Evidence map›Paper›PMID 34552055›Full record

ArticleSignal transduction and targeted therapy2021

SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells via enhancing B-cell metabolism.

Yukai Jing, Li Luo, Ying Chen, Lisa S Westerberg, Peng Zhou, Zhiping Xu, Andrés A Herrada, Chan-Sik Park, Masato Kubo, Heng Mei and 8 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 55 citations in OpenAlex.

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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

18 authors at 11 institutions in 6 countries.

Yukai Jing *Department of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Li Luo *Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Ying ChenCenter for Biosafety Mega-Science, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, People's Republic of China.
Lisa S WesterbergDepartment of Microbiology Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Peng ZhouCenter for Biosafety Mega-Science, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, People's Republic of China.ORCID 0000-0001-9863-4201
Zhiping XuWuhan Metware Biotechnology Co., Ltd, Wuhan, People's Republic of China.
Andrés A HerradaLymphatic and Inflammation Research Laboratory, Facultad de Ciencias de la Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Talca, Chile.
Chan-Sik ParkDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Masato KuboLaboratory for Cytokine Regulation, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Kanagawa, Japan.
Heng MeiInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Yu HuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.ORCID 0000-0002-2815-4568
Pamela Pui-Wah LeeDepartment of Paediatrics and Adolescent Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China.
Bing ZhengDepartment of Immunology, School of Medicine, Yangtze University, Jingzhou, Hubei Province, People's Republic of China.
Zhiwei SuiCenter for Advanced Measurement Science, National Institute of Metrology, Beijing, People's Republic of China.
Wei XiaoDepartment of Respiratory, The First Affiliated Hospital of Yangtze University, Jingzhou, Hubei Province, People's Republic of China.
Quan GongDepartment of Immunology, School of Medicine, Yangtze University, Jingzhou, Hubei Province, People's Republic of China.
Zhongxin LuDepartment of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. 2826862499@qq.com.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. ChaohongLiu80@126.com.
Yangtze University · CNCentral Hospital of Wuhan · CNChinese Academy of Sciences · CNHuazhong University of Science and Technology · CNUnion Hospital · CNChinese University of Hong Kong · HKKarolinska Institutet · SENational Institute of Metrology · CNRIKEN Center for Integrative Medical Sciences · JPUlsan College · KRUniversidad Autónoma de Chile · CL

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31900654
6 · The paper itself

Abstract

The SARS-CoV-2 infection causes severe immune disruption. However, it is unclear if disrupted immune regulation still exists and pertains in recovered COVID-19 patients. In our study, we have characterized the immune phenotype of B cells from 15 recovered COVID-19 patients, and found that healthy controls and recovered patients had similar B-cell populations before and after BCR stimulation, but the frequencies of PBC in patients were significantly increased when compared to healthy controls before stimulation. However, the percentage of unswitched memory B cells was decreased in recovered patients but not changed in healthy controls upon BCR stimulation. Interestingly, we found that CD19 expression was significantly reduced in almost all the B-cell subsets in recovered patients. Moreover, the BCR signaling and early B-cell response were disrupted upon BCR stimulation. Mechanistically, we found that the reduced CD19 expression was caused by the dysregulation of cell metabolism. In conclusion, we found that SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells via enhancing B-cell metabolism, which may provide a new intervention target to cure COVID-19.

Indexed as

AnimalsAntigens, CD19B-LymphocytesChlorocebus aethiopsCOVID-19Down-RegulationFemaleHumansImmunologic Deficiency SyndromesImmunologic MemoryMaleMiceMice, TransgenicReceptors, Antigen, B-CellSARS-CoV-2Vero CellsAntigens, CD19CD19 antigen, mouseCD19 molecule, humanReceptors, Antigen, B-Cell

Identifiers

PMID34552055
PMCPMC8456405
OpenAlexW3199311682

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.