Evidence map›Paper›PMID 30323338›Full record

ArticleNature immunology2018

Characterization of a potent and highly unusual minimally enhancing antibody directed against dengue virus.

Max Renner, Aleksandra Flanagan, Wanwisa Dejnirattisai, Chunya Puttikhunt, Watchara Kasinrerk, Piyada Supasa, Wiyada Wongwiwat, Kriangkrai Chawansuntati, Thaneeya Duangchinda, Alison Cowper and 6 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Pharmaceuticals (Basel, Switzerland) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Max RennerDivision of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Aleksandra FlanaganDivision of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Wanwisa DejnirattisaiNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Chunya PuttikhuntMedical Biotechnology Research Unit, National Center for Genetic Engineering and Biotechnology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Watchara KasinrerkBiomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, Chiang Mai University, Chiang Mai, Thailand.
Piyada SupasaNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Wiyada WongwiwatNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Kriangkrai ChawansuntatiMedical Biotechnology Research Unit, National Center for Genetic Engineering and Biotechnology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Thaneeya DuangchindaMedical Biotechnology Research Unit, National Center for Genetic Engineering and Biotechnology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Alison CowperNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Claire M MidgleyNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Prida MalasitMedical Biotechnology Research Unit, National Center for Genetic Engineering and Biotechnology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Juha T HuiskonenDivision of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Juthathip MongkolsapayaNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. juthathip.mongkolsapaya@well.ox.ac.uk.
Gavin R ScreatonNuffield Department of Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. gavin.screaton@medsci.ox.ac.uk.
Jonathan M GrimesDivision of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. jonathan@strubi.ox.ac.uk.ORCID http://orcid.org/0000-0001-9698-0389
Centre for Human Genetics · GBSiriraj Hospital · THChiang Mai University · TH

Funding

Wellcome Trust 080721Wellcome Trust 093305Wellcome Trust 200835Wellcome Trust 203141Wellcome Trust 203224Wellcome Trust 204703
6 · The paper itself

Abstract

Dengue virus is a major pathogen, and severe infections can lead to life-threatening dengue hemorrhagic fever. Dengue virus exists as four serotypes, and dengue hemorrhagic fever is often associated with secondary heterologous infections. Antibody-dependent enhancement (ADE) may drive higher viral loads in these secondary infections and is purported to result from antibodies that recognize dengue virus but fail to fully neutralize it. Here we characterize two antibodies, 2C8 and 3H5, that bind to the envelope protein. Antibody 3H5 is highly unusual as it not only is potently neutralizing but also promotes little if any ADE, whereas antibody 2C8 has strong capacity to promote ADE. We show that 3H5 shows resilient binding in endosomal pH conditions and neutralizes at low occupancy. Immunocomplexes of 3H5 and dengue virus do not efficiently interact with Fcγ receptors, which we propose is due to the binding mode of 3H5 and constitutes the primary mechanism of how ADE is avoided.

Indexed as

Antibodies, NeutralizingAntibodies, ViralAntibody-Dependent EnhancementDengue VirusHumansAntibodies, NeutralizingAntibodies, Viral

Identifiers

PMID30323338
PMCPMC7051845
OpenAlexW2895384398

What OpenQuestion holds

Textmetadata
LicenceTDM
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.