Evidence map›Paper›PMID 34936684›Full record

ArticlePloS one2021

SARS-CoV-2 spike-specific memory B cells express higher levels of T-bet and FcRL5 after non-severe COVID-19 as compared to severe disease.

Raphael A Reyes, Kathleen Clarke, S Jake Gonzales, Angelene M Cantwell, Rolando Garza, Gabriel Catano, Robin E Tragus, Thomas F Patterson, Sebastiaan Bol, Evelien M Bunnik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-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, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  8. Differences in phenotype between long-lived memory B cells againstbioRxiv : the preprint server for biology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Raphael A ReyesDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.ORCID 0000-0002-2234-4758
Kathleen ClarkeDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
S Jake GonzalesDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.ORCID 0000-0002-6621-4103
Angelene M CantwellDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.ORCID 0000-0001-5122-6112
Rolando GarzaDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Gabriel CatanoDepartment of Medicine, Division of Infectious Diseases, The University of Texas Health Science Center at San Antonio, University Health System, San Antonio, Texas, United States of America.ORCID 0000-0001-6047-2286
Robin E TragusDepartment of Medicine, Division of Infectious Diseases, The University of Texas Health Science Center at San Antonio, University Health System, San Antonio, Texas, United States of America.ORCID 0000-0001-6980-9164
Thomas F PattersonDepartment of Medicine, Division of Infectious Diseases, The University of Texas Health Science Center at San Antonio, University Health System, San Antonio, Texas, United States of America.
Sebastiaan BolDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.ORCID 0000-0002-3843-6657
Evelien M BunnikDepartment of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.ORCID 0000-0003-4003-3053
The University of Texas Health Science Center at San Antonio · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
NRSA Training Core (TL1)TL1TR002647 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHUN, YONG-HEE PATRICIA, FREI, CHRISTOPHER R. · 2018 to 2022
$1.8M
NCATS NIH HHS TL1 TR002647NCATS NIH HHS UL1 TR001120NCI NIH HHS P30 CA054174NIAID NIH HHS HHSN272201400008C
6 · The paper itself

Abstract

SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the memory B cell compartment between recovery and five months post-symptom onset. Using high-parameter spectral flow cytometry, we analyzed the phenotype of memory B cells with reactivity against the SARS-CoV-2 spike protein or the spike receptor binding domain (RBD) in recovered individuals who had been hospitalized with non-severe (n = 8) or severe (n = 5) COVID-19. One month after symptom onset, a substantial proportion of spike-specific IgG+ B cells showed an activated phenotype. In individuals who experienced non-severe disease, spike-specific IgG+ B cells showed increased expression of markers associated with durable B cell memory, including T-bet and FcRL5, as compared to individuals who experienced severe disease. While the frequency of T-bet+ spike-specific IgG+ B cells differed between the two groups, these cells predominantly showed an activated switched memory B cell phenotype in both groups. Five months post-symptom onset, the majority of spike-specific memory B cells had a resting phenotype and the percentage of spike-specific T-bet+ IgG+ memory B cells decreased to baseline levels. Collectively, our results highlight subtle differences in the B cells response after non-severe and severe COVID-19 and suggest that the memory B cell response elicited during non-severe COVID-19 may be of higher quality than the response after severe disease.

Indexed as

AdultAgedAntibodies, ViralBiomarkersB-LymphocytesCOVID-19FemaleFlow CytometryHospitalizationHumansImmunoglobulin GImmunologic MemoryMaleMemory B CellsMiddle AgedReceptors, FcAntibodies, ViralBiomarkersFCRL5 protein, humanImmunoglobulin GReceptors, FcSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2T-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID34936684
PMCPMC8694470
OpenAlexW4200598759

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.