Serveur d'exploration sur le Covid à Stanford

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Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections.

Identifieur interne : 000002 ( Main/Exploration ); précédent : 000001; suivant : 000003

Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections.

Auteurs : Simone A. Thair [États-Unis] ; Yudong D. He [États-Unis] ; Yehudit Hasin-Brumshtein [États-Unis] ; Suraj Sakaram [États-Unis] ; Rushika Pandya [États-Unis] ; Jiaying Toh [États-Unis] ; David Rawling [États-Unis] ; Melissa Remmel [États-Unis] ; Sabrina Coyle [États-Unis] ; George N. Dalekos [Grèce] ; Ioannis Koutsodimitropoulos [Grèce] ; Glykeria Vlachogianni [Grèce] ; Eleni Gkeka [Grèce] ; Eleni Karakike [Grèce] ; Georgia Damoraki [Grèce] ; Nikolaos Antonakos [Grèce] ; Purvesh Khatri [États-Unis] ; Evangelos J. Giamarellos-Bourboulis [Grèce] ; Timothy E. Sweeney [États-Unis]

Source :

RBID : pubmed:33437935

Abstract

The pandemic 2019 novel coronavirus disease (COVID-19) shares certain clinical characteristics with other acute viral infections. We studied the whole-blood transcriptomic host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using RNAseq from 24 healthy controls and 62 prospectively enrolled patients with COVID-19. We then compared these data to non-COVID-19 viral infections, curated from 23 independent studies profiling 1,855 blood samples covering six viruses (influenza, respiratory syncytial virus (RSV), human rhinovirus (HRV), severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1), Ebola, dengue). We show gene expression changes in COVID-19 versus non-COVID-19 viral infections are highly correlated (r = 0.74, p < 0.001). However, we also found 416 genes specific to COVID-19. Inspection of top genes revealed dynamic immune evasion and counter host responses specific to COVID-19. Statistical deconvolution of cell proportions maps many cell type proportions concordantly shifting. Discordantly increased in COVID-19 were CD56bright natural killer cells and M2 macrophages. The concordant and discordant responses mapped out here provide a window to explore the pathophysiology of the host response to SARS-CoV-2.

DOI: 10.1016/j.isci.2020.101947
PubMed: 33437935
PubMed Central: PMC7786129


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<name sortKey="Koutsodimitropoulos, Ioannis" sort="Koutsodimitropoulos, Ioannis" uniqKey="Koutsodimitropoulos I" first="Ioannis" last="Koutsodimitropoulos">Ioannis Koutsodimitropoulos</name>
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<div type="abstract" xml:lang="en">The pandemic 2019 novel coronavirus disease (COVID-19) shares certain clinical characteristics with other acute viral infections. We studied the whole-blood transcriptomic host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using RNAseq from 24 healthy controls and 62 prospectively enrolled patients with COVID-19. We then compared these data to non-COVID-19 viral infections, curated from 23 independent studies profiling 1,855 blood samples covering six viruses (influenza, respiratory syncytial virus (RSV), human rhinovirus (HRV), severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1), Ebola, dengue). We show gene expression changes in COVID-19 versus non-COVID-19 viral infections are highly correlated (r = 0.74, p < 0.001). However, we also found 416 genes specific to COVID-19. Inspection of top genes revealed dynamic immune evasion and counter host responses specific to COVID-19. Statistical deconvolution of cell proportions maps many cell type proportions concordantly shifting. Discordantly increased in COVID-19 were CD56
<sup>bright</sup>
natural killer cells and M2 macrophages. The concordant and discordant responses mapped out here provide a window to explore the pathophysiology of the host response to SARS-CoV-2.</div>
</front>
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<AbstractText>The pandemic 2019 novel coronavirus disease (COVID-19) shares certain clinical characteristics with other acute viral infections. We studied the whole-blood transcriptomic host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using RNAseq from 24 healthy controls and 62 prospectively enrolled patients with COVID-19. We then compared these data to non-COVID-19 viral infections, curated from 23 independent studies profiling 1,855 blood samples covering six viruses (influenza, respiratory syncytial virus (RSV), human rhinovirus (HRV), severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1), Ebola, dengue). We show gene expression changes in COVID-19 versus non-COVID-19 viral infections are highly correlated (r = 0.74, p < 0.001). However, we also found 416 genes specific to COVID-19. Inspection of top genes revealed dynamic immune evasion and counter host responses specific to COVID-19. Statistical deconvolution of cell proportions maps many cell type proportions concordantly shifting. Discordantly increased in COVID-19 were CD56
<sup>bright</sup>
natural killer cells and M2 macrophages. The concordant and discordant responses mapped out here provide a window to explore the pathophysiology of the host response to SARS-CoV-2.</AbstractText>
<CopyrightInformation>© 2020 The Authors.</CopyrightInformation>
</Abstract>
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<LastName>Thair</LastName>
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<ForeName>Yudong D</ForeName>
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<ForeName>Jiaying</ForeName>
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<AffiliationInfo>
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<LastName>Dalekos</LastName>
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<Affiliation>Department of Internal Medicine, University of Thessaly, Larissa General Hospital, Greece.</Affiliation>
</AffiliationInfo>
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<LastName>Koutsodimitropoulos</LastName>
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<LastName>Vlachogianni</LastName>
<ForeName>Glykeria</ForeName>
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<LastName>Gkeka</LastName>
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<Affiliation>4th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, 124 62 Athens, Greece.</Affiliation>
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<LastName>Damoraki</LastName>
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<Affiliation>4th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, 124 62 Athens, Greece.</Affiliation>
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<Author ValidYN="Y">
<LastName>Antonakos</LastName>
<ForeName>Nikolaos</ForeName>
<Initials>N</Initials>
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<Affiliation>4th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, 124 62 Athens, Greece.</Affiliation>
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<AffiliationInfo>
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<Affiliation>4th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, 124 62 Athens, Greece.</Affiliation>
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<LastName>Sweeney</LastName>
<ForeName>Timothy E</ForeName>
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<Affiliation>Inflammatix, Inc., 863 Mitten Road, Suite 104, Burlingame, CA 94010, USA.</Affiliation>
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<CoiStatement>S.A.T., Y.D.H., Y.H., S.S., R.P., D.R., M.R., S.C., and T.E.S. are employees of and stockholders in Inflammatix, Inc. P.K. reports being a shareholder and a consultant to Inflammatix, Inc. E.J.G.B. reports receiving honoraria from 10.13039/100006483AbbVie 10.13039/100011408USA, Abbott CH, InflaRx GmbH, MSD Greece, XBiotech Inc., and 10.13039/501100006546Angelini Italy; independent educational grants from 10.13039/100006483AbbVie, Abbott, 10.13039/501100006044Astellas Pharma Europe, AxisShield, bioMérieux Inc, InflaRx GmbH, and XBiotech Inc; and funding from the FrameWork 7 program HemoSpec (granted to the National and Kapodistrian University of Athens), the 10.13039/501100007601Horizon 2020 Marie-Curie Project European Sepsis Academy (granted to the National and Kapodistrian University of Athens), and the 10.13039/501100007601Horizon 2020 European Grant ImmunoSep (granted to the Hellenic Institute for the Study of Sepsis). The other authors declare no competing interests.</CoiStatement>
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