AI Article Synopsis
- Studies show that the immune response to SARS-CoV-2 can impact how severe the disease becomes, but the exact molecular mechanisms are still not fully understood.
- Research identified that MDA5 and LGP2 are crucial sensors for triggering the interferon (IFN) response when lung cells are infected with SARS-CoV-2, which occurs with a delay.
- Key transcription factors like IRF3, IRF5, and NF-κB/p65 play essential roles in regulating the IFN response during SARS-CoV-2 infection, highlighting important aspects of the immune recognition process.
Article 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.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7832566 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2020.108628 | DOI Listing |
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