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Rescooped by Gilbert C FAURE from Virus World
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SARS-CoV-2 and Innate Immunity: the Good, the Bad, and the “Goldilocks” - Review

SARS-CoV-2 and Innate Immunity: the Good, the Bad, and the “Goldilocks” - Review | Immunology | Scoop.it
From www.nature.com - November 25, 2023 2:42 AM

An ancient conflict between hosts and pathogens has driven the innate and adaptive arms of immunity. Knowledge about this interplay can not only help us identify biological mechanisms but also reveal pathogen vulnerabilities that can be leveraged therapeutically. The humoral response to SARS-CoV-2 infection has been the focus of intense research, and the role of the innate immune system has received significantly less attention. Here, we review current knowledge of the innate immune response to SARS-CoV-2 infection and the various means SARS-CoV-2 employs to evade innate defense systems. We also consider the role of innate immunity in SARS-CoV-2 vaccines and in the phenomenon of long COVID.

 

Published in Cell. Mol. Immunology (Nov. 20, 2023):

https://doi.org/10.1038/s41423-023-01104-y 


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Gilbert C FAURE's comment, November 25, 2023 4:42 AM
intéressant pour aborder le sujet de l'immunité innée dans le covid
Gilbert C FAURE's comment, November 25, 2023 4:44 AM
voir les rôles des interférons dans les réponses antivirales...
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Rescooped by Gilbert C FAURE from Virus World
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Evasion of Type-I Interferon by SARS-CoV-2

Evasion of Type-I Interferon by SARS-CoV-2 | Immunology | Scoop.it
From www.cell.com - September 23, 2020 4:40 AM
The coronavirus disease 2019 (COVID-19) is determined by SARS-CoV-2 replication and host immune response, but studies evaluating viral evasion of immune response are lacking. Here we employed unbiased screening to identify SARS-CoV-2 proteins that antagonize type-I interferon (IFN-I) response. Three proteins were found to antagonize IFN-I production via distinct mechanisms: nsp6 binds TBK1 to suppress IRF3 phosphorylation; nsp13 binds and blocks TBK1 phosphorylation; and ORF6 binds importin KPNA2 to inhibit IRF3 nuclear translocation.
 
Two sets of viral proteins were identified to antagonize IFN-I signaling through blocking STAT1/STAT2 phosphorylation or nuclear translocation. Remarkably, SARS-CoV-2 nsp1 and nsp6 suppressed IFN-I signaling more efficiently than SARS-CoV and MERS-CoV. Thus, when treated with IFN-I, a SARS-CoV2 replicon replicated to a higher level than chimeric replicons containing nsp1 or nsp6 from SARS-CoV or MERS-CoV. Altogether, the study has provided insights on SARS-CoV-2 evasion of IFN-I response and its potential impact on viral transmission and pathogenesis.
 
Published in Cell Reports (September 19, 2020):

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