ArticleJournal of neurovirology2020
Enterovirus A71 capsid protein VP1 increases blood-brain barrier permeability and virus receptor vimentin on the brain endothelial cells.
Article in Journal of neurovirology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Crosstalk between vimentin and keratins in viral infection: Implications across the viral life cycle.Virulence · 2026Review
- Desmin mutations in cardiomyocytes increase susceptibility to coxsackievirus B3 infection by impairing antiviral IFN-β response and upregulating viral receptors expression.Stem cell research & therapy · 2026Article
- Animal models for enterovirus 71: Mechanisms, immunity, and applications.Human vaccines & immunotherapeutics · 2025Review
- Review
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- Overview of the Trending Enteric Viruses and Their Pathogenesis in Intestinal Epithelial Cell Infection.Biomedicines · 2024Review
- MiR-181a Negatively Regulates Claudin-3 to FacilitateViruses · 2024Article
- The key mechanisms of multi-system responses triggered by central nervous system damage in hand, foot, and mouth disease severity.Infectious medicine · 2024Review
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- The VP1 Protein of Porcine Teschovirus Inhibits the Innate Immune Response to Viral Infection by Blocking MDA5 Activation.Transboundary and emerging diseases · 2024Article
- IP-10 acts early in CV-A16 infection to induce BBB destruction and promote virus entry into the CNS by increasing TNF-α expression.Frontiers in immunology · 2024Article
- The molecular biophysics of extracellular vimentin and its role in pathogen-host interactions.Current opinion in cell biology · 2023Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Complete genome analysis of echovirus 30 strains isolated from hand-foot-and-mouth disease in Yunnan province, China.Virology journal · 2023Article
- Tight Junctions, the Key Factor in Virus-Related Disease.Pathogens (Basel, Switzerland) · 2022Review
- Effects of host vimentin on Eimeria tenella sporozoite invasion.Parasites & vectors · 2022Article
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
- Vimentin Inhibits Dengue Virus Type 2 Invasion of the Blood-Brain Barrier.Frontiers in cellular and infection microbiology · 2022Article
- The pathogenesis and virulence of enterovirus-D68 infection.Virulence · 2021Review
- Ginsenoside Rg1 ameliorates blood-brain barrier disruption and traumatic brain injuryActa pharmaceutica Sinica. B · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus A71 (EV-A71) is the major cause of severe hand-foot-and-mouth diseases (HFMD), especially encephalitis and other nervous system diseases. EV-A71 capsid protein VP1 mediates virus attachment and is the important virulence factor in the EV-A71pathogenesis. In this study, we explored the roles of VP1 in the permeability of blood-brain barrier (BBB). Sera albumin, Evans blue, and dextran leaked into brain parenchyma of the 1-week-old C57BL/6J mice intracranially injected with VP1 recombinant protein. VP1 also increased the permeability of the brain endothelial cells monolayer, an in vitro BBB model. Tight junction protein claudin-5 was reduced in the brain tissues or brain endothelial cells treated with VP1. In contrast, VP1 increased the expression of virus receptor vimentin, which could be blocked with VP1 neutralization antibody. Vimentin expression in the VP1-treated brain endothelial cells was regulated by TGF-β/Smad-3 and NF-κB signal pathways. Moreover, vimentin over-expression was accompanied with compromised BBB. From these studies, we conclude that EV-A71 virus capsid protein VP1 disrupted BBB and increased virus receptor vimentin, which both may contribute to the virus entrance into brain and EV-A71 CNS infection.
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