ArticlePLoS pathogens2013
Enterovirus 71 protease 2Apro targets MAVS to inhibit anti-viral type I interferon responses.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 164 papers.
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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
164 citing papers in PubMed, 228 citations in OpenAlex.
- Immune Evasion by Neurotropic Viruses: Molecular Strategies, Cellular Targets, and Consequences for CNS Infection.International journal of molecular sciences · 2026Review
- Enteroviruses antagonize the host restriction factor ABL2 via proteasomal degradation to facilitate viral replication.Virologica Sinica · 2026Article
- An ancient anthozoan protein reveals an alternative evolutionary path of antiviral signalling.Nature ecology & evolution · 2026Article
- Information-Entropy-Based Single Amino Acid Polymorphism Analysis Reveals Functional Variance of Enterovirus 2A Proteases.Microorganisms · 2026Article
- Modeling human enterovirus A71 infection using an intestinal microphysiological system.Journal of virology · 2026Article
- Bovine viral diarrhea virus suppresses type I IFN production by inducing MAVS degradation via autophagy mediated by the ROS-endoplasmic reticulum stress axis.Journal of virology · 2026Article
- Prohibitins: emerging host targets of bacteria and viruses at the plasma membrane, mitochondria, and cytoplasm.Microbial cell (Graz, Austria) · 2026Article
- Ubiquitin-specific protease 5 promotes EV-A71 replication by de-ubiquitinating MAVS and IRF3.Virologica Sinica · 2025Article
- Review
- The multifaceted role of the viral 2A protease in enterovirus replication and antagonism of host antiviral responses.PLoS pathogens · 2025Article
- The structural protein VP3 of enterovirus D68 interacts with MAVS to inhibit the NF-κB signaling pathway.Journal of virology · 2025Article
- Pull-Down Techniques for Determining Virus-Host Protein Interactions.Methods in molecular biology (Clifton, N.J.) · 2025Article
- MAVS signaling shapes microglia responses to neurotropic virus infection.Journal of neuroinflammation · 2024Article
- Natural-Target-Mimicking Translocation-Based Fluorescent Sensor for Detection of SARS-CoV-2 PLpro Protease Activity and Virus Infection in Living Cells.International journal of molecular sciences · 2024Article
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- The EV71 2A protease occupies the central cleft of SETD3 and disrupts SETD3-actin interaction.Nature communications · 2024Article
- Correction: Enterovirus 71 Protease 2Apro Targets MAVS to Inhibit Anti-Viral Type I Interferon Responses.PLoS pathogens · 2024Article
- Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Multiple functions of the nonstructural protein 3D in picornavirus infection.Frontiers in immunology · 2024Review
104 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is the major causative pathogen of hand, foot, and mouth disease (HFMD). Its pathogenicity is not fully understood, but innate immune evasion is likely a key factor. Strategies to circumvent the initiation and effector phases of anti-viral innate immunity are well known; less well known is whether EV71 evades the signal transduction phase regulated by a sophisticated interplay of cellular and viral proteins. Here, we show that EV71 inhibits anti-viral type I interferon (IFN) responses by targeting the mitochondrial anti-viral signaling (MAVS) protein--a unique adaptor molecule activated upon retinoic acid induced gene-I (RIG-I) and melanoma differentiation associated gene (MDA-5) viral recognition receptor signaling--upstream of type I interferon production. MAVS was cleaved and released from mitochondria during EV71 infection. An in vitro cleavage assay demonstrated that the viral 2A protease (2A(pro)), but not the mutant 2A(pro) (2A(pro)-110) containing an inactivated catalytic site, cleaved MAVS. The Protease-Glo assay revealed that MAVS was cleaved at 3 residues between the proline-rich and transmembrane domains, and the resulting fragmentation effectively inactivated downstream signaling. In addition to MAVS cleavage, we found that EV71 infection also induced morphologic and functional changes to the mitochondria. The EV71 structural protein VP1 was detected on purified mitochondria, suggesting not only a novel role for mitochondria in the EV71 replication cycle but also an explanation of how EV71-derived 2A(pro) could approach MAVS. Taken together, our findings reveal a novel strategy employed by EV71 to escape host anti-viral innate immunity that complements the known EV71-mediated immune-evasion mechanisms.
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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.