SARS-CoV-2 infection induces beta cell transdifferentiation
Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vi...
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| Published in | Cell metabolism Vol. 33; no. 8; pp. 1577 - 1591.e7 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
03.08.2021
Cell Press |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.
[Display omitted]
•SARS-CoV-2 viral antigen is detected in beta cells of autopsies of COVID-19 subjects•SARS-CoV-2 infection causes beta cell transdifferentiation•SARS-CoV-2-induced beta cell transdifferentiation is mediated by eIF2 pathway•Trans-ISRIB reverses SARS-CoV-2 infection-induced beta cell transdifferentiation
Here, Tang et al. reported the detection of SARS-CoV-2 viral antigen in autopsy samples from COVID-19 subjects. In addition, SARS-CoV-2 infection induces eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that can be reversed by trans-ISRIB. |
|---|---|
| AbstractList | Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from
ex vivo
infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with
trans
-integrated stress response inhibitor (
trans
-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.
•
SARS-CoV-2 viral antigen is detected in beta cells of autopsies of COVID-19 subjects
•
SARS-CoV-2 infection causes beta cell transdifferentiation
•
SARS-CoV-2-induced beta cell transdifferentiation is mediated by eIF2 pathway
•
Trans
-ISRIB reverses SARS-CoV-2 infection-induced beta cell transdifferentiation
Here, Tang et al. reported the detection of SARS-CoV-2 viral antigen in autopsy samples from COVID-19 subjects. In addition, SARS-CoV-2 infection induces eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that can be reversed by
trans
-ISRIB. Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19. Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19. Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19. [Display omitted] •SARS-CoV-2 viral antigen is detected in beta cells of autopsies of COVID-19 subjects•SARS-CoV-2 infection causes beta cell transdifferentiation•SARS-CoV-2-induced beta cell transdifferentiation is mediated by eIF2 pathway•Trans-ISRIB reverses SARS-CoV-2 infection-induced beta cell transdifferentiation Here, Tang et al. reported the detection of SARS-CoV-2 viral antigen in autopsy samples from COVID-19 subjects. In addition, SARS-CoV-2 infection induces eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that can be reversed by trans-ISRIB. |
| Author | Erdos, Michael R. Chong, Angie Chi Nok Narisu, Narisu Naji, Ali Lacko, Lauretta A. tenOever, Benjamin R. Collins, Francis S. Uhl, Skyler Liu, Chengyang Bonnycastle, Lori L. Evans, Todd Chen, Shuibing Lim, Jean K. Bram, Yaron Chandar, Vasuretha Xiang, Jenny Acklin, Joshua A. Borczuk, Alain C. Li, Bo Zhang, Tuo Min, Zaw Schwartz, Robert E. Xue, Dongxiang Vandana, J. Jeya Tang, Xuming |
| Author_xml | – sequence: 1 givenname: Xuming surname: Tang fullname: Tang, Xuming organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 2 givenname: Skyler surname: Uhl fullname: Uhl, Skyler organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA – sequence: 3 givenname: Tuo surname: Zhang fullname: Zhang, Tuo organization: Genomics Resources Core Facility, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 4 givenname: Dongxiang surname: Xue fullname: Xue, Dongxiang organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 5 givenname: Bo surname: Li fullname: Li, Bo organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 6 givenname: J. Jeya surname: Vandana fullname: Vandana, J. Jeya organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 7 givenname: Joshua A. surname: Acklin fullname: Acklin, Joshua A. organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA – sequence: 8 givenname: Lori L. surname: Bonnycastle fullname: Bonnycastle, Lori L. organization: The Center for Precision Health Research, National Human Genome Research Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA – sequence: 9 givenname: Narisu surname: Narisu fullname: Narisu, Narisu organization: The Center for Precision Health Research, National Human Genome Research Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA – sequence: 10 givenname: Michael R. surname: Erdos fullname: Erdos, Michael R. organization: The Center for Precision Health Research, National Human Genome Research Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA – sequence: 11 givenname: Yaron surname: Bram fullname: Bram, Yaron organization: Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 12 givenname: Vasuretha surname: Chandar fullname: Chandar, Vasuretha organization: Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 13 givenname: Angie Chi Nok surname: Chong fullname: Chong, Angie Chi Nok organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 14 givenname: Lauretta A. surname: Lacko fullname: Lacko, Lauretta A. organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 15 givenname: Zaw surname: Min fullname: Min, Zaw organization: Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA – sequence: 16 givenname: Jean K. surname: Lim fullname: Lim, Jean K. organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA – sequence: 17 givenname: Alain C. surname: Borczuk fullname: Borczuk, Alain C. organization: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 18 givenname: Jenny surname: Xiang fullname: Xiang, Jenny organization: Genomics Resources Core Facility, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 19 givenname: Ali surname: Naji fullname: Naji, Ali organization: Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA – sequence: 20 givenname: Francis S. surname: Collins fullname: Collins, Francis S. organization: The Center for Precision Health Research, National Human Genome Research Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA – sequence: 21 givenname: Todd surname: Evans fullname: Evans, Todd organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 22 givenname: Chengyang surname: Liu fullname: Liu, Chengyang email: chliu@pennmedicine.upenn.edu organization: Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA – sequence: 23 givenname: Benjamin R. surname: tenOever fullname: tenOever, Benjamin R. email: benjamin.tenoever@mssm.edu organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA – sequence: 24 givenname: Robert E. surname: Schwartz fullname: Schwartz, Robert E. email: rec2025@med.cornell.edu organization: Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA – sequence: 25 givenname: Shuibing surname: Chen fullname: Chen, Shuibing email: shc2034@med.cornell.edu organization: Department of Surgery, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34081913$$D View this record in MEDLINE/PubMed |
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| ISSN | 1550-4131 1932-7420 |
| IngestDate | Thu Aug 21 18:00:00 EDT 2025 Thu Jul 10 17:38:18 EDT 2025 Mon Jul 21 06:00:17 EDT 2025 Thu Apr 24 23:03:58 EDT 2025 Tue Jul 01 03:58:19 EDT 2025 Fri Feb 23 02:39:54 EST 2024 |
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| Issue | 8 |
| Keywords | COVID-19 PRSS1 insulin human islets trypsin 1 diabetes EgIF2 |
| Language | English |
| License | This is an open access article under the CC BY license. Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
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| OpenAccessLink | https://www.sciencedirect.com/science/article/pii/S1550413121002321 |
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| PublicationTitle | Cell metabolism |
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| Snippet | Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral... |
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| SubjectTerms | Acetamides - pharmacology Adolescent Adult Aged Aged, 80 and over Animals Cell Transdifferentiation - drug effects Chlorocebus aethiops Clinical and Translational Report COVID-19 COVID-19 - mortality COVID-19 - virology Cyclohexylamines - pharmacology Cytokines - metabolism diabetes EgIF2 Eukaryotic Initiation Factor-2 - metabolism Female Glucagon Host-Pathogen Interactions human islets Humans insulin Insulin - metabolism Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Insulin-Secreting Cells - pathology Insulin-Secreting Cells - virology Male Middle Aged Phenotype PRSS1 SARS-CoV-2 - pathogenicity Signal Transduction Tissue Culture Techniques Trypsin - metabolism trypsin 1 Vero Cells Young Adult |
| Title | SARS-CoV-2 infection induces beta cell transdifferentiation |
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