ReviewFrontiers in cellular and infection microbiology2017
Molecular Mechanisms of Foot-and-Mouth Disease Virus Targeting the Host Antiviral Response.
Review in Frontiers in cellular and infection microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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
38 citing papers in PubMed, 45 citations in OpenAlex.
- STING1 negatively regulates translation and replication of foot-and-mouth disease virus independently of interferon and is antagonized by the viral proteins 3C and 2B.Virologica Sinica · 2026Article
- RNA helicase DDX5 regulates the translation and genomic replication of foot-and-mouth disease virus.Journal of virology · 2026Article
- Genome-wide CRISPR screen identifies RNF24 as a critical host factor for foot-and-mouth disease virus entry.Frontiers in cell and developmental biology · 2026Article
- An integrated structural and immunoinformatic approach to design a multi-epitope based vaccine against the foot-and-mouth disease virus.Scientific reports · 2025Article
- Dicer is cleaved by the Leader protease encoded by foot-and-mouth disease virus to promote infection in mammalian cells.Science advances · 2025Article
- The pathogenesis of foot-and-mouth disease virus: current understandings and knowledge gaps.Veterinary research · 2025Review
- Heat shock protein A1 inhibits the replication of foot-and-mouth disease virus by degrading viral RNA polymerase 3D through chaperone-mediated autophagy.Journal of virology · 2025Article
- Foot-and-mouth disease in Asia.Virus research · 2025Review
- Review
- Modifying miRs for effective reprogramming of fibroblasts to cardiomyocytes.Molecular therapy. Nucleic acids · 2024Article
- The antiviral response triggered by the cGAS/STING pathway is subverted by the foot-and-mouth disease virus proteases.Cellular and molecular life sciences : CMLS · 2024Article
- Nuclear ribonucleoprotein RALY downregulates foot-and-mouth disease virus replication but antagonized by viral 3C protease.Microbiology spectrum · 2024Article
- A genome-wide CRISPR screening uncovers that TOB1 acts as a key host factor for FMDV infection via both IFN and EGFR mediated pathways.PLoS pathogens · 2024Article
- Article
- The Host Protein CAD Regulates the Replication of FMDV through the Function of Pyrimidines'Journal of virology · 2023Article
- Reprogramming viral immune evasion for a rational design of next-generation vaccines for RNA viruses.Frontiers in immunology · 2023Review
- Structure-based virtual screening and molecular dynamics studies to explore potential natural inhibitors against 3C protease of foot-and-mouth disease virus.Frontiers in veterinary science · 2023Article
- The prevalence of foot-and-mouth disease in Asia.Frontiers in veterinary science · 2023Review
- Fibroblast growth factor 11 inhibits foot-and-mouth disease virus gene expression and replication in vitro.The Journal of veterinary medical science · 2022Article
- Mutation of FMDV LFrontiers in veterinary science · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foot-and-mouth disease virus (FMDV) is the causative agent of an acute vesicular disease affecting pigs, cattle and other domestic, and wild animals worldwide. The aim of the host interferon (IFN) response is to limit viral replication and spread. Detection of the viral genome and products by specialized cellular sensors initiates a signaling cascade that leads to a rapid antiviral response involving the secretion of type I- and type III-IFNs and other antiviral cytokines with antiproliferative and immunomodulatory functions. During co-evolution with their hosts, viruses have acquired strategies to actively counteract host antiviral responses and the balance between innate response and viral antagonism may determine the outcome of disease and pathogenesis. FMDV proteases Lpro and 3C have been found to antagonize the host IFN response by a repertoire of mechanisms. Moreover, the putative role of other viral proteins in IFN antagonism is being recently unveiled, uncovering sophisticated immune evasion strategies different to those reported to date for other members of the
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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.