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4 results on '"Allon, Samuel J."'

1. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics.

Author

Muus C, Luecken MD, Eraslan G, Sikkema L, Waghray A, Heimberg G, Kobayashi Y, Vaishnav ED, Subramanian A, Smillie C, Jagadeesh KA, Duong ET, Fiskin E, Torlai Triglia E, Ansari M, Cai P, Lin B, Buchanan J, Chen S, Shu J, Haber AL, Chung H, Montoro DT, Adams T, Aliee H, Allon SJ, Andrusivova Z, Angelidis I, Ashenberg O, Bassler K, Bécavin C, Benhar I, Bergenstråhle J, Bergenstråhle L, Bolt L, Braun E, Bui LT, Callori S, Chaffin M, Chichelnitskiy E, Chiou J, Conlon TM, Cuoco MS, Cuomo ASE, Deprez M, Duclos G, Fine D, Fischer DS, Ghazanfar S, Gillich A, Giotti B, Gould J, Guo M, Gutierrez AJ, Habermann AC, Harvey T, He P, Hou X, Hu L, Hu Y, Jaiswal A, Ji L, Jiang P, Kapellos TS, Kuo CS, Larsson L, Leney-Greene MA, Lim K, Litviňuková M, Ludwig LS, Lukassen S, Luo W, Maatz H, Madissoon E, Mamanova L, Manakongtreecheep K, Leroy S, Mayr CH, Mbano IM, McAdams AM, Nabhan AN, Nyquist SK, Penland L, Poirion OB, Poli S, Qi C, Queen R, Reichart D, Rosas I, Schupp JC, Shea CV, Shi X, Sinha R, Sit RV, Slowikowski K, Slyper M, Smith NP, Sountoulidis A, Strunz M, Sullivan TB, Sun D, Talavera-López C, Tan P, Tantivit J, Travaglini KJ, Tucker NR, Vernon KA, Wadsworth MH, Waldman J, Wang X, Xu K, Yan W, Zhao W, and Ziegler CGK

Subjects
Adult, Aged, Aged, 80 and over, Alveolar Epithelial Cells metabolism, Alveolar Epithelial Cells virology, Angiotensin-Converting Enzyme 2 genetics, Angiotensin-Converting Enzyme 2 metabolism, COVID-19 pathology, COVID-19 virology, Cathepsin L genetics, Cathepsin L metabolism, Datasets as Topic statistics & numerical data, Demography, Female, Gene Expression Profiling statistics & numerical data, Humans, Lung metabolism, Lung virology, Male, Middle Aged, Organ Specificity genetics, Respiratory System metabolism, Respiratory System virology, Sequence Analysis, RNA methods, Serine Endopeptidases genetics, Serine Endopeptidases metabolism, Single-Cell Analysis methods, COVID-19 epidemiology, COVID-19 genetics, Host-Pathogen Interactions genetics, SARS-CoV-2 physiology, Sequence Analysis, RNA statistics & numerical data, Single-Cell Analysis statistics & numerical data, Virus Internalization
Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing studies with 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals. This revealed cell-type-specific associations of age, sex and smoking with expression levels of ACE2, TMPRSS2 and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar type 2 cells. Expression programs shared by ACE2 + TMPRSS2 + cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

Published
2021
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2. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues

Author

Ziegler, Carly GK, Allon, Samuel J, Nyquist, Sarah K, Mbano, Ian M, Miao, Vincent N, Tzouanas, Constantine N, Cao, Yuming, Yousif, Ashraf S, Bals, Julia, Hauser, Blake M, Feldman, Jared, Muus, Christoph, Wadsworth, Marc H, Kazer, Samuel W, Hughes, Travis K, Doran, Benjamin, Gatter, G James, Vukovic, Marko, Taliaferro, Faith, Mead, Benjamin E, Guo, Zhiru, Wang, Jennifer P, Gras, Delphine, Plaisant, Magali, Ansari, Meshal, Angelidis, Ilias, Adler, Heiko, Sucre, Jennifer MS, Taylor, Chase J, Lin, Brian, Waghray, Avinash, Mitsialis, Vanessa, Dwyer, Daniel F, Buchheit, Kathleen M, Boyce, Joshua A, Barrett, Nora A, Laidlaw, Tanya M, Carroll, Shaina L, Colonna, Lucrezia, Tkachev, Victor, Peterson, Christopher W, Yu, Alison, Zheng, Hengqi Betty, Gideon, Hannah P, Winchell, Caylin G, Lin, Philana Ling, Bingle, Colin D, Snapper, Scott B, Kropski, Jonathan A, Theis, Fabian J, Schiller, Herbert B, Zaragosi, Laure-Emmanuelle, Barbry, Pascal, Leslie, Alasdair, Kiem, Hans-Peter, Flynn, JoAnne L, Fortune, Sarah M, Berger, Bonnie, Finberg, Robert W, Kean, Leslie S, Garber, Manuel, Schmidt, Aaron G, Lingwood, Daniel, Shalek, Alex K, Ordovas-Montanes, Jose, HCA Lung Biological Network. Electronic Address: Lung-Network@Humancellatlas.Org, HCA Lung Biological Network, Yousif, Ashraf S [0000-0001-9215-3853], Hauser, Blake M [0000-0002-0100-1684], Kazer, Samuel W [0000-0002-7380-9594], Sucre, Jennifer MS [0000-0002-6613-1439], Tkachev, Victor [0000-0001-6011-0576], Zheng, Hengqi Betty [0000-0003-0575-6475], Bingle, Colin D [0000-0002-5405-6988], and Apollo - University of Cambridge Repository

Subjects
Adolescent, Pneumonia, Viral, ACE2, non-human primate, HIV Infections, Peptidyl-Dipeptidase A, Cell Line, ISG, Betacoronavirus, Mice, scRNA-seq, Influenza, Human, Animals, Humans, Tuberculosis, human, Child, Lung, Pandemics, mouse, Cells, Cultured, SARS-CoV-2, Serine Endopeptidases, COVID-19, interferon, Mycobacterium tuberculosis, respiratory system, Macaca mulatta, Up-Regulation, Nasal Mucosa, Enterocytes, Alveolar Epithelial Cells, Interferon Type I, Receptors, Virus, Angiotensin-Converting Enzyme 2, Goblet Cells, Single-Cell Analysis, influenza, Coronavirus Infections
Abstract

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.

Published
2020
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3. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics

Author

Christoph, Muus, Luecken , Malte D., Gökcen, Eraslan, Lisa, Sikkema, Avinash, Waghray, Graham, Heimberg, Yoshihiko, Kobayashi, Eeshit Dhaval Vaishnav, Ayshwarya, Subramanian, Christopher, Smillie, Jagadeesh, Karthik A., Elizabeth Thu Duong, Evgenij, Fiskin, Elena Torlai Triglia, Meshal, Ansari, Peiwen, Cai, Brian, Lin, Justin, Buchanan, Sijia, Chen, Jian, Shu, Haber, Adam L., Hattie, Chung, Montoro, Daniel T., Taylor, Adams, Hananeh, Aliee, Allon, Samuel J., Zaneta, Andrusivova, Ilias, Angelidis, Orr, Ashenberg, Kevin, Bassler, Christophe, Bécavin, Inbal, Benhar, Joseph, Bergenstråhle, Ludvig, Bergenstråhle, Liam, Bolt, Emelie, Braun, Bui, Linh T., Steven, Callori, Mark, Chaffin, Evgeny, Chichelnitskiy, Joshua, Chiou, Conlon, Thomas M., Cuoco, Michael S., Cuomo, Anna S. E., Marie, Deprez, Grant, Duclos, Denise, Fine, Fischer, David S., Shila, Ghazanfar, Astrid, Gillich, Bruno, Giotti, Joshua, Gould, Minzhe, Guo, Gutierrez, Austin J., Habermann, Arun C., Tyler, Harvey, Peng, He, Xiaomeng, Hou, Lijuan, Hu, Yan, Hu, Alok, Jaiswal, Lu, Ji, Peiyong, Jiang, Kapellos, Theodoros S., Kuo, Christin S., Ludvig, Larsson, Leney-Greene, Michael A., Kyungtae, Lim, Monika, Litviňuková, Ludwig, Leif S., Soeren, Lukassen, Wendy, Luo, Henrike, Maatz, Elo, Madissoon, Lira, Mamanova, Kasidet, Manakongtreecheep, Sylvie, Leroy, Mayr, Christoph H., Mbano, Ian M., Mcadams, Alexi M., Nabhan, Ahmad N., Nyquist, Sarah K., Lolita, Penland, Poirion, Olivier B., Sergio, Poli, Cancan, Qi, Rachel, Queen, Daniel, Reichart, Ivan, Rosas, Schupp, Jonas C., Shea, Conor V., Xingyi, Shi, Rahul, Sinha, Sit, Rene V., Kamil, Slowikowski, Michal, Slyper, Smith, Neal P., Alex, Sountoulidis, Maximilian, Strunz, Sullivan, Travis B., Dawei, Sun, Carlos, Talavera-López, Peng, Tan, Jessica, Tantivit, Travaglini, Kyle J., Tucker, Nathan R., Vernon, Katherine A., Wadsworth, Marc H., Julia, Waldman, Xiuting, Wang, Ke, Xu, Wenjun, Yan, William, Zhao, Ziegler, Carly G. K., The NHLBI LungMap Consortium, Zerti, Darin, The Human Cell Atlas Lung Biological Network, and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
0301 basic medicine, Male, Cathepsin L, Respiratory System, Datasets as Topic, Lung/metabolism, Sequence Analysis, RNA/methods, Organ Specificity/genetics, 0302 clinical medicine, 80 and over, Respiratory system, Lung, COVID-19/epidemiology, Aged, 80 and over, Serine Endopeptidases, General Medicine, respiratory system, Middle Aged, Host-Pathogen Interactions/genetics, 3. Good health, Angiotensin-Converting Enzyme 2/genetics, medicine.anatomical_structure, Datasets as Topic/statistics & numerical data, Respiratory System/metabolism, Organ Specificity, Cathepsin L/genetics, 030220 oncology & carcinogenesis, Host-Pathogen Interactions, Tumor necrosis factor alpha, Female, Angiotensin-Converting Enzyme 2, Single-Cell Analysis, RNA/methods, Sequence Analysis, Adult, Alveolar Epithelial Cells/metabolism, Serine Endopeptidases/genetics, Biology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Immune system, Viral entry, Parenchyma, medicine, Humans, Gene Expression Profiling/statistics & numerical data, Aged, Demography, SARS-CoV-2, Sequence Analysis, RNA, Gene Expression Profiling, Single-Cell Analysis/methods, COVID-19, Virus Internalization, Gene expression profiling, 030104 developmental biology, Alveolar Epithelial Cells, Immunology, Tissue tropism, SARS-CoV-2/physiology
Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing studies with 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals. This revealed cell-type-specific associations of age, sex and smoking with expression levels of ACE2, TMPRSS2 and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar type 2 cells. Expression programs shared by ACE2+TMPRSS2+ cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

Full Text
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4. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues.

Author

Ziegler, Carly G.K., Allon, Samuel J., Nyquist, Sarah K., Mbano, Ian M., Miao, Vincent N., Tzouanas, Constantine N., Cao, Yuming, Yousif, Ashraf S., Bals, Julia, Hauser, Blake M., Feldman, Jared, Muus, Christoph, Wadsworth II, Marc H., Kazer, Samuel W., Hughes, Travis K., Doran, Benjamin, Gatter, G. James, Vukovic, Marko, Taliaferro, Faith, and Mead, Benjamin E.

Subjects
*SARS-CoV-2, *INTERFERON receptors, *EPITHELIAL cells, *HUMAN genes, *VIRUS diseases, *TYPE I interferons
Abstract

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. • 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 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. [ABSTRACT FROM AUTHOR]

Published
2020
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