunopathology in a mouse model of severe influenza.The Journal of experimental medicine · 2021Article
- Review
109 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis C virus (HCV), a member of the Flaviviridae family, is a single-stranded positive-sense RNA virus that infects >170 million people worldwide and causes acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Despite its ability to block the innate host response in infected hepatocyte cell lines in vitro, HCV induces a strong type 1 interferon (IFN) response in the infected liver. The source of IFN in vivo and how it is induced are currently undefined. Here we report that HCV-infected cells trigger a robust IFN response in plasmacytoid dendritic cells (pDCs) by a mechanism that requires active viral replication, direct cell-cell contact, and Toll-like receptor 7 signaling, and we show that the activated pDC supernatant inhibits HCV infection in an IFN receptor-dependent manner. Importantly, the same events are triggered by HCV subgenomic replicon cells but not by free virus particles, suggesting the existence of a novel cell-cell RNA transfer process whereby HCV-infected cells can activate pDCs to produce IFN without infecting them. These results may explain how HCV induces IFN production in the liver, and they reveal a heretofore unsuspected aspect of the innate host response to viruses that can subvert the classical sensing machinery in the cells they infect, and do not infect or directly activate pDCs.
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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.