ArticleThe Journal of biological chemistry2011
The essential role of clathrin-mediated endocytosis in the infectious entry of human enterovirus 71.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 143 citations in OpenAlex.
- Target-Based Antiviral Drug Development Against Human Respiratory Viruses.Pathogens (Basel, Switzerland) · 2026Review
- EV-D68 exploits clathrin-mediated endocytosis and compensatory macropinocytosis for cellular entry.Journal of virology · 2026Article
- Insulin receptor trafficking and interactions in muscle cells.Journal of the Endocrine Society · 2026Article
- AP2: an indispensable host factor in virus infection.Journal of virology · 2026Review
- Genistein inhibits the replication of enterovirus A71.Frontiers in pharmacology · 2026Article
- Reframing clathrin-mediated viral entry: evidence standards, context dependence and host-directed vulnerabilities.Frontiers in cellular and infection microbiology · 2026Review
- Selenium Nanoparticles as Versatile Delivery Tools.Pharmaceutics · 2025Review
- Antiviral candidates for enterovirus 71: targeting viral proteome and stage-specific lifecycle interventions.Virology journal · 2025Review
- SNX10 enhances HCoV-OC43 infection by facilitating viral entry and inhibiting virus-triggered autophagy.Virologica Sinica · 2025Article
- Enterovirus A71 priorities, challenges, and future opportunities in humoral immunity and vaccine development.NPJ vaccines · 2025Review
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Endosome rupture enables enteroviruses from the family Picornaviridae to infect cells.Communications biology · 2024Article
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- N-terminal acetyltransferase 6 facilitates enterovirus 71 replication by regulating PI4KB expression and replication organelle biogenesis.Journal of virology · 2024Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Enterovirus A71 does not meet the uncoating receptor SCARB2 at the cell surface.PLoS pathogens · 2024Article
- Targeting pyroptosis with nanoparticles to alleviate neuroinflammatory for preventing secondary damage following traumatic brain injury.Science advances · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- A tradeoff between enterovirus A71 particle stability and cell entry.Nature communications · 2023Article
- Engineered vitamin E-tethered non-immunogenic facial lipopeptide for developing improved siRNA based combination therapy against metastatic breast cancer.Chemical science · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is currently known about the infectious entry process of human enterovirus 71 (HEV71) into host cells, which may represent potential anti-viral targeting sites. In this study a targeted small-interfering RNA (siRNA) screening platform assay was established and validated to identify and profile key cellular genes involved in processes of endocytosis, cytoskeletal dynamics, and endosomal trafficking essential for HEV71 infection. Screen evaluation was conducted via the expression of well characterized dominant-negative mutants, bioimaging studies (double-labeled immunofluorescence assays, transmission electron microscopy analysis), secondary siRNA-based dosage dependence studies, and drug inhibition assays. The infectious entry of HEV71 into rhabdomyosarcoma cells was shown to be significantly inhibited by siRNAs targeting genes associated with clathrin-mediated endocytosis (CME) that include AP2A1, ARRB1, CLTC, CLTCL1, SYNJ1, ARPC5, PAK1, ROCK1, and WASF1. The functional role of CME was verified by the observation of strong co-localization between HEV71 particles and clathrin as well as dose-dependent inhibition of HEV71 infection upon siRNA knockdown of CME-associated genes. HEV71 entry by CME was further confirmed via inhibition by dominant-negative EPS15 mutants and treatment of CME drug inhibitors, with more than 80% inhibition observed at 20 μm chlorpromazine. Furthermore, HEV71 infection was shown to be sensitive to the disruption of human genes in regulating early to late endosomal trafficking as well as endosomal acidic pH. The identification of clathrin-mediated endocytosis as the entry pathway for HEV71 infection of susceptible host cells contributes to a better understanding of HEV71 pathogenesis and enables future development of anti-viral strategies against HEV71 infection.
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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.