ArticleJournal of virology2018
Fibronectin Facilitates Enterovirus 71 Infection by Mediating Viral Entry.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 45 citations in OpenAlex.
- Rational Design of Broad-Spectrum Anti-Enteroviral Molecular Glues Targeting Enteroviral RNAi Suppressors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- The multifaceted roles of fibronectin in viral pathogenesis.Archives of virology · 2026Review
- Review
- Review
- Severe enterovirus A71 infection is associated with dysfunction of T cell immune response and alleviated by Astragaloside A.Virologica Sinica · 2025Article
- A skin organoid-based infection platform identifies an inhibitor specific for HFMD.Nature communications · 2025Article
- Tribbles pseudokinase 3 promotes enterovirus A71 infection via dual mechanisms.Emerging microbes & infections · 2024Article
- Genomic and biogeographic characterisation of the novel prasinovirus Mantoniella tinhauana virus 1.Environmental microbiology reports · 2024Article
- C1QTNF5 is a novel attachment factor that facilitates the entry of influenza A virus.Virologica Sinica · 2024Article
- Enterovirus A71 does not meet the uncoating receptor SCARB2 at the cell surface.PLoS pathogens · 2024Article
- Interaction of species A rotavirus VP4 with the cellular proteins vimentin and actin related protein 2 discovered by a proximity interactome assay.Journal of virology · 2023Article
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Variant enterovirus A71 found in immune-suppressed patient binds to heparan sulfate and exhibits neurotropism in B-cell-depleted mice.Cell reports · 2023Article
- Review
- Article
- Chemokine PF4 Inhibits EV71 and CA16 Infections at the Entry Stage.Journal of virology · 2022Article
- SLC35B2 Acts in a Dual Role in the Host Sulfation Required for EV71 Infection.Journal of virology · 2022Article
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
- Molecular Docking of SP40 Peptide towards Cellular Receptors for Enterovirus 71 (EV-A71).Molecules (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibronectin (FN) is a high-molecular-weight extracellular matrix protein that contains the RGDS motif, which is required to bind to integrins. Synthetic RGDS peptides have been reported to compete with FN to bind to the cell surface and inhibit the function of FN. Here, we identified that synthetic RGDS peptides significantly inhibit human enterovirus 71 (EV71) infection in cell cultures. In addition, mice treated with RGDS peptides and infected with EV71 had a significantly higher survival rate and a lower viral load than the control group. Because RGDS peptides affect the function of FN, we questioned whether FN may play a role in virus infection. Our study indicates that overexpression of FN enhanced EV71 infection. In contrast, knockout of FN significantly reduced viral yield and decreased the viral binding to host cells. Furthermore, EV71 entry, rather than intracellular viral replication, was blocked by FN inhibitor pretreatment. Next, we found that FN could interact with the EV71 capsid protein VP1, and further truncated-mutation assays indicated that the D2 domain of FN could interact with the N-terminal fragment of VP1. Taken together, our results demonstrate that the host factor FN binds to EV71 particles and facilitates EV71 entry, providing a potential therapy target for EV71 infection.
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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.