ArticleJournal of cellular and molecular medicine2016
Hepatitis C virus NS3-4A inhibits the peroxisomal MAVS-dependent antiviral signalling response.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- MAVS oligomerization drives a faster and more efficient antiviral signaling activation at peroxisomes compared to mitochondria.The FEBS journal · 2026Article
- Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Hepatitis C virus-associated cardiomyopathy: A review of pathogenesis.World journal of virology · 2025Article
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- From viruses to cancer: exploring the role of the hepatitis C virus NS3 protein in carcinogenesis.Infectious agents and cancer · 2024Review
- Article
- HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024Review
- Dengue Virus 2 NS2B Targets MAVS and IKKε to Evade the Antiviral Innate Immune Response.Journal of microbiology and biotechnology · 2023Article
- Host-mediated RNA editing in viruses.Biology direct · 2023Review
- Tools to Investigate the Peroxisome-Dependent Antiviral Response.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Host mitochondria: more than an organelle in SARS-CoV-2 infection.Frontiers in cellular and infection microbiology · 2023Review
- Peroxisomes and Viruses: Overview on Current Knowledge and Experimental Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Hepatitis C virus and intracellular antiviral response.Current opinion in virology · 2022Review
- Article
- Human Cytomegalovirus vMIA Inhibits MAVS Oligomerization at Peroxisomes in an MFF-Dependent Manner.Frontiers in cell and developmental biology · 2022Article
- Infection of Glia by Human Pegivirus Suppresses Peroxisomal and Antiviral Signaling Pathways.Journal of virology · 2021Article
- Mitochondria and Mitochondrial DNA: Key Elements in the Pathogenesis and Exacerbation of the Inflammatory State Caused by COVID-19.Medicina (Kaunas, Lithuania) · 2021Review
- Circular RNA circPIKfyve acts as a sponge of miR-21-3p to enhance antiviral immunity through regulating MAVS in teleost fish.Journal of virology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) is the cause of one of the most prevalent viral infections worldwide. Upon infection, the HCV genome activates the RIG-I-MAVS signalling pathway leading to the production of direct antiviral effectors which prevent important steps in viral propagation. MAVS localizes at peroxisomes and mitochondria and coordinate the activation of an effective antiviral response: peroxisomal MAVS is responsible for a rapid but short-termed antiviral response, while the mitochondrial MAVS is associated with the activation of a stable response with delayed kinetics. The HCV NS3-4A protease was shown to specifically cleave the mitochondrial MAVS, inhibiting the downstream response. In this study, we have analysed whether HCV NS3-4A is also able to cleave the peroxisomal MAVS and whether this would have any effect on the cellular antiviral response. We show that NS3-4A is indeed able to specifically cleave this protein and release it into the cytosol, a mechanism that seems to occur at a similar kinetic rate as the cleavage of the mitochondrial MAVS. Under these conditions, RIG-I-like receptor (RLR) signalling from peroxisomes is blocked and antiviral gene expression is inhibited. Our results also show that NS3-4A is able to localize at peroxisomes in the absence of MAVS. However, mutation studies have shown that this localization pattern is preferred in the presence of a fully cleavable MAVS. These findings present evidence of a viral evasion strategy that disrupts RLR signalling on peroxisomes and provide an excellent example of how a single viral evasion strategy can block innate immune signalling from different organelles.
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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.