MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells.
Cell Rep
; 34(2): 108628, 2021 01 12.
Article
in English
| MEDLINE | ID: covidwho-1036973
ABSTRACT
Recent studies have profiled the innate immune signatures in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and suggest that cellular responses to viral challenge may affect disease severity. Yet the molecular events that underlie cellular recognition and response to SARS-CoV-2 infection remain to be elucidated. Here, we find that SARS-CoV-2 replication induces a delayed interferon (IFN) response in lung epithelial cells. By screening 16 putative sensors involved in sensing of RNA virus infection, we found that MDA5 and LGP2 primarily regulate IFN induction in response to SARS-CoV-2 infection. Further analyses revealed that viral intermediates specifically activate the IFN response through MDA5-mediated sensing. Additionally, we find that IRF3, IRF5, and NF-κB/p65 are the key transcription factors regulating the IFN response during SARS-CoV-2 infection. In summary, these findings provide critical insights into the molecular basis of the innate immune recognition and signaling response to SARS-CoV-2.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Interferon-Induced Helicase, IFIH1
/
SARS-CoV-2
/
Immunity, Innate
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Cell Rep
Year:
2021
Document Type:
Article
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