ArticleProceedings of the National Academy of Sciences of the United States of America2016
Enterovirus D68 receptor requirements unveiled by haploid genetics.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 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.
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Who cites it
70 citing papers in PubMed, 104 citations in OpenAlex.
- A dual-receptor checkpoint primes enterovirus D68 for respiratory cell entry.Nature communications · 2026Article
- Decoding the complex receptor landscape of enterovirus D68.PLoS pathogens · 2026Review
- Enterovirus D68 receptor usage: from static attachment to dynamic entry.Journal of virology · 2026Review
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Elucidating the role of human skeletal muscles in the pathogenesis of enterovirus D68 infection.Life science alliance · 2025Article
- Sialic Acid-Containing Glycolipids Extend the Receptor Repertoire of Enterovirus-D68.ACS infectious diseases · 2025Article
- The use of sialic acids as attachment factors is a common feature ofJournal of virology · 2025Article
- MFSD6 is an entry receptor for enterovirus D68.Nature · 2025Article
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- Enteroviruses: epidemic potential, challenges and opportunities with vaccines.Journal of biomedical science · 2024Review
- Pharmacological activation of TLR7 exerts inhibition on the replication of EV-D68 in respiratory cells.Journal of virology · 2024Article
- N-terminal acetyltransferase 6 facilitates enterovirus 71 replication by regulating PI4KB expression and replication organelle biogenesis.Journal of virology · 2024Article
- Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1.Journal of virology · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Identification of four neutralizing antigenic sites on the enterovirus D68 capsid.Journal of virology · 2023Article
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- Pterostilbene, an active constituent of blueberries, enhances innate immune activation and restricts enterovirus D68 infection.Frontiers in immunology · 2023Article
- Cellular glycan modification by B3GAT1 broadly restricts influenza virus infection.Nature communications · 2022Article
- Enterovirus D68 Infection in Human Primary Airway and Brain Organoids: No Additional Role for Heparan Sulfate Binding for Neurotropism.Microbiology spectrum · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrection for Baggen et al., Enterovirus D68 receptor requirements unveiled by haploid genetics.2016 · de Haan Xander, Cornelis A M [corrected to de Haan, Cornelis A M]
Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
Enterovirus D68 (EV-D68) is an emerging pathogen that can cause severe respiratory disease and is associated with cases of paralysis, especially among children. Heretofore, information on host factor requirements for EV-D68 infection is scarce. Haploid genetic screening is a powerful tool to reveal factors involved in the entry of pathogens. We performed a genome-wide haploid screen with the EV-D68 prototype Fermon strain to obtain a comprehensive overview of cellular factors supporting EV-D68 infection. We identified and confirmed several genes involved in sialic acid (Sia) biosynthesis, transport, and conjugation to be essential for infection. Moreover, by using knockout cell lines and gene reconstitution, we showed that both α2,6- and α2,3-linked Sia can be used as functional cellular EV-D68 receptors. Importantly, the screen did not reveal a specific protein receptor, suggesting that EV-D68 can use multiple redundant sialylated receptors. Upon testing recent clinical strains, we identified strains that showed a similar Sia dependency, whereas others could infect cells lacking surface Sia, indicating they can use an alternative, nonsialylated receptor. Nevertheless, these Sia-independent strains were still able to bind Sia on human erythrocytes, raising the possibility that these viruses can use multiple receptors. Sequence comparison of Sia-dependent and Sia-independent EV-D68 strains showed that many changes occurred near the canyon that might allow alternative receptor binding. Collectively, our findings provide insights into the identity of the EV-D68 receptor and suggest the possible existence of Sia-independent viruses, which are essential for understanding tropism and disease.
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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.