CovidFranceV1, Main, Exploration, bibRecord, 000C51

Interplay between SARS-CoV-2 and the type I interferon response.

Identifieur interne : 000C51 ( Main/Exploration ); précédent : 000C50; suivant : 000C52

Interplay between SARS-CoV-2 and the type I interferon response.

Auteurs : Margarida Sa Ribero [France] ; Nolwenn Jouvenet [France] ; Marlène Dreux [France] ; Sébastien Nisole [France]

Source :

PLoS pathogens [ 1553-7374 ] ; 2020.

RBID : pubmed:32726355

Descripteurs français

KwdFr :
- Antiviraux (usage thérapeutique), Betacoronavirus (effets des médicaments et des substances chimiques), Betacoronavirus (immunologie), Betacoronavirus (isolement et purification), Cellules dendritiques (effets des médicaments et des substances chimiques), Cellules dendritiques (immunologie), Humains (MeSH), Immunité innée (effets des médicaments et des substances chimiques), Immunité innée (immunologie), Infections à coronavirus (immunologie), Infections à coronavirus (traitement médicamenteux), Infections à coronavirus (virologie), Interféron de type I (usage thérapeutique), Pandémies (MeSH), Pneumopathie virale (immunologie), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (virologie), Pronostic (MeSH).
MESH :
- effets des médicaments et des substances chimiques : Betacoronavirus, Cellules dendritiques, Immunité innée.
- immunologie : Betacoronavirus, Cellules dendritiques, Immunité innée, Infections à coronavirus, Pneumopathie virale.
- isolement et purification : Betacoronavirus.
- traitement médicamenteux : Infections à coronavirus, Pneumopathie virale.
- usage thérapeutique : Antiviraux, Interféron de type I.
- virologie : Infections à coronavirus, Pneumopathie virale.
- Humains, Pandémies, Pronostic.

English descriptors

KwdEn :
- Antiviral Agents (therapeutic use), Betacoronavirus (drug effects), Betacoronavirus (immunology), Betacoronavirus (isolation & purification), Coronavirus Infections (drug therapy), Coronavirus Infections (immunology), Coronavirus Infections (virology), Dendritic Cells (drug effects), Dendritic Cells (immunology), Humans (MeSH), Immunity, Innate (drug effects), Immunity, Innate (immunology), Interferon Type I (therapeutic use), Pandemics (MeSH), Pneumonia, Viral (drug therapy), Pneumonia, Viral (immunology), Pneumonia, Viral (virology), Prognosis (MeSH).
MESH :
- chemical , therapeutic use : Antiviral Agents, Interferon Type I.
- drug effects : Betacoronavirus, Dendritic Cells, Immunity, Innate.
- drug therapy : Coronavirus Infections, Pneumonia, Viral.
- immunology : Betacoronavirus, Coronavirus Infections, Dendritic Cells, Immunity, Innate, Pneumonia, Viral.
- isolation & purification : Betacoronavirus.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Humans, Pandemics, Prognosis.

Abstract

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.

DOI: 10.1371/journal.ppat.1008737
PubMed: 32726355
PubMed Central: PMC7390284

Affiliations:

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

to stream Main, to step Corpus: 000802
to stream Main, to step Curation: 000802

Le document en format XML

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<front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.</div>
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<Abstract><AbstractText>The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.</AbstractText>
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Interplay between SARS-CoV-2 and the type I interferon response.

Interplay between SARS-CoV-2 and the type I interferon response.

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