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An Autoantigen Profile of Human A549 Lung Cells Reveals Viral and Host Etiologic Molecular Attributes of Autoimmunity in COVID-19

View ORCID ProfileJulia Y. Wang, Wei Zhang, Michael W. Roehrl, Victor B. Roehrl, View ORCID ProfileMichael H. Roehrl
doi: https://doi.org/10.1101/2021.02.21.432171
Julia Y. Wang
1Curandis, New York, USA
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  • For correspondence: julia@curandis.com roehrlm@mskcc.org
Wei Zhang
2Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guizhou, China
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Michael W. Roehrl
1Curandis, New York, USA
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Victor B. Roehrl
1Curandis, New York, USA
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Michael H. Roehrl
3Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, USA
4Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, USA
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  • For correspondence: julia@curandis.com roehrlm@mskcc.org
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Abstract

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.

Competing Interest Statement

JYW is the founder and Chief Scientific Officer of Curandis. WZ was supported by the NIH and declares no competing interests. MWR and VBR are volunteers of Curandis. MHR is a member of the Scientific Advisory Boards of Trans-Hit, Proscia, and Universal DX, but these companies have no relation to the study.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted February 22, 2021.
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An Autoantigen Profile of Human A549 Lung Cells Reveals Viral and Host Etiologic Molecular Attributes of Autoimmunity in COVID-19
Julia Y. Wang, Wei Zhang, Michael W. Roehrl, Victor B. Roehrl, Michael H. Roehrl
bioRxiv 2021.02.21.432171; doi: https://doi.org/10.1101/2021.02.21.432171
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An Autoantigen Profile of Human A549 Lung Cells Reveals Viral and Host Etiologic Molecular Attributes of Autoimmunity in COVID-19
Julia Y. Wang, Wei Zhang, Michael W. Roehrl, Victor B. Roehrl, Michael H. Roehrl
bioRxiv 2021.02.21.432171; doi: https://doi.org/10.1101/2021.02.21.432171

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