ArticleBMC microbiology2012
Cell surface sialylation affects binding of enterovirus 71 to rhabdomyosarcoma and neuroblastoma cells.
Article in BMC microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Plasminogen deficiency reduces disease severity and immune responses in enterovirus A71-infected mice.Microbiology spectrum · 2025Article
- Severe enterovirus A71 pathogenesis and immune responses in human nucleolin transgenic mice.Medical microbiology and immunology · 2025Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Receptors and Host Factors for Enterovirus Infection: Implications for Cancer Therapy.Cancers · 2024Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Review
- Amino acid variation at VP1-145 of enterovirus A71 determines the viral infectivity and receptor usage in a primary human intestinal model.Frontiers in microbiology · 2023Article
- SLC35B2 Acts in a Dual Role in the Host Sulfation Required for EV71 Infection.Journal of virology · 2022Article
- Carbohydrate Ligands for COVID-19 Spike Proteins.Viruses · 2022Article
- Adaptation and Virulence of Enterovirus-A71.Viruses · 2021Review
- ICAM-1 induced rearrangements of capsid and genome prime rhinovirus 14 for activation and uncoating.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Use of Oseltamivir as Adjunctive Therapy for the Treatment of Hand-Food-and-Mouth Disease: A Meta-Analysis of Randomized Clinical Trials.Frontiers in pharmacology · 2021Article
- Heparan sulfate attachment receptor is a major selection factor for attenuated enterovirus 71 mutants during cell culture adaptation.PLoS pathogens · 2020Article
- Molecular Pathogenicity of Enteroviruses Causing Neurological Disease.Frontiers in microbiology · 2020Review
- Electrostatic interactions at the five-fold axis alter heparin-binding phenotype and drive enterovirus A71 virulence in mice.PLoS pathogens · 2019Article
- Viral Factors Important for Efficient Replication of Influenza A Viruses in Cells of the Central Nervous System.Journal of virology · 2019Article
- Review
- Cell surface α2,3-linked sialic acid facilitates Zika virus internalization.Emerging microbes & infections · 2019Article
- Amino Acid Variation at VP1-145 of Enterovirus 71 Determines Attachment Receptor Usage and Neurovirulence in Human Scavenger Receptor B2 Transgenic Mice.Journal of virology · 2018Article
- VP1 Amino Acid Residue 145 of Enterovirus 71 Is a Key Residue for Its Receptor Attachment and Resistance to Neutralizing Antibody during Cynomolgus Monkey Infection.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnterovirus 71 (EV71) is a major causative agent of hand-foot-and-mouth disease (HFMD), and infection of EV71 to central nerve system (CNS) may result in a high mortality in children less than 2 years old. Although there are two highly glycosylated membrane proteins, SCARB2 and PSGL-1, which have been identified as the cellular and functional receptors of EV71, the role of glycosylation in EV71 infection is still unclear.
resultsWe demonstrated that the attachment of EV71 to RD and SK-N-SH cells was diminished after the removal of cell surface sialic acids by neuraminidase. Sialic acid specific lectins, Maackia amurensis (MAA) and Sambucus Nigra (SNA), could compete with EV71 and restrained the binding of EV71 significantly. Preincubation of RD cells with fetuin also reduced the binding of EV71. In addition, we found that SCARB2 was a sialylated glycoprotein and interaction between SCARB2 and EV71 was retarded after desialylation.
conclusionsIn this study, we demonstrated that cell surface sialic acids assist in the attachment of EV71 to host cells. Cell surface sialylation should be a key regulator that facilitates the binding and infection of EV71 to RD and SK-N-SH cells.
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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.