ArticleViruses2021
Inhibition of MAVS Aggregation-Mediated Type-I Interferon Signaling by Foot-and-Mouth Disease Virus VP3.
Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Foot-and-mouth disease virus VP4 interferes with host interferon response by targeting the nuclear translocation of interferon regulatory factor 3 (IRF3).Veterinary research · 2026Article
- FMDV VP3 Induces IL-10 Expression in Porcine Macrophages via PI3K Interaction and PI3K/AKT-mTOR Pathway Activation.Viruses · 2026Article
- Novel strategies for PEDV to interfere with host antiviral immunity through Caspase-1.Virulence · 2025Article
- Interferon-stimulated gene MCL1 inhibits foot-and-mouth disease virus replication by modulating mitochondrial dynamics and autophagy.Journal of virology · 2025Article
- MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication.Veterinary research · 2025Article
- Review
- Use of virus-like particles and nanoparticle-based vaccines for combating picornavirus infections.Veterinary research · 2024Review
- African swine fever virus B175L inhibits the type I interferon pathway by targeting STING and 2'3'-cGAMP.Journal of virology · 2023Article
- A novel protein encoded by circVPS13D attenuates antiviral innate immunity by targeting MAVS in teleost fish.Journal of virology · 2023Article
- Identification of Orbivirus Non-Structural Protein 5 (NS5), Its Role and Interaction with RNA/DNA in Infected Cells.International journal of molecular sciences · 2023Article
- Flavivirus prM interacts with MDA5 and MAVS to inhibit RLR antiviral signaling.Cell & bioscience · 2023Article
- Foot-and-Mouth Disease Virus: Molecular Interplays with IFN Response and the Importance of the Model.Viruses · 2022Review
- Foot-and-mouth disease virus non-structural protein 2B downregulates the RLR signaling pathwayFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a structural protein of the Foot-and-mouth disease virus (FMDV), VP3 plays a vital role in virus assembly and inhibiting the interferon (IFN) signal transduction to promote FMDV replication. Previous studies demonstrated that FMDV VP3 blocks the type-I IFN response by inhibiting the mRNA expression of the mitochondrial antiviral-signaling protein (MAVS); however, the underlying mechanism is poorly understood. Here, we describe the specificity of FMDV VP3 interaction with the transmembrane (TM) domain of MAVS as FMDV driven type-I IFN inhibitory mechanism for its effective replication. The TM domain of MAVS governs the mitochondria localization of MAVS, and it is a key factor in type-I IFN signaling transduction via MAVS aggregation. Thereby, the interaction of FMDV VP3 with the TM domain of MAVS leads to the inhibition of MAVS mitochondria localization, self-association, and aggregation, resulting in the suppression of type-I IFN response. Collectively, these results provide a clear understanding of a key molecular mechanism used by the FMDV VP3 for the suppression of IFN responses via targeting MAVS.
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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.