An autoantigen profile of human A549 lung cells reveals viral and host etiologic molecular attributes of autoimmunity in COVID-19.

Tytuł:: An autoantigen profile of human A549 lung cells reveals viral and host etiologic molecular attributes of autoimmunity in COVID-19.
Autorzy:: Wang JY; Curandis, New York, USA. Electronic address: .
Zhang W; Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guizhou, China.
Roehrl MW; Curandis, New York, USA.
Roehrl VB; Curandis, New York, USA.
Roehrl MH; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, USA; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, USA. Electronic address: .
Źródło:: Journal of autoimmunity [J Autoimmun] 2021 Jun; Vol. 120, pp. 102644. Date of Electronic Publication: 2021 Apr 27.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: London : Academic Press
Original Publication: London ; San Diego : Academic Press, c1988-
MeSH Terms:: Autoimmunity*
Autoantigens/*immunology
COVID-19/*immunology
Lung/*immunology
SARS-CoV-2/*physiology
Signal Transduction/*immunology
Virus Replication/*immunology
A549 Cells ; COVID-19/pathology ; Humans ; Lung/pathology ; Lung/virology
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Grant Information:: P30 CA008748 United States CA NCI NIH HHS; R21 CA251992 United States CA NCI NIH HHS
Contributed Indexing:: Keywords: Atlas; Autoantigens; Autoimmunity; COVID-19; Lung; Resource
Substance Nomenclature:: 0 (Autoantigens)
Entry Date(s):: Date Created: 20210510 Date Completed: 20210524 Latest Revision: 20221221
Update Code:: 20240105
PubMed Central ID:: PMC8075847
DOI:: 10.1016/j.jaut.2021.102644
PMID:: 33971585
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We aim to establish a comprehensive COVID-19 autoantigen atlas in order to understand autoimmune diseases caused by SARS-CoV-2 infection. Based on the unique affinity between dermatan sulfate and autoantigens, we identified 348 proteins from human lung A549 cells, of which 198 are known targets of autoantibodies. Comparison with current COVID data identified 291 proteins that are altered at protein or transcript level in SARS-CoV-2 infection, with 191 being known autoantigens. These known and putative autoantigens are significantly associated with viral replication and trafficking processes, including gene expression, ribonucleoprotein biogenesis, mRNA metabolism, translation, vesicle and vesicle-mediated transport, and apoptosis. They are also associated with cytoskeleton, platelet degranulation, IL-12 signaling, and smooth muscle contraction. Host proteins that interact with and that are perturbed by viral proteins are a major source of autoantigens. Orf3 induces the largest number of protein alterations, Orf9 affects the mitochondrial ribosome, and they and E, M, N, and Nsp proteins affect protein localization to membrane, immune responses, and apoptosis. Phosphorylation and ubiquitination alterations by viral infection define major molecular changes in autoantigen origination. This study provides a large list of autoantigens as well as new targets for future investigation, e.g., UBA1, UCHL1, USP7, CDK11A, PRKDC, PLD3, PSAT1, RAB1A, SLC2A1, platelet activating factor acetylhydrolase, and mitochondrial ribosomal proteins. This study illustrates how viral infection can modify host cellular proteins extensively, yield diverse autoantigens, and trigger a myriad of autoimmune sequelae. Our work provides a rich resource for studies into "long COVID" and related autoimmune sequelae.
(Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Update of: bioRxiv. 2021 Feb 22;:. (PMID: 33655248)

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