ArticleJournal of virology2012
Foot-and-mouth disease virus induces autophagosomes during cell entry via a class III phosphatidylinositol 3-kinase-independent pathway.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 114 citations in OpenAlex.
- Interactions between the 2C protein of foot-and-mouth disease virus and components of the viral replication machinery are mediated by endoplasmic reticulum-derived membranes.The Journal of general virology · 2026Article
- Sichuan pepper, Zanthoxylum bungeanum Maxim., suppresses human coronavirus OC43 infection by inhibiting viral entry and impairing autolysosome accumulation.Chinese medicine · 2026Article
- Autophagy machinery as exploited by viruses.Autophagy reports · 2025Article
- VPS34-mediated autophagosome-lysosome fusion facilitates classical swine fever virus replication.Journal of virology · 2025Article
- Interactions between the 2C protein of FMDV and components of the viral replication machinery are mediated by ER-derived membranes.bioRxiv : the preprint server for biology · 2025Article
- Interferon-stimulated gene MCL1 inhibits foot-and-mouth disease virus replication by modulating mitochondrial dynamics and autophagy.Journal of virology · 2025Article
- Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights.Cells · 2025Review
- Retinol binding protein 4 restricts PCV2 replication via selective autophagy degradation of viral ORF1 protein.Communications biology · 2024Article
- The multifaceted roles of selective autophagy receptors in viral infections.Journal of virology · 2024Review
- Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024Review
- Silencing RNA-Mediated Knockdown of IFITM3 Enhances Senecavirus A Replication.Pathogens (Basel, Switzerland) · 2024Article
- Molecular basis for the different PCV2 susceptibility of T-lymphoblasts in Landrace and Piétrain pigs.Veterinary research · 2024Article
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
- CDKL5 regulates p62-mediated selective autophagy and confers protection against neurotropic viruses.The Journal of clinical investigation · 2024Article
- The Role of the NRF2 Pathway in the Pathogenesis of Viral Respiratory Infections.Pathogens (Basel, Switzerland) · 2023Review
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- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
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- Seneca Valley virus 3CFrontiers in microbiology · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Autophagy is an intracellular pathway that can contribute to innate antiviral immunity by delivering viruses to lysosomes for degradation or can be beneficial for viruses by providing specialized membranes for virus replication. Here, we show that the picornavirus foot-and-mouth disease virus (FMDV) induces the formation of autophagosomes. Induction was dependent on Atg5, involved processing of LC3 to LC3II, and led to a redistribution of LC3 from the cytosol to punctate vesicles indicative of authentic autophagosomes. Furthermore, FMDV yields were reduced in cells lacking Atg5, suggesting that autophagy may facilitate FMDV infection. However, induction of autophagosomes by FMDV appeared to differ from starvation, as the generation of LC3 punctae was not inhibited by wortmannin, implying that FMDV-induced autophagosome formation does not require the class III phosphatidylinositol 3-kinase (PI3-kinase) activity of vps34. Unlike other picornaviruses, for which there is strong evidence that autophagosome formation is linked to expression of viral nonstructural proteins, FMDV induced autophagosomes very early during infection. Furthermore, autophagosomes could be triggered by either UV-inactivated virus or empty FMDV capsids, suggesting that autophagosome formation was activated during cell entry. Unlike other picornaviruses, FMDV-induced autophagosomes did not colocalize with the viral 3A or 3D protein. In contrast, ∼50% of the autophagosomes induced by FMDV colocalized with VP1. LC3 and VP1 also colocalized with the cellular adaptor protein p62, which normally targets ubiquitinated proteins to autophagosomes. These results suggest that FMDV induces autophagosomes during cell entry to facilitate infection, but not to provide membranes for replication.
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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.