Evidence map›Paper›PMID 32315970›Full record

ArticleEBioMedicine2020

Transcriptional and clonal characterization of B cell plasmablast diversity following primary and secondary natural DENV infection.

Adam T Waickman, Gregory D Gromowski, Wiriya Rutvisuttinunt, Tao Li, Hayden Siegfried, Kaitlin Victor, Caitlin Kuklis, Methee Gomootsukavadee, Michael K McCracken, Benjamin Gabriel and 15 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2020. 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 5 institutions in 2 countries.

Adam T WaickmanViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States. Electronic address: adam.t.waickman.ctr@mail.mil.
Gregory D GromowskiViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Wiriya RutvisuttinuntViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Tao LiViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Hayden SiegfriedViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Kaitlin VictorViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Caitlin KuklisViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Methee GomootsukavadeeDepartment of Virology, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand.
Michael K McCrackenViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Benjamin GabrielDepartment of Cell and Molecular Biology, Institute for Immunology and Informatics, University of Rhode Island, Providence, RI, United States.
Anuja MathewDepartment of Cell and Molecular Biology, Institute for Immunology and Informatics, University of Rhode Island, Providence, RI, United States.
Ariadna Grinyo I EscuerIntegral Molecular, Philadelphia, PA, United States.
Mallorie E FouchIntegral Molecular, Philadelphia, PA, United States.
Jenny LiangIntegral Molecular, Philadelphia, PA, United States.
Stefan FernandezDepartment of Virology, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand.
Edgar DavidsonIntegral Molecular, Philadelphia, PA, United States.
Benjamin J DoranzIntegral Molecular, Philadelphia, PA, United States.
Anon SrikiatkhachornDepartment of Cell and Molecular Biology, Institute for Immunology and Informatics, University of Rhode Island, Providence, RI, United States; Faculty of Medicine, King Mongkut's Institute of Technology Ladkrabang, Bangkok, Thailand.
Timothy EndyDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, USA.
Stephen J ThomasInstitute for Global Health and Translational Sciences, State University of New York Upstate Medical University, Syracuse, New York, USA.
Damon EllisonViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Alan L RothmanDepartment of Cell and Molecular Biology, Institute for Immunology and Informatics, University of Rhode Island, Providence, RI, United States.
Richard G JarmanViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Jeffrey R CurrierViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Heather FribergViral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, MD, United States.
Walter Reed Army Institute of Research · USIntegral Molecular (United States) · USUniversity of Rhode Island · USArmed Forces Research Institute of Medical Science · THSUNY Upstate Medical University · US

Funding

VIRAL DETERMINANTS OF SEVERE DENGUE DISEASEP01AI034533 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ROTHMAN, ALAN L · 1994 to 2022
$42.0M
NIAID NIH HHS HHSN272201400058CNIAID NIH HHS P01 AI034533
6 · The paper itself

Abstract

Antibody-mediated humoral immunity is thought to play a central role in mediating the immunopathogenesis of acute DENV infection, but limited data are available on the diversity, specificity, and functionality of the antibody response at the molecular level elicited by primary or secondary DENV infection. In order to close this functional gap in our understanding of DENV-specific humoral immunity, we utilized high-throughput single cell RNA sequencing to investigate B cells circulating in both primary and secondary natural DENV infections. We captured full-length paired immunoglobulin receptor sequence data from 9,027 B cells from a total of 6 subjects, including 2,717 plasmablasts. In addition to IgG and IgM class-switched cells, we unexpectedly found a high proportion of the DENV-elicited plasmablasts expressing IgA, principally in individuals with primary DENV infections. These IgA class-switched cells were extensively hypermutated even in individuals with a serologically confirmed primary DENV infection. Utilizing a combination of conventional biochemical assays and high-throughput shotgun mutagenesis, we determined that DENV-reactive IgA class-switched antibodies represent a significant fraction of DENV-reactive Igs generated in response to DENV infection, and that they exhibit a comparable epitope specificity to DENV-reactive IgG antibodies. These results provide insight into the molecular-level diversity of DENV-elicited humoral immunity and identify a heretofore unappreciated IgA plasmablast response to DENV infection.

Indexed as

B-LymphocytesCells, CulturedDengueHumansImmunity, HumoralImmunoglobulinsRNA-SeqSingle-Cell AnalysisTranscriptomeImmunoglobulinsDengueIgAMonoclonal antibodyPlasmablastSingle-cell RNA sequencing

Identifiers

PMID32315970
PMCPMC7170960
OpenAlexW3016975593

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.