Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19

Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response...

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Published inCell Vol. 181; no. 5; pp. 1036 - 1045.e9
Main Authors Blanco-Melo, Daniel, Nilsson-Payant, Benjamin E., Liu, Wen-Chun, Uhl, Skyler, Hoagland, Daisy, Møller, Rasmus, Jordan, Tristan X., Oishi, Kohei, Panis, Maryline, Sachs, David, Wang, Taia T., Schwartz, Robert E., Lim, Jean K., Albrecht, Randy A., tenOever, Benjamin R.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 28.05.2020
Subjects
animal models
Animals
Betacoronavirus - physiology
blood serum
Cells, Cultured
chemokines
Chemokines - genetics
Chemokines - immunology
Coronavirus
Coronavirus infections
Coronavirus Infections - genetics
Coronavirus Infections - immunology
COVID-19
Disease Models, Animal
ferret
Host-Pathogen Interactions
Humans
IL6
Immunity, Innate
inflammation
Inflammation - virology
interferon
interferons
Interferons - genetics
Interferons - immunology
interleukin-6
pandemic
Pandemics
patients
Pneumonia, Viral - genetics
Pneumonia, Viral - immunology
RNA Viruses - classification
RNA Viruses - immunology
SARS-CoV-2
transcription (genetics)
Transcription, Genetic
transcriptomics
virus-host interactions
viruses
COVID-19
SARS-CoV-2
IL6
Coronavirus
virus-host interactions
transcriptomics
interferon
chemokines
ferret
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Abstract Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19. [Display omitted] •SARS-CoV-2 infection induces low IFN-I and -III levels with a moderate ISG response•Strong chemokine expression is consistent across in vitro, ex vivo, and in vivo models•Low innate antiviral defenses and high pro-inflammatory cues contribute to COVID-19 In comparison to other respiratory viruses, SARS-CoV-2 infection drives a lower antiviral transcriptional response that is marked by low IFN-I and IFN-III levels and elevated chemokine expression, which could explain the pro-inflammatory disease state associated with COVID-19.
AbstractList Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19. • SARS-CoV-2 infection induces low IFN-I and -III levels with a moderate ISG response • Strong chemokine expression is consistent across in vitro , ex vivo , and in vivo models • Low innate antiviral defenses and high pro-inflammatory cues contribute to COVID-19 In comparison to other respiratory viruses, SARS-CoV-2 infection drives a lower antiviral transcriptional response that is marked by low IFN-I and IFN-III levels and elevated chemokine expression, which could explain the pro-inflammatory disease state associated with COVID-19.
Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19. [Display omitted] •SARS-CoV-2 infection induces low IFN-I and -III levels with a moderate ISG response•Strong chemokine expression is consistent across in vitro, ex vivo, and in vivo models•Low innate antiviral defenses and high pro-inflammatory cues contribute to COVID-19 In comparison to other respiratory viruses, SARS-CoV-2 infection drives a lower antiviral transcriptional response that is marked by low IFN-I and IFN-III levels and elevated chemokine expression, which could explain the pro-inflammatory disease state associated with COVID-19.
Author Hoagland, Daisy
Albrecht, Randy A.
Panis, Maryline
Wang, Taia T.
Møller, Rasmus
Nilsson-Payant, Benjamin E.
Sachs, David
Schwartz, Robert E.
tenOever, Benjamin R.
Blanco-Melo, Daniel
Liu, Wen-Chun
Uhl, Skyler
Jordan, Tristan X.
Oishi, Kohei
Lim, Jean K.
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Issue 5
Keywords COVID-19
SARS-CoV-2
IL6
Coronavirus
virus-host interactions
transcriptomics
interferon
chemokines
ferret
Language English
License Copyright © 2020 Elsevier Inc. All rights reserved.
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These authors contributed equally
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References Corman, Landt, Kaiser, Molenkamp, Meijer, Chu, Bleicker, Brünink, Schneider, Schmidt (bib6) 2020; 25
Kamitani, Narayanan, Huang, Lokugamage, Ikegami, Ito, Kubo, Makino (bib20) 2006; 103
Witten, Tibshirani, Hastie (bib48) 2009; 10
García-Sastre, Egorov, Matassov, Brandt, Levy, Durbin, Palese, Muster (bib12) 1998; 252
Lazear, Schoggins, Diamond (bib26) 2019; 50
Wolfel, Corman, Guggemos, Seilmaier, Zange, Muller, Niemeyer, Jones, Vollmar, Rothe (bib49) 2020
Cui, Li, Shi (bib7) 2019; 17
Lokugamage, Hage, Schindewolf, Rajsbaum, Menachery (bib30) 2020
Harcourt, Tamin, Lu, Kamili, Sakthivel, Murray, Queen, Tao, Paden, Zhang (bib15) 2020
Zhu, Zhang, Wang, Li, Yang, Song, Zhao, Huang, Shi, Lu (bib53) 2020; 382
Law, Cheung, Ng, Sia, Chan, Luk, Nicholls, Peiris, Lau (bib25) 2005; 106
Hallak, Collins, Knudson, Peeples (bib14) 2000; 271
Szklarczyk, Gable, Lyon, Junge, Wyder, Huerta-Cepas, Simonovic, Doncheva, Morris, Bork (bib43) 2019; 47
(bib36) 2020; 41
Frieman, Baric (bib9) 2008; 72
tenOever (bib44) 2016; 19
Menachery, Eisfeld, Schäfer, Josset, Sims, Proll, Fan, Li, Neumann, Tilton (bib33) 2014; 5
Blanco-Melo, Nilsson-Payant, Uhl, Escudero-Pèrez, Olschewski, Thibault, Panis, Rosenthal, Muñoz-Fontela, Lee (bib2) 2020
Xu, Shi, Wang, Zhang, Huang, Zhang, Liu, Zhao, Liu, Zhu (bib51) 2020; 8
Sokol, Luster (bib42) 2015; 7
Norelli, Camisa, Barbiera, Falcone, Purevdorj, Genua, Sanvito, Ponzoni, Doglioni, Cristofori (bib35) 2018; 24
Lu, Zhang, Du, Zhang, Li, Qu, Zhang, Wang, Bao, Li (bib32) 2020
Love, Huber, Anders (bib31) 2014; 15
García-Sastre (bib11) 2017; 22
Varble, Albrecht, Backes, Crumiller, Bouvier, Sachs, García-Sastre, tenOever (bib45) 2014; 16
Weiss, Navas-Martin (bib46) 2005; 69
Wu, Zhao, Yu, Chen, Wang, Song, Hu, Tao, Tian, Pei (bib50) 2020; 579
Langmead, Salzberg (bib24) 2012; 9
Montecino-Rodriguez, Berent-Maoz, Dorshkind (bib34) 2013; 123
Sharma, tenOever, Grandvaux, Zhou, Lin, Hiscott (bib41) 2003; 300
Langlois, Albrecht, Kimble, Sutton, Shapiro, Finch, Angel, Chua, Gonzalez-Reiche, Xu (bib23) 2013; 31
Liao, Liu, Yuan, Wen, Xu, Zhao, Chen, Li, Wang, Wang (bib28) 2020
Channappanavar, Fehr, Vijay, Mack, Zhao, Meyerholz, Perlman (bib3) 2016; 19
Proudfoot (bib38) 2002; 2
Giavridis, van der Stegen, Eyquem, Hamieh, Piersigilli, Sadelain (bib13) 2018; 24
Pascal, Coleman, Mujica, Kamat, Badithe, Fairhurst, Hunt, Strein, Berrebi, Sisk (bib37) 2015; 112
Hur (bib17) 2019; 37
Wickham (bib47) 2016
Kim, Kim, Kim, Kim, Park, Yu, Chang, Kim, Lee, Casel (bib21) 2020
Yoshida, Lareau, Ramirez, Rose, Maier, Wroblewska, Desland, Chudnovskiy, Mortha, Dominguez (bib52) 2019; 176
de Wit, van Doremalen, Falzarano, Munster (bib8) 2016; 14
Jing, Shaheen, Drake, Chen, Gravenstein, Deng (bib19) 2009; 70
Chen, Zhou, Dong, Qu, Gong, Han, Qiu, Wang, Liu, Wei (bib4) 2020; 395
Janeway, Medzhitov (bib18) 2002; 20
Lefrançais, Ortiz-Muñoz, Caudrillier, Mallavia, Liu, Sayah, Thornton, Headley, David, Coughlin (bib27) 2017; 544
Amanat, Krammer (bib1) 2020; 52
Qin, Zhou, Hu, Zhang, Yang, Tao, Xie, Ma, Shang, Wang (bib40) 2020
Qian, Travanty, Oko, Edeen, Berglund, Wang, Ito, Holmes, Mason (bib39) 2013; 48
Liu, Nachbagauer, Stadlbauer, Solórzano, Berlanda-Scorza, García-Sastre, Palese, Krammer, Albrecht (bib29) 2019; 10
Frieman, Chen, Morrison, Whitmore, Funkhouser, Ward, Lamirande, Roberts, Heise, Subbarao, Baric (bib10) 2010; 6
Kopecky-Bromberg, Martínez-Sobrido, Frieman, Baric, Palese (bib22) 2007; 81
Hoffmann, Kleine-Weber, Schroeder, Krüger, Herrler, Erichsen, Schiergens, Herrler, Wu, Nitsche (bib16) 2020; 181
Chu, Pan, Cheng, Hui, Krishnan, Liu, Ng, Wan, Yang, Wang (bib5) 2020; 66
References_xml – volume: 106
  start-page: 2366
  year: 2005
  end-page: 2374
  ident: bib25
  article-title: Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells
  publication-title: Blood
– year: 2020
  ident: bib30
  article-title: SARS-CoV-2 is sensitive to type I interferon pretreatment
  publication-title: bioRxiv
– volume: 271
  start-page: 264
  year: 2000
  end-page: 275
  ident: bib14
  article-title: Iduronic acid-containing glycosaminoglycans on target cells are required for efficient respiratory syncytial virus infection
  publication-title: Virology
– volume: 81
  start-page: 548
  year: 2007
  end-page: 557
  ident: bib22
  article-title: Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists
  publication-title: J. Virol.
– volume: 69
  start-page: 635
  year: 2005
  end-page: 664
  ident: bib46
  article-title: Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus
  publication-title: Microbiol. Mol. Biol. Rev.
– volume: 52
  start-page: 583
  year: 2020
  end-page: 589
  ident: bib1
  article-title: SARS-CoV-2 Vaccines: Status Report
  publication-title: Immunity
– year: 2020
  ident: bib21
  article-title: Infection and rapid transmission of SARS-CoV-2 in ferrets
  publication-title: Cell Host Microbe
– volume: 300
  start-page: 1148
  year: 2003
  end-page: 1151
  ident: bib41
  article-title: Triggering the interferon antiviral response through an IKK-related pathway
  publication-title: Science
– volume: 15
  start-page: 550
  year: 2014
  ident: bib31
  article-title: Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
  publication-title: Genome Biol.
– volume: 181
  start-page: 271
  year: 2020
  end-page: 280.e8
  ident: bib16
  article-title: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor
  publication-title: Cell
– volume: 112
  start-page: 8738
  year: 2015
  end-page: 8743
  ident: bib37
  article-title: Pre- and postexposure efficacy of fully human antibodies against Spike protein in a novel humanized mouse model of MERS-CoV infection
  publication-title: Proc. Natl. Acad. Sci. USA
– volume: 31
  start-page: 844
  year: 2013
  end-page: 847
  ident: bib23
  article-title: MicroRNA-based strategy to mitigate the risk of gain-of-function influenza studies
  publication-title: Nat. Biotechnol.
– volume: 72
  start-page: 672
  year: 2008
  end-page: 685
  ident: bib9
  article-title: Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation
  publication-title: Microbiol. Mol. Biol. Rev.
– volume: 37
  start-page: 349
  year: 2019
  end-page: 375
  ident: bib17
  article-title: Double-Stranded RNA Sensors and Modulators in Innate Immunity
  publication-title: Annu. Rev. Immunol.
– volume: 7
  year: 2015
  ident: bib42
  article-title: The chemokine system in innate immunity
  publication-title: Cold Spring Harb. Perspect. Biol.
– volume: 10
  start-page: 515
  year: 2009
  end-page: 534
  ident: bib48
  article-title: A penalized matrix decomposition, with applications to sparse principal components and canonical correlation analysis
  publication-title: Biostatistics
– volume: 14
  start-page: 523
  year: 2016
  end-page: 534
  ident: bib8
  article-title: SARS and MERS: recent insights into emerging coronaviruses
  publication-title: Nat. Rev. Microbiol.
– volume: 123
  start-page: 958
  year: 2013
  end-page: 965
  ident: bib34
  article-title: Causes, consequences, and reversal of immune system aging
  publication-title: J. Clin. Invest.
– volume: 9
  start-page: 357
  year: 2012
  end-page: 359
  ident: bib24
  article-title: Fast gapped-read alignment with Bowtie 2
  publication-title: Nat. Methods
– volume: 544
  start-page: 105
  year: 2017
  end-page: 109
  ident: bib27
  article-title: The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors
  publication-title: Nature
– volume: 50
  start-page: 907
  year: 2019
  end-page: 923
  ident: bib26
  article-title: Shared and Distinct Functions of Type I and Type III Interferons
  publication-title: Immunity
– volume: 395
  start-page: 507
  year: 2020
  end-page: 513
  ident: bib4
  article-title: Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study
  publication-title: Lancet
– volume: 24
  start-page: 739
  year: 2018
  end-page: 748
  ident: bib35
  article-title: Monocyte-derived IL-1 and IL-6 are differentially required for cytokine-release syndrome and neurotoxicity due to CAR T cells
  publication-title: Nat. Med.
– volume: 6
  start-page: e1000849
  year: 2010
  ident: bib10
  article-title: SARS-CoV pathogenesis is regulated by a STAT1 dependent but a type I, II and III interferon receptor independent mechanism
  publication-title: PLoS Pathog.
– volume: 25
  start-page: 25
  year: 2020
  ident: bib6
  article-title: Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR
  publication-title: Euro Surveill.
– volume: 47
  start-page: D607
  year: 2019
  end-page: D613
  ident: bib43
  article-title: STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets
  publication-title: Nucleic Acids Res.
– volume: 48
  start-page: 742
  year: 2013
  end-page: 748
  ident: bib39
  article-title: Innate immune response of human alveolar type II cells infected with severe acute respiratory syndrome-coronavirus
  publication-title: Am. J. Respir. Cell Mol. Biol.
– volume: 382
  start-page: 727
  year: 2020
  end-page: 733
  ident: bib53
  article-title: A Novel Coronavirus from Patients with Pneumonia in China, 2019
  publication-title: N. Engl. J. Med.
– volume: 8
  start-page: 420
  year: 2020
  end-page: 422
  ident: bib51
  article-title: Pathological findings of COVID-19 associated with acute respiratory distress syndrome
  publication-title: Lancet Respir. Med.
– year: 2020
  ident: bib32
  article-title: SARS-CoV-2 Infection in Children
  publication-title: N. Engl. J. Med.
– volume: 176
  start-page: 897
  year: 2019
  end-page: 912.e20
  ident: bib52
  article-title: The cis-Regulatory Atlas of the Mouse Immune System
  publication-title: Cell
– volume: 5
  year: 2014
  ident: bib33
  article-title: Pathogenic influenza viruses and coronaviruses utilize similar and contrasting approaches to control interferon-stimulated gene responses
  publication-title: MBio
– year: 2020
  ident: bib49
  article-title: Virological assessment of hospitalized patients with COVID-2019
  publication-title: Nature
– volume: 20
  start-page: 197
  year: 2002
  end-page: 216
  ident: bib18
  article-title: Innate immune recognition
  publication-title: Annu. Rev. Immunol.
– volume: 41
  start-page: 145
  year: 2020
  end-page: 151
  ident: bib36
  article-title: The epidemiological characteristics of an outbreak of 2019 novel coronavirus diseases (COVID-19) in China
  publication-title: Zhonghua Liu Xing Bing Xue Za Zhi
– year: 2020
  ident: bib15
  article-title: Severe Acute Respiratory Syndrome Coronavirus 2 from Patient with 2019 Novel Coronavirus Disease, United States
  publication-title: Emerg. Infect. Dis.
– volume: 66
  start-page: 549
  year: 2020
  end-page: 555
  ident: bib5
  article-title: Molecular Diagnosis of a Novel Coronavirus (2019-nCoV) Causing an Outbreak of Pneumonia
  publication-title: Clin. Chem.
– volume: 17
  start-page: 181
  year: 2019
  end-page: 192
  ident: bib7
  article-title: Origin and evolution of pathogenic coronaviruses
  publication-title: Nat. Rev. Microbiol.
– year: 2016
  ident: bib47
  article-title: ggplot2: Elegant Graphics for Data Analysis
– volume: 24
  start-page: 731
  year: 2018
  end-page: 738
  ident: bib13
  article-title: CAR T cell-induced cytokine release syndrome is mediated by macrophages and abated by IL-1 blockade
  publication-title: Nat. Med.
– year: 2020
  ident: bib40
  article-title: Dysregulation of immune response in patients with COVID-19 in Wuhan, China
  publication-title: Clin. Infect. Dis.
– volume: 70
  start-page: 777
  year: 2009
  end-page: 784
  ident: bib19
  article-title: Aging is associated with a numerical and functional decline in plasmacytoid dendritic cells, whereas myeloid dendritic cells are relatively unaltered in human peripheral blood
  publication-title: Hum. Immunol.
– volume: 579
  start-page: 265
  year: 2020
  end-page: 269
  ident: bib50
  article-title: A new coronavirus associated with human respiratory disease in China
  publication-title: Nature
– volume: 22
  start-page: 176
  year: 2017
  end-page: 184
  ident: bib11
  article-title: Ten Strategies of Interferon Evasion by Viruses
  publication-title: Cell Host Microbe
– year: 2020
  ident: bib28
  article-title: The landscape of lung bronchoalveolar immune cells in COVID-19 revealed by single-cell RNA sequencing
  publication-title: medRxiv
– year: 2020
  ident: bib2
  article-title: An inability to maintain the ribonucleoprotein genomic structure is responsible for host detection of negative-sense RNA viruses
  publication-title: bioRxiv
– volume: 19
  start-page: 181
  year: 2016
  end-page: 193
  ident: bib3
  article-title: Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice
  publication-title: Cell Host Microbe
– volume: 16
  start-page: 691
  year: 2014
  end-page: 700
  ident: bib45
  article-title: Influenza A virus transmission bottlenecks are defined by infection route and recipient host
  publication-title: Cell Host Microbe
– volume: 10
  start-page: 756
  year: 2019
  ident: bib29
  article-title: Sequential Immunization With Live-Attenuated Chimeric Hemagglutinin-Based Vaccines Confers Heterosubtypic Immunity Against Influenza A Viruses in a Preclinical Ferret Model
  publication-title: Front. Immunol.
– volume: 2
  start-page: 106
  year: 2002
  end-page: 115
  ident: bib38
  article-title: Chemokine receptors: multifaceted therapeutic targets
  publication-title: Nat. Rev. Immunol.
– volume: 252
  start-page: 324
  year: 1998
  end-page: 330
  ident: bib12
  article-title: Influenza A virus lacking the NS1 gene replicates in interferon-deficient systems
  publication-title: Virology
– volume: 19
  start-page: 142
  year: 2016
  end-page: 149
  ident: bib44
  article-title: The Evolution of Antiviral Defense Systems
  publication-title: Cell Host Microbe
– volume: 103
  start-page: 12885
  year: 2006
  end-page: 12890
  ident: bib20
  article-title: Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation
  publication-title: Proc. Natl. Acad. Sci. USA
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Snippet Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information...
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SubjectTerms animal models
Animals
Betacoronavirus - physiology
blood serum
Cells, Cultured
chemokines
Chemokines - genetics
Chemokines - immunology
Coronavirus
Coronavirus infections
Coronavirus Infections - genetics
Coronavirus Infections - immunology
COVID-19
Disease Models, Animal
ferret
Host-Pathogen Interactions
Humans
IL6
Immunity, Innate
inflammation
Inflammation - virology
interferon
interferons
Interferons - genetics
Interferons - immunology
interleukin-6
pandemic
Pandemics
patients
Pneumonia, Viral - genetics
Pneumonia, Viral - immunology
RNA Viruses - classification
RNA Viruses - immunology
SARS-CoV-2
transcription (genetics)
Transcription, Genetic
transcriptomics
virus-host interactions
viruses
Title Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19
URI https://dx.doi.org/10.1016/j.cell.2020.04.026
https://www.ncbi.nlm.nih.gov/pubmed/32416070
https://www.proquest.com/docview/2404040767
https://www.proquest.com/docview/2439393808
https://pubmed.ncbi.nlm.nih.gov/PMC7227586
Volume 181
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