Transcriptional landscape of SARS-CoV-2 infection dismantles pathogenic pathways activated by the virus, proposes unique sex-specific differences and predicts tailored therapeutic strategies.
Identifieur interne : 000021 ( Main/Exploration ); précédent : 000020; suivant : 000022Transcriptional landscape of SARS-CoV-2 infection dismantles pathogenic pathways activated by the virus, proposes unique sex-specific differences and predicts tailored therapeutic strategies.
Auteurs : Paolo Fagone [Italie] ; Rosella Ciurleo [Italie] ; Salvo Danilo Lombardo [Autriche] ; Carmelo Iacobello [Italie] ; Concetta Ilenia Palermo [Italie] ; Yehuda Shoenfeld [Russie] ; Klaus Bendtzen [Danemark] ; Placido Bramanti [Italie] ; Ferdinando Nicoletti [Italie]Source :
- Autoimmunity reviews [ 1873-0183 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (MeSH), Cellules cultivées (MeSH), Cellules épithéliales (virologie), Découverte de médicament (MeSH), Facteurs sexuels (MeSH), Femelle (MeSH), Humains (MeSH), Infections à coronavirus (anatomopathologie), Infections à coronavirus (génétique), Infections à coronavirus (mortalité), Mâle (MeSH), Pandémies (MeSH), Pneumopathie virale (anatomopathologie), Pneumopathie virale (génétique), Pneumopathie virale (mortalité), Poumon (cytologie), Syndrome respiratoire aigu sévère (MeSH), Sérine-thréonine kinases TOR (MeSH), Transcriptome (MeSH).
- MESH :
- anatomopathologie : Infections à coronavirus, Pneumopathie virale.
- cytologie : Poumon.
- génétique : Infections à coronavirus, Pneumopathie virale.
- mortalité : Infections à coronavirus, Pneumopathie virale.
- virologie : Cellules épithéliales.
- Betacoronavirus, Cellules cultivées, Découverte de médicament, Facteurs sexuels, Femelle, Humains, Mâle, Pandémies, Syndrome respiratoire aigu sévère, Sérine-thréonine kinases TOR, Transcriptome.
English descriptors
- KwdEn :
- Betacoronavirus (MeSH), Cells, Cultured (MeSH), Coronavirus Infections (genetics), Coronavirus Infections (mortality), Coronavirus Infections (pathology), Drug Discovery (MeSH), Epithelial Cells (virology), Female (MeSH), Humans (MeSH), Lung (cytology), Male (MeSH), Pandemics (MeSH), Pneumonia, Viral (genetics), Pneumonia, Viral (mortality), Pneumonia, Viral (pathology), Severe Acute Respiratory Syndrome (MeSH), Sex Factors (MeSH), TOR Serine-Threonine Kinases (MeSH), Transcriptome (MeSH).
- MESH :
- chemical : TOR Serine-Threonine Kinases.
- cytology : Lung.
- genetics : Coronavirus Infections, Pneumonia, Viral.
- mortality : Coronavirus Infections, Pneumonia, Viral.
- pathology : Coronavirus Infections, Pneumonia, Viral.
- virology : Epithelial Cells.
- Betacoronavirus, Cells, Cultured, Drug Discovery, Female, Humans, Male, Pandemics, Severe Acute Respiratory Syndrome, Sex Factors, Transcriptome.
Abstract
The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has posed a serious threat to global health. As no specific therapeutics are yet available to control disease evolution, more in-depth understanding of the pathogenic mechanisms induced by SARS-CoV-2 will help to characterize new targets for the management of COVID-19. The present study identified a specific set of biological pathways altered in primary human lung epithelium upon SARS-CoV-2 infection, and a comparison with SARS-CoV from the 2003 pandemic was studied. The transcriptomic profiles were also exploited as possible novel therapeutic targets, and anti-signature perturbation analysis predicted potential drugs to control disease progression. Among them, Mitogen-activated protein kinase kinase (MEK), serine-threonine kinase (AKT), mammalian target of rapamycin (mTOR) and I kappa B Kinase (IKK) inhibitors emerged as candidate drugs. Finally, sex-specific differences that may underlie the higher COVID-19 mortality in men are proposed.
DOI: 10.1016/j.autrev.2020.102571
PubMed: 32376402
PubMed Central: PMC7252184
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Coronavirus Infections (genetics)</term>
<term>Coronavirus Infections (mortality)</term>
<term>Coronavirus Infections (pathology)</term>
<term>Drug Discovery (MeSH)</term>
<term>Epithelial Cells (virology)</term>
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<term>Pneumonia, Viral (mortality)</term>
<term>Pneumonia, Viral (pathology)</term>
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<term>Découverte de médicament (MeSH)</term>
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<front><div type="abstract" xml:lang="en">The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has posed a serious threat to global health. As no specific therapeutics are yet available to control disease evolution, more in-depth understanding of the pathogenic mechanisms induced by SARS-CoV-2 will help to characterize new targets for the management of COVID-19. The present study identified a specific set of biological pathways altered in primary human lung epithelium upon SARS-CoV-2 infection, and a comparison with SARS-CoV from the 2003 pandemic was studied. The transcriptomic profiles were also exploited as possible novel therapeutic targets, and anti-signature perturbation analysis predicted potential drugs to control disease progression. Among them, Mitogen-activated protein kinase kinase (MEK), serine-threonine kinase (AKT), mammalian target of rapamycin (mTOR) and I kappa B Kinase (IKK) inhibitors emerged as candidate drugs. Finally, sex-specific differences that may underlie the higher COVID-19 mortality in men are proposed.</div>
</front>
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<Abstract><AbstractText>The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has posed a serious threat to global health. As no specific therapeutics are yet available to control disease evolution, more in-depth understanding of the pathogenic mechanisms induced by SARS-CoV-2 will help to characterize new targets for the management of COVID-19. The present study identified a specific set of biological pathways altered in primary human lung epithelium upon SARS-CoV-2 infection, and a comparison with SARS-CoV from the 2003 pandemic was studied. The transcriptomic profiles were also exploited as possible novel therapeutic targets, and anti-signature perturbation analysis predicted potential drugs to control disease progression. Among them, Mitogen-activated protein kinase kinase (MEK), serine-threonine kinase (AKT), mammalian target of rapamycin (mTOR) and I kappa B Kinase (IKK) inhibitors emerged as candidate drugs. Finally, sex-specific differences that may underlie the higher COVID-19 mortality in men are proposed.</AbstractText>
<CopyrightInformation>Copyright © 2020 Elsevier B.V. All rights reserved.</CopyrightInformation>
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<ForeName>Paolo</ForeName>
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</AffiliationInfo>
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<ForeName>Rosella</ForeName>
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<AffiliationInfo><Affiliation>IRCCS Centro Neurolesi Bonino Pulejo, C.da Casazza, 98124 Messina, Italy. Electronic address: rossella.ciurleo@irccsme.it.</Affiliation>
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<Author ValidYN="Y"><LastName>Lombardo</LastName>
<ForeName>Salvo Danilo</ForeName>
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<AffiliationInfo><Affiliation>CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, A-1090 Vienna, Austria. Electronic address: SLombardo@cemm.oeaw.ac.at.</Affiliation>
</AffiliationInfo>
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<ForeName>Carmelo</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>UOC Malattie Infettive, AO Cannizzaro, Catania, Italy.</Affiliation>
</AffiliationInfo>
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<Keyword MajorTopicYN="N">SARS</Keyword>
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<CoiStatement>Declaration of Competing Interest The authors declare no conflict of interest.</CoiStatement>
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