Evidence map›Paper›PMID 29284752›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Role of enhanced receptor engagement in the evolution of a pandemic acute hemorrhagic conjunctivitis virus.

Jim Baggen, Daniel L Hurdiss, Georg Zocher, Nitesh Mistry, Richard W Roberts, Jasper J Slager, Hongbo Guo, Arno L W van Vliet, Maryam Wahedi, Kimberley Benschop and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 61 citations in OpenAlex.

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  4. ITAFProceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 5 countries.

Jim BaggenVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Daniel L HurdissAstbury Centre for Structural Molecular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom.ORCID 0000-0003-3834-5808
Georg ZocherInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Nitesh MistryDivision of Virology, Department of Clinical Microbiology, Umeå University, 90187 Umeå, Sweden.
Richard W RobertsVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Jasper J SlagerVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Hongbo GuoVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Arno L W van VlietVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Maryam WahediVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Kimberley BenschopCentre for Infectious Disease Control, National Institute for Public Health and the Environment, 3720BA Bilthoven, The Netherlands.
Erwin DuizerCentre for Infectious Disease Control, National Institute for Public Health and the Environment, 3720BA Bilthoven, The Netherlands.
Cornelis A M de HaanVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Erik de VriesVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
José M CasasnovasDepartment of Macromolecular Structures, Centro Nacional de Biotecnología, Campus Universidad Autónoma de Madrid, 28049 Madrid, Spain.
Raoul J de GrootVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Niklas ArnbergDivision of Virology, Department of Clinical Microbiology, Umeå University, 90187 Umeå, Sweden.ORCID 0000-0002-7069-6678
Thilo StehleInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Neil A RansonAstbury Centre for Structural Molecular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom.ORCID 0000-0002-3640-5275
Hendrik Jan ThibautVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands.
Frank J M van KuppeveldVirology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584CL Utrecht, The Netherlands; F.J.M.vanKuppeveld@uu.nl.
Utrecht University · NLNational Institute for Public Health and the Environment · NLUmeå University · SEUniversity of Leeds · GBUniversity of Tübingen · DECentro Nacional de Biotecnología · ES

Funding

Wellcome Trust 102572/B/13/ZWellcome Trust 108466Wellcome Trust 108466/Z/15/Z
6 · The paper itself

Abstract

Acute hemorrhagic conjunctivitis (AHC) is a painful, contagious eye disease, with millions of cases in the last decades. Coxsackievirus A24 (CV-A24) was not originally associated with human disease, but in 1970 a pathogenic "variant" (CV-A24v) emerged, which is now the main cause of AHC. Initially, this variant circulated only in Southeast Asia, but it later spread worldwide, accounting for numerous AHC outbreaks and two pandemics. While both CV-A24 variant and nonvariant strains still circulate in humans, only variant strains cause AHC for reasons that are yet unknown. Since receptors are important determinants of viral tropism, we set out to map the CV-A24 receptor repertoire and establish whether changes in receptor preference have led to the increased pathogenicity and rapid spread of CV-A24v. Here, we identify ICAM-1 as an essential receptor for both AHC-causing and non-AHC strains. We provide a high-resolution cryo-EM structure of a virus-ICAM-1 complex, which revealed critical ICAM-1-binding residues. These data could help identify a possible conserved mode of receptor engagement among ICAM-1-binding enteroviruses and rhinoviruses. Moreover, we identify a single capsid substitution that has been adopted by all pandemic CV-A24v strains and we reveal that this adaptation enhances the capacity of CV-A24v to bind sialic acid. Our data elucidate the CV-A24v receptor repertoire and point to a role of enhanced receptor engagement in the adaptation to the eye, possibly enabling pandemic spread.

Indexed as

Amino Acid SequenceCapsid ProteinsConjunctivitis, Acute HemorrhagicCryoelectron MicroscopyDisease OutbreaksEnterovirus C, HumanHumansIntercellular Adhesion Molecule-1MutationN-Acetylneuraminic AcidPandemicsPhylogenyProtein BindingReceptors, VirusSequence Homology, Amino AcidViral TropismCapsid ProteinsIntercellular Adhesion Molecule-1N-Acetylneuraminic AcidReceptors, Virusconjunctivitiscoxsackievirus A24vICAM-1receptorsialic acid

Identifiers

PMID29284752
PMCPMC5777043
OpenAlexW2778474843

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.