Asset Details
Do you wish to reserve the book?
Activation and evasion of type I interferon responses by SARS-CoV-2
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Activation and evasion of type I interferon responses by SARS-CoV-2
Do you wish to request the book?
Activation and evasion of type I interferon responses by SARS-CoV-2
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Activation and evasion of type I interferon responses by SARS-CoV-2
2020
Overview
The pandemic of COVID-19 has posed an unprecedented threat to global public health. However, the interplay between the viral pathogen of COVID-19, SARS-CoV-2, and host innate immunity is poorly understood. Here we show that SARS-CoV-2 induces overt but delayed type-I interferon (IFN) responses. By screening 23 viral proteins, we find that SARS-CoV-2 NSP1, NSP3, NSP12, NSP13, NSP14, ORF3, ORF6 and M protein inhibit Sendai virus-induced IFN-β promoter activation, whereas NSP2 and S protein exert opposite effects. Further analyses suggest that ORF6 inhibits both type I IFN production and downstream signaling, and that the C-terminus region of ORF6 is critical for its antagonistic effect. Finally, we find that IFN-β treatment effectively blocks SARS-CoV-2 replication. In summary, our study shows that SARS-CoV-2 perturbs host innate immune response via both its structural and nonstructural proteins, and thus provides insights into the pathogenesis of SARS-CoV-2.
The pandemic of SARS-CoV-2 post a significant threat to public health. Here the authors show, by screening 23 viral proteins, that both structural and non-structural SARS-CoV-2 proteins are capable of modulating host innate immunity and type interferon responses, with this information serves to warrant further studies on SARS-CoV-2 pathogenesis.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/109
/ 14/19
/ 38/77
/ 82/80
/ Betacoronavirus - immunology
/ Betacoronavirus - metabolism
/ Betacoronavirus - physiology
/ Coronavirus Infections - immunology
/ Coronavirus Infections - virology
/ COVID-19
/ Humanities and Social Sciences
/ Humans
/ Immunity
/ Interferon Type I - metabolism
/ Interferon-beta - metabolism
/ Interferon-beta - pharmacology
/ Mutation
/ Pneumonia, Viral - immunology
/ Proteins
/ Science
/ Severe acute respiratory syndrome coronavirus 2
/ Signal Transduction - drug effects
/ Virus Replication - drug effects
/ Viruses
