An association between a positive direct antiglobulin test and HLA-DR12 in COVID-19.


Journal

Annals of hematology
ISSN: 1432-0584
Titre abrégé: Ann Hematol
Pays: Germany
ID NLM: 9107334

Informations de publication

Date de publication:
Sep 2022
Historique:
received: 14 03 2022
accepted: 28 06 2022
pubmed: 15 7 2022
medline: 17 8 2022
entrez: 14 7 2022
Statut: ppublish

Résumé

SARS-CoV-2 infection has been reported to be associated with a positive direct antiglobulin test (DAT). In this study, an analysis of 40 consecutive coronavirus disease 2019 (COVID-19) cases from December 2020 to September 2021 in Japan revealed that patients of 70 years and over were predisposed to a positive DAT. DAT positivity was related to a decrease in the hemoglobin level. Anemia in DAT-positive COVID-19 patients was attributed to hemolysis, which was corroborated by high reticulocyte counts and an increase in the red blood cell distribution width. Human leukocyte antigen (HLA)-DRB1*12:01 and DRB1*12:02 were exclusively found in DAT-positive COVID-19 patients. In silico assays for the Spike protein of SARS-CoV-2 predicted several common core peptides that met the criteria for a B cell epitope and strong binding to both HLA-DRB1*12:01 and DRB1*12:02. Among these peptides, the amino acids sequence TSNFR, which is found within the S1 subunit of SARS-CoV-2 Spike protein, is shared by human blood group antigen Rhesus (Rh) CE polypeptides. In vitro analysis showed that the expression of HLA-DR in CD4

Identifiants

pubmed: 35833981
doi: 10.1007/s00277-022-04921-9
pii: 10.1007/s00277-022-04921-9
pmc: PMC9281373
doi:

Substances chimiques

Epitopes, T-Lymphocyte 0
HLA-DR Serological Subtypes 0
HLA-DR12 antigen 0
Spike Glycoprotein, Coronavirus 0
spike protein, SARS-CoV-2 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1959-1969

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Hideaki Matsuura (H)

Department of Blood Transfusion, Fujita Health University Hospital, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.
Department of Cellular and Molecular Biology, Fujita Health University School of Medical Sciences, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.

Sumie Fujii (S)

Department of Transfusion Medicine and Cell Therapy, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.

Yusuke Matsui (Y)

Gladstone Institute of Virology and Immunology, University of California, San Francisco, San Francisco, CA, USA.

Yukari Sugiura (Y)

Department of Blood Transfusion, Fujita Health University Hospital, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.

Hidehiko Akiyama (H)

Department of Cellular and Molecular Biology, Fujita Health University School of Medical Sciences, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.

Yasuo Miura (Y)

Department of Blood Transfusion, Fujita Health University Hospital, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan. ymiura@fujita-hu.ac.jp.
Department of Transfusion Medicine and Cell Therapy, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan. ymiura@fujita-hu.ac.jp.

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