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description Publicationkeyboard_double_arrow_right Article 2020 France, France, Germany, United States, United Kingdom, Netherlands, FrancePublisher:Elsevier BV Funded by:NIH | The Role of IL-5 and Loca..., NIH | Administrative Core, NIH | Prostaglandin D2: A Key M... +20 projectsNIH| The Role of IL-5 and Local Nasal Polyp Immunoglobulin Production in Aspirin-Exacerbated Respiratory Disease ,NIH| Administrative Core ,NIH| Prostaglandin D2: A Key Mediator of Aspirin-Exacerbated Respiratory Disease ,NIH| Defining and Exploiting a Genetic Template for an HIV Vaccine ,NSF| Graduate Research Fellowship Program ,NIH| Contribution of CD8 T cells in Controlling Tuberculosis ,NIH| Innate-like BCR activity as a template for universal vaccination against influenza virus ,NIH| The inflammatory role of the platelet in aspirin-exacerbated respiratory disease. ,NIH| Eicosanoid Networks in Aspirin Exacerbated Respiratory Disease ,NIH| CDRH3-independent B cell stimulation to selectively expand VRC01 lineages from a fully humanized immunoglobulin repertoire ,NIH| CysLT and P2Y Receptors in Lung Inflammation ,NIH| Medical Scientist Training Program ,NIH| Novel Biologic Therapies for BMT: Mechanistic Evaluation in Rhesus Macaques ,NIH| An integrated multiplexed genomic assay for low input clinical samples1 ,NIH| Curing HIV Through Allogeneic Hematopoietic Stem Cell Transplantation ,ANR| SAHARRA ,NIH| BELIEVE: Bench to Bed Enhanced Lymphocyte Infusions to Engineer Viral Eradication ,NIH| The Role of IL-5 and Local Nasal Polyp Immunoglobulin Production in Aspirin-Exacerbated Respiratory Disease ,NIH| Pathophysiologic and therapeutic mechanisms of aspirin exacerbated respiratory d* ,NIH| Next Generation HSC Gene Therapy for HIV Control and Eradication ,NIH| Structure based prediction of the interactome ,NIH| Optimizing EP receptor subtype targeting for asthma therapy ,NIH| Cell and Gene Therapy for HIV CureCarly G. K. Ziegler; Samuel J. Allon; Sarah K. Nyquist; Ian M. Mbano; Vincent N. Miao; Constantine N. Tzouanas; Yuming Cao; Ashraf S. Yousif; Julia Bals; Blake M. Hauser; Jared Feldman; Christoph Muus; Marc H. Wadsworth; Samuel W. Kazer; Travis K. Hughes; Benjamin Doran; G. James Gatter; Marko Vukovic; Faith Taliaferro; Benjamin E. Mead; Zhiru Guo; Jennifer P. Wang; Delphine Gras; Magali Plaisant; Meshal Ansari; Ilias Angelidis; Heiko Adler; Jennifer M.S. Sucre; Chase J. Taylor; Brian M. Lin; Avinash Waghray; Vanessa Mitsialis; Daniel F. Dwyer; Kathleen M. Buchheit; Joshua A. Boyce; Nora A. Barrett; Tanya M. Laidlaw; Shaina L. Carroll; Lucrezia Colonna; Victor Tkachev; Christopher W. Peterson; Alison Yu; Hengqi Betty Zheng; Hannah P. Gideon; Caylin G. Winchell; Philana Ling Lin; Colin D. Bingle; Scott B. Snapper; Jonathan A. Kropski; Fabian J. Theis; Herbert B. Schiller; Laure-Emmanuelle Zaragosi; Pascal Barbry; Alasdair Leslie; Hans-Peter Kiem; JoAnne L. Flynn; Sarah M. Fortune; Bonnie Berger; Robert W. Finberg; Leslie S. Kean; Manuel Garber; Aaron G. Schmidt; Daniel Lingwood; Alex K. Shalek; Jose Ordovas-Montanes; Nicholas E. Banovich; Alvis Brazma; Tushar J. Desai; Thu Elizabeth Duong; Oliver Eickelberg; Christine S. Falk; Michael Farzan; Ian A. Glass; Muzlifah Haniffa; Peter Horvath; Deborah T. Hung; Naftali Kaminski; Mark A. Krasnow; Malte Kühnemund; Robert Lafyatis; Haeock Lee; Sylvie Leroy; Sten Linnarson; Joakim Lundeberg; Kerstin B. Meyer; Alexander V. Misharin; Martijn C. Nawijn; Marko Nikolic; Dana Pe'er; Joseph E. Powell; Stephen R. Quake; Jay Rajagopal; Purushothama Rao Tata; Emma L. Rawlins; Aviv Regev; Paul A. Reyfman; Mauricio Rojas; Orit Rosen; Kourosh Saeb-Parsy; Christos Samakovlis; Herbert B. Schiller; Joachim L. Schultze; Max A. Seibold; Douglas P. Shepherd; Jason R. Spence; Avrum Spira; Xin Sun; Sarah A. Teichmann; Fabian J. Theis; Alexander M. Tsankov; Maarten van den Berge; Michael von Papen; Jeffrey A. Whitsett; Ramnik J. Xavier; Yan Xu; Kun Zhang;pmid: 32413319
pmc: PMC7252096
Summary There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection. Analysis of single-cell RNA-seq datasets from human, non-human primate, and mouse barrier tissues identifies putative cellular targets of SARS-CoV-2 on the basis of ACE2 and TMPRSS2 expression. ACE2 represents a previously unappreciated interferon-stimulated gene in human, but not mouse, epithelial tissues, identifying anti-viral induction of a host tissue-protective mechanism, but also a potential means for viral exploitation of the host response. Highlights • Meta-analysis of human, non-human primate, and mouse single-cell RNA-seq datasets for putative SARS-CoV-2 targets • Type II pneumocytes, nasal secretory cells, and absorptive enterocytes are ACE2 + TMPRSS2 + • Interferon and influenza increase ACE2 in human nasal epithelia and lung tissue • Mouse Ace2 is not upregulated by interferon, raising implications for disease modeling Graphical Abstract
NARCIS; Cell arrow_drop_down NARCIS; CellArticle . 2020CORE (RIOXX-UK Aggregator)Article . 2020License: CC BY NC NDData sources: CORE (RIOXX-UK Aggregator)Europe PubMed CentralArticle . 2020Full-Text: http://europepmc.org/articles/PMC7252096Data sources: PubMed CentralPublication Server of Helmholtz Zentrum München (PuSH)Article . 2020Data sources: Publication Server of Helmholtz Zentrum München (PuSH)add ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.This Research product is the result of merged Research products in OpenAIRE.
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For further information contact us at helpdesk@openaire.euAccess RoutesGreen hybrid 2K citations 1,920 popularity Top 0.01% influence Top 0.1% impulse Top 0.01% Powered by BIP!visibility 25visibility views 25 download downloads 83 Powered bymore_vert NARCIS; Cell arrow_drop_down NARCIS; CellArticle . 2020CORE (RIOXX-UK Aggregator)Article . 2020License: CC BY NC NDData sources: CORE (RIOXX-UK Aggregator)Europe PubMed CentralArticle . 2020Full-Text: http://europepmc.org/articles/PMC7252096Data sources: PubMed CentralPublication Server of Helmholtz Zentrum München (PuSH)Article . 2020Data sources: Publication Server of Helmholtz Zentrum München (PuSH)add ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
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description Publicationkeyboard_double_arrow_right Article 2020 France, France, Germany, United States, United Kingdom, Netherlands, FrancePublisher:Elsevier BV Funded by:NIH | The Role of IL-5 and Loca..., NIH | Administrative Core, NIH | Prostaglandin D2: A Key M... +20 projectsNIH| The Role of IL-5 and Local Nasal Polyp Immunoglobulin Production in Aspirin-Exacerbated Respiratory Disease ,NIH| Administrative Core ,NIH| Prostaglandin D2: A Key Mediator of Aspirin-Exacerbated Respiratory Disease ,NIH| Defining and Exploiting a Genetic Template for an HIV Vaccine ,NSF| Graduate Research Fellowship Program ,NIH| Contribution of CD8 T cells in Controlling Tuberculosis ,NIH| Innate-like BCR activity as a template for universal vaccination against influenza virus ,NIH| The inflammatory role of the platelet in aspirin-exacerbated respiratory disease. ,NIH| Eicosanoid Networks in Aspirin Exacerbated Respiratory Disease ,NIH| CDRH3-independent B cell stimulation to selectively expand VRC01 lineages from a fully humanized immunoglobulin repertoire ,NIH| CysLT and P2Y Receptors in Lung Inflammation ,NIH| Medical Scientist Training Program ,NIH| Novel Biologic Therapies for BMT: Mechanistic Evaluation in Rhesus Macaques ,NIH| An integrated multiplexed genomic assay for low input clinical samples1 ,NIH| Curing HIV Through Allogeneic Hematopoietic Stem Cell Transplantation ,ANR| SAHARRA ,NIH| BELIEVE: Bench to Bed Enhanced Lymphocyte Infusions to Engineer Viral Eradication ,NIH| The Role of IL-5 and Local Nasal Polyp Immunoglobulin Production in Aspirin-Exacerbated Respiratory Disease ,NIH| Pathophysiologic and therapeutic mechanisms of aspirin exacerbated respiratory d* ,NIH| Next Generation HSC Gene Therapy for HIV Control and Eradication ,NIH| Structure based prediction of the interactome ,NIH| Optimizing EP receptor subtype targeting for asthma therapy ,NIH| Cell and Gene Therapy for HIV CureCarly G. K. Ziegler; Samuel J. Allon; Sarah K. Nyquist; Ian M. Mbano; Vincent N. Miao; Constantine N. Tzouanas; Yuming Cao; Ashraf S. Yousif; Julia Bals; Blake M. Hauser; Jared Feldman; Christoph Muus; Marc H. Wadsworth; Samuel W. Kazer; Travis K. Hughes; Benjamin Doran; G. James Gatter; Marko Vukovic; Faith Taliaferro; Benjamin E. Mead; Zhiru Guo; Jennifer P. Wang; Delphine Gras; Magali Plaisant; Meshal Ansari; Ilias Angelidis; Heiko Adler; Jennifer M.S. Sucre; Chase J. Taylor; Brian M. Lin; Avinash Waghray; Vanessa Mitsialis; Daniel F. Dwyer; Kathleen M. Buchheit; Joshua A. Boyce; Nora A. Barrett; Tanya M. Laidlaw; Shaina L. Carroll; Lucrezia Colonna; Victor Tkachev; Christopher W. Peterson; Alison Yu; Hengqi Betty Zheng; Hannah P. Gideon; Caylin G. Winchell; Philana Ling Lin; Colin D. Bingle; Scott B. Snapper; Jonathan A. Kropski; Fabian J. Theis; Herbert B. Schiller; Laure-Emmanuelle Zaragosi; Pascal Barbry; Alasdair Leslie; Hans-Peter Kiem; JoAnne L. Flynn; Sarah M. Fortune; Bonnie Berger; Robert W. Finberg; Leslie S. Kean; Manuel Garber; Aaron G. Schmidt; Daniel Lingwood; Alex K. Shalek; Jose Ordovas-Montanes; Nicholas E. Banovich; Alvis Brazma; Tushar J. Desai; Thu Elizabeth Duong; Oliver Eickelberg; Christine S. Falk; Michael Farzan; Ian A. Glass; Muzlifah Haniffa; Peter Horvath; Deborah T. Hung; Naftali Kaminski; Mark A. Krasnow; Malte Kühnemund; Robert Lafyatis; Haeock Lee; Sylvie Leroy; Sten Linnarson; Joakim Lundeberg; Kerstin B. Meyer; Alexander V. Misharin; Martijn C. Nawijn; Marko Nikolic; Dana Pe'er; Joseph E. Powell; Stephen R. Quake; Jay Rajagopal; Purushothama Rao Tata; Emma L. Rawlins; Aviv Regev; Paul A. Reyfman; Mauricio Rojas; Orit Rosen; Kourosh Saeb-Parsy; Christos Samakovlis; Herbert B. Schiller; Joachim L. Schultze; Max A. Seibold; Douglas P. Shepherd; Jason R. Spence; Avrum Spira; Xin Sun; Sarah A. Teichmann; Fabian J. Theis; Alexander M. Tsankov; Maarten van den Berge; Michael von Papen; Jeffrey A. Whitsett; Ramnik J. Xavier; Yan Xu; Kun Zhang;pmid: 32413319
pmc: PMC7252096
Summary There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection. Analysis of single-cell RNA-seq datasets from human, non-human primate, and mouse barrier tissues identifies putative cellular targets of SARS-CoV-2 on the basis of ACE2 and TMPRSS2 expression. ACE2 represents a previously unappreciated interferon-stimulated gene in human, but not mouse, epithelial tissues, identifying anti-viral induction of a host tissue-protective mechanism, but also a potential means for viral exploitation of the host response. Highlights • Meta-analysis of human, non-human primate, and mouse single-cell RNA-seq datasets for putative SARS-CoV-2 targets • Type II pneumocytes, nasal secretory cells, and absorptive enterocytes are ACE2 + TMPRSS2 + • Interferon and influenza increase ACE2 in human nasal epithelia and lung tissue • Mouse Ace2 is not upregulated by interferon, raising implications for disease modeling Graphical Abstract
NARCIS; Cell arrow_drop_down NARCIS; CellArticle . 2020CORE (RIOXX-UK Aggregator)Article . 2020License: CC BY NC NDData sources: CORE (RIOXX-UK Aggregator)Europe PubMed CentralArticle . 2020Full-Text: http://europepmc.org/articles/PMC7252096Data sources: PubMed CentralPublication Server of Helmholtz Zentrum München (PuSH)Article . 2020Data sources: Publication Server of Helmholtz Zentrum München (PuSH)add ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.All Research productsarrow_drop_down <script type="text/javascript"> <!-- document.write('<div id="oa_widget"></div>'); document.write('<script type="text/javascript" src="https://www.openaire.eu/index.php?option=com_openaire&view=widget&format=raw&projectId=10.1016/j.cell.2020.04.035&type=result"></script>'); --> </script>
For further information contact us at helpdesk@openaire.euAccess RoutesGreen hybrid 2K citations 1,920 popularity Top 0.01% influence Top 0.1% impulse Top 0.01% Powered by BIP!visibility 25visibility views 25 download downloads 83 Powered bymore_vert NARCIS; Cell arrow_drop_down NARCIS; CellArticle . 2020CORE (RIOXX-UK Aggregator)Article . 2020License: CC BY NC NDData sources: CORE (RIOXX-UK Aggregator)Europe PubMed CentralArticle . 2020Full-Text: http://europepmc.org/articles/PMC7252096Data sources: PubMed CentralPublication Server of Helmholtz Zentrum München (PuSH)Article . 2020Data sources: Publication Server of Helmholtz Zentrum München (PuSH)add ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.All Research productsarrow_drop_down <script type="text/javascript"> <!-- document.write('<div id="oa_widget"></div>'); document.write('<script type="text/javascript" src="https://www.openaire.eu/index.php?option=com_openaire&view=widget&format=raw&projectId=10.1016/j.cell.2020.04.035&type=result"></script>'); --> </script>
For further information contact us at helpdesk@openaire.eu