ArticleProceedings of the National Academy of Sciences of the United States of America2017
Systematic identification of anti-interferon function on hepatitis C virus genome reveals p7 as an immune evasion protein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- A chromosome-level genome assembly of the Hispid cotton rat (Sigmodon hispidus), a model for human pathogenic virus infections.BMC biology · 2025Article
- Hepatitis C Virus and the Host: A Mutual Endurance Leaving Indelible Scars in the Host's Immunity.International journal of molecular sciences · 2023Review
- Interferon inhibits a model RNA virus via a limited set of inducible effector genes.EMBO reports · 2023Article
- Whole-genome sequencing identifies interferon-induced protein IFI6/IFI27-like as a strong candidate gene for VNN resistance in European sea bass.Genetics, selection, evolution : GSE · 2023Article
- A Human and Rhesus Macaque Interferon-Stimulated Gene Screen Shows That Over-Expression ofViruses · 2022Article
- Toll-like Receptor Response to Hepatitis C Virus Infection: A Recent Overview.International journal of molecular sciences · 2022Review
- Unravelling the Immunomodulatory Effects of Viral Ion Channels, towards the Treatment of Disease.Viruses · 2021Review
- Applications of Deep Mutational Scanning in Virology.Viruses · 2021Review
- Inhibitor Development against p7 Channel in Hepatitis C Virus.Molecules (Basel, Switzerland) · 2021Article
- Acute Infection of Viral Pathogens and Their Innate Immune Escape.Frontiers in microbiology · 2021Review
- mRNA display with library of even-distribution reveals cellular interactors of influenza virus NS1.Nature communications · 2020Article
- Hepatitis C Virus: Evading the Intracellular Innate Immunity.Journal of clinical medicine · 2020Review
- The role of spatial structure in the evolution of viral innate immunity evasion: A diffusion-reaction cellular automaton model.PLoS computational biology · 2020Article
- Virus Control of Cell Metabolism for Replication and Evasion of Host Immune Responses.Frontiers in cellular and infection microbiology · 2019Review
- A CRISPR screen identifies IFI6 as an ER-resident interferon effector that blocks flavivirus replication.Nature microbiology · 2018Article
- Modelling how responsiveness to interferon improves interferon-free treatment of hepatitis C virus infection.PLoS computational biology · 2018Article
- Article
- Mitochondrial Proteins Coded by Human Tumor Viruses.Frontiers in microbiology · 2018Review
- Recent advances in antiviral interferon-stimulated gene biology.F1000Research · 2018Review
- The amino-terminus of the hepatitis C virus (HCV) p7 viroporin and its cleavage from glycoprotein E2-p7 precursor determine specific infectivity and secretion levels of HCV particle types.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
Abstract
Hepatitis C virus (HCV) encodes mechanisms to evade the multilayered antiviral actions of the host immune system. Great progress has been made in elucidating the strategies HCV employs to down-regulate interferon (IFN) production, impede IFN signaling transduction, and impair IFN-stimulated gene (ISG) expression. However, there is a limited understanding of the mechanisms governing how viral proteins counteract the antiviral functions of downstream IFN effectors due to the lack of an efficient approach to identify such interactions systematically. To study the mechanisms by which HCV antagonizes the IFN responses, we have developed a high-throughput profiling platform that enables mapping of HCV sequences critical for anti-IFN function at high resolution. Genome-wide profiling performed with a 15-nt insertion mutant library of HCV showed that mutations in the p7 region conferred high levels of IFN sensitivity, which could be alleviated by the expression of WT p7 protein. This finding suggests that p7 protein of HCV has an immune evasion function. By screening a liver-specific ISG library, we identified that IFI6-16 significantly inhibits the replication of p7 mutant viruses without affecting WT virus replication. In contrast, knockout of IFI6-16 reversed the IFN hypersensitivity of p7 mutant virus. In addition, p7 was found to be coimmunoprecipitated with IFI6-16 and to counteract the function of IFI6-16 by depolarizing the mitochondria potential. Our data suggest that p7 is a critical immune evasion protein that suppresses the antiviral IFN function by counteracting the function of IFI6-16.
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