ArticleEMBO reports2021
Enterovirus-A71 exploits peripherin and Rac1 to invade the central nervous system.
Article in EMBO reports, 2021. 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 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Historical evolution, research hotspots and emerging trends of pediatric hand, foot, and mouth disease: a bibliometric worldview since the 21st century.Frontiers in medicine · 2025Pooled it
- Article
- Host transcriptomic analysis reveals a defective intracellular environment that limits SARS-CoV-2 replication in CFTR-deficient airway epithelium.Frontiers in cellular and infection microbiology · 2026Article
- Epidemiological and genetic characterizations of hand, foot, and mouth disease and acute respiratory infections due to CV-A6 infection in Henan Province, China between 2021 and 2022.BMC pediatrics · 2025Article
- Ex vivo study of neuroinvasive and neurotropic viruses: what is current and what is next.FEMS microbiology reviews · 2025Review
- Enterovirus-A71 preferentially infects and replicates in human motor neurons, inducing neurodegeneration by ferroptosis.Emerging microbes & infections · 2024Article
- Understanding neurotropic enteric viruses: routes of infection and mechanisms of attenuation.Cellular and molecular life sciences : CMLS · 2024Review
- Enterovirus-A71 exploits RAB11 to recruit chaperones for virus morphogenesis.Journal of biomedical science · 2024Article
- Histone deacetylase inhibitor boosts anticancer potential of fusogenic oncolytic vaccinia virus by enhancing cell-cell fusion.Cancer science · 2024Article
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- Pathogenesis of enterovirus infection in central nervous system.Biosafety and health · 2023Review
- Role of the Intermediate Filament Protein Peripherin in Health and Disease.International journal of molecular sciences · 2022Review
- Molecular Mechanisms in the Genesis of Seizures and Epilepsy Associated With Viral Infection.Frontiers in molecular neuroscience · 2022Review
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
- 6-Thioguanine Inhibits Herpes Simplex Virus 1 Infection of Eyes.Microbiology spectrum · 2021Article
- Enterovirus-A71 exploits peripherin and Rac1 to invade the central nervous system.EMBO reports · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Enterovirus-A71 (EV-A71) has been associated with severe neurological forms of hand, foot, and mouth disease (HFMD). EV-A71 infects motor neurons at neuromuscular junctions (NMJs) to invade the central nervous system (CNS). Here, we investigate the role of peripherin (PRPH) during EV-A71 infection, a type III intermediate neurofilament involved in neurodegenerative conditions. In mice infected with EV-A71, PRPH co-localizes with viral particles in the muscles at NMJs and in the spinal cord. In motor neuron-like and neuroblastoma cell lines, surface-expressed PRPH facilitates viral entry, while intracellular PRPH influences viral genome replication through interactions with structural and non-structural viral components. Importantly, PRPH does not play a role during infection with coxsackievirus A16, another causative agent of HFMD rarely associated with neurological complications, suggesting that EV-A71 ability to exploit PRPH represents a unique attribute for successful CNS invasion. Finally, we show that EV-A71 also exploits some of the many PRPH-interacting partners. Of these, small GTP-binding protein Rac1 represents a potential druggable host target to limit neuroinvasion of EV-A71.
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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.