ArticleCell reports2023
Variant enterovirus A71 found in immune-suppressed patient binds to heparan sulfate and exhibits neurotropism in B-cell-depleted mice.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Establishment of an oral enterovirus 71 (EV71) infection model in immunocompetent mice for antiviral therapy evaluation.Journal of virology · 2026Article
- Serial passagingFrontiers in cellular and infection microbiology · 2026Article
- Enterovirus A71 priorities, challenges, and future opportunities in humoral immunity and vaccine development.NPJ vaccines · 2025Review
- Sialic Acid-Containing Glycolipids Extend the Receptor Repertoire of Enterovirus-D68.ACS infectious diseases · 2025Article
- Pilaralisib inhibits the replication of enteroviruses by targeting the PI3K/AKT signaling pathway.Virology journal · 2025Article
- Article
- Novel virulence determinants in VP1 regulate the assembly of enterovirus-A71.Journal of virology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Enterovirus A71 (EV-A71) causes hand, foot, and mouth disease outbreaks with neurological complications and deaths. We previously isolated an EV-A71 variant in the stool, cerebrospinal fluid, and blood of an immunocompromised patient who had a leucine-to-arginine substitution on the VP1 capsid protein, resulting in increased heparin sulfate binding. We show here that this mutation increases the virus's pathogenicity in orally infected mice with depleted B cells, which mimics the patient's immune status, and increases susceptibility to neutralizing antibodies. However, a double mutant with even greater heparin sulfate affinity is not pathogenic, suggesting that increased heparin sulfate affinity may trap virions in peripheral tissues and reduce neurovirulence. This research sheds light on the increased pathogenicity of variant with heparin sulfate (HS)-binding ability in individuals with decreased B cell immunity.
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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.