Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium
Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathog...
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| Published in: | Nature communications Vol. 11; no. 1; pp. 5139 - 18 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
12.10.2020
Nature Portfolio |
| Subjects: | |
| ISSN: | 2041-1723, 2041-1723 |
| Online Access: | Get full text |
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| Abstract | Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both
ACE2
and
TMPRSS2
, that vary in frequency across world populations. We find
TMPRSS2
is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates
ACE2
expression. IL-13 and virus infection mediated effects on
ACE2
expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of
IL6
and
ACE2
. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes.
ACE2 and TMPRSS2 have received recent attention as entry factors for SARS-CoV-2. Here the authors analyze nasal airway transcriptome data from 695 children determining ACE2 and TMPRSS2 expression is induced by viral and type2 inflammation, respectively, and both exhibit eQTLs that vary across world populations. |
|---|---|
| AbstractList | Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes.Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes. Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes. ACE2 and TMPRSS2 have received recent attention as entry factors for SARS-CoV-2. Here the authors analyze nasal airway transcriptome data from 695 children determining ACE2 and TMPRSS2 expression is induced by viral and type2 inflammation, respectively, and both exhibit eQTLs that vary across world populations. Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2 , that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2 . Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes. Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2 , that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2 . Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes. ACE2 and TMPRSS2 have received recent attention as entry factors for SARS-CoV-2. Here the authors analyze nasal airway transcriptome data from 695 children determining ACE2 and TMPRSS2 expression is induced by viral and type2 inflammation, respectively, and both exhibit eQTLs that vary across world populations. ACE2 and TMPRSS2 have received recent attention as entry factors for SARS-CoV-2. Here the authors analyze nasal airway transcriptome data from 695 children determining ACE2 and TMPRSS2 expression is induced by viral and type2 inflammation, respectively, and both exhibit eQTLs that vary across world populations. Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes. |
| ArticleNumber | 5139 |
| Author | Pruesse, Elmar Rodriguez-Santana, Jose DeFord, Peter Rios, Cydney L. Zody, Michael C. Li, Yingchun Abecasis, Gonçalo Medina, Vivian Germer, Soren Wechsler, Michael E. Eng, Celeste Mak, Angel C. Y. Kumar, Rajesh Sajuthi, Satria P. Nolin, James D. Salazar, Sandra Burchard, Esteban G. Rice, Kenneth M. Jackson, Nathan D. Seibold, Max A. Nickerson, Deborah A. Wohlford, Eric M. Huntsman, Scott Kang, Hyun Min Everman, Jamie L. Oh, Sam Plender, Elizabeth G. Montgomery, Michael T. |
| Author_xml | – sequence: 1 givenname: Satria P. surname: Sajuthi fullname: Sajuthi, Satria P. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 2 givenname: Peter orcidid: 0000-0003-1445-7135 surname: DeFord fullname: DeFord, Peter organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 3 givenname: Yingchun surname: Li fullname: Li, Yingchun organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 4 givenname: Nathan D. surname: Jackson fullname: Jackson, Nathan D. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 5 givenname: Michael T. orcidid: 0000-0002-6748-2329 surname: Montgomery fullname: Montgomery, Michael T. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 6 givenname: Jamie L. orcidid: 0000-0002-1935-4672 surname: Everman fullname: Everman, Jamie L. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 7 givenname: Cydney L. surname: Rios fullname: Rios, Cydney L. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 8 givenname: Elmar surname: Pruesse fullname: Pruesse, Elmar organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 9 givenname: James D. orcidid: 0000-0002-6611-1550 surname: Nolin fullname: Nolin, James D. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 10 givenname: Elizabeth G. surname: Plender fullname: Plender, Elizabeth G. organization: Center for Genes, Environment, and Health, National Jewish Health – sequence: 11 givenname: Michael E. surname: Wechsler fullname: Wechsler, Michael E. organization: Department of Medicine, National Jewish Health – sequence: 12 givenname: Angel C. Y. orcidid: 0000-0002-5372-4198 surname: Mak fullname: Mak, Angel C. Y. organization: Department of Medicine, University of California San Francisco – sequence: 13 givenname: Celeste surname: Eng fullname: Eng, Celeste organization: Department of Medicine, University of California San Francisco – sequence: 14 givenname: Sandra surname: Salazar fullname: Salazar, Sandra organization: Department of Medicine, University of California San Francisco – sequence: 15 givenname: Vivian surname: Medina fullname: Medina, Vivian organization: Centro de Neumología Pediátrica – sequence: 16 givenname: Eric M. surname: Wohlford fullname: Wohlford, Eric M. organization: Department of Medicine, University of California San Francisco, Division of Pediatric Allergy and Immunology, University of California San Francisco – sequence: 17 givenname: Scott surname: Huntsman fullname: Huntsman, Scott organization: Department of Medicine, University of California San Francisco – sequence: 18 givenname: Deborah A. surname: Nickerson fullname: Nickerson, Deborah A. organization: Department of Genome Sciences, University of Washington, Northwest Genomics Center, Brotman Baty Institute – sequence: 19 givenname: Soren surname: Germer fullname: Germer, Soren organization: New York Genome Center – sequence: 20 givenname: Michael C. surname: Zody fullname: Zody, Michael C. organization: New York Genome Center – sequence: 21 givenname: Gonçalo orcidid: 0000-0003-1509-1825 surname: Abecasis fullname: Abecasis, Gonçalo organization: Center for Statistical Genetics, University of Michigan – sequence: 22 givenname: Hyun Min surname: Kang fullname: Kang, Hyun Min organization: Center for Statistical Genetics, University of Michigan – sequence: 23 givenname: Kenneth M. orcidid: 0000-0002-3071-7278 surname: Rice fullname: Rice, Kenneth M. organization: Department of Biostatistics, University of Washington – sequence: 24 givenname: Rajesh surname: Kumar fullname: Kumar, Rajesh organization: Department of Pediatrics, Ann and Robert H. Lurie Children’s Hospital of Chicago, Northwestern University – sequence: 25 givenname: Sam orcidid: 0000-0002-2815-6037 surname: Oh fullname: Oh, Sam organization: Department of Medicine, University of California San Francisco – sequence: 26 givenname: Jose surname: Rodriguez-Santana fullname: Rodriguez-Santana, Jose organization: Centro de Neumología Pediátrica – sequence: 27 givenname: Esteban G. surname: Burchard fullname: Burchard, Esteban G. organization: Department of Medicine, University of California San Francisco, Department of Bioengineering and Therapeutic Sciences, University of California San Francisco – sequence: 28 givenname: Max A. orcidid: 0000-0002-8685-4263 surname: Seibold fullname: Seibold, Max A. email: seiboldm@njhealth.org organization: Center for Genes, Environment, and Health, National Jewish Health, Department of Pediatrics, National Jewish Health, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado-AMC |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33046696$$D View this record in MEDLINE/PubMed |
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| Snippet | Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the... ACE2 and TMPRSS2 have received recent attention as entry factors for SARS-CoV-2. Here the authors analyze nasal airway transcriptome data from 695 children... |
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| SubjectTerms | 13/106 38 38/91 631/208/200 631/337/2019 631/80/304 692/699/255/2514 Angiotensin-Converting Enzyme 2 Betacoronavirus - physiology Child Coronavirus Infections - metabolism Coronavirus Infections - pathology Coronavirus Infections - virology COVID-19 Epithelial Cells - metabolism Gene Expression Profiling Gene Expression Regulation Genetic Variation Host-Pathogen Interactions Humanities and Social Sciences Humans Inflammation Interferons - metabolism Interleukin-13 - metabolism Middle Aged multidisciplinary Nasal Mucosa - metabolism Nasal Mucosa - pathology Pandemics Peptidyl-Dipeptidase A - genetics Peptidyl-Dipeptidase A - metabolism Pneumonia, Viral - metabolism Pneumonia, Viral - pathology Pneumonia, Viral - virology SARS-CoV-2 Science Science (multidisciplinary) Serine Endopeptidases - genetics Serine Endopeptidases - metabolism Virus Internalization |
| Title | Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium |
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