Innate immunity
Which sensor starts IFN against SARS-CoV-2 in lung cells?
Open access · cc by · source: Europe PMC
SARS-CoV-2 triggers delayed IFN mainly via MDA5/LGP2 sensing of viral intermediates, with IRF3/IRF5/NF-κB p65 as key TFs.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
MDA5/LGP2 dominate IFN induction to SARS-CoV-2 in lung epithelial cells.
Sensor screens showed MDA5 and LGP2 primarily regulate IFN induction to SARS-CoV-2, with delayed IFN and IRF3/IRF5/NF-κB p65 as key transcription factors.
Evidence for the claim as stated.
Interferon programs reshape host gene expression during viral defense.
Host-defense work shows interferon-mediated down-regulation as part of antiviral control—effector-layer evidence beside sensor identity.
Scope note — IFN effector programs ≠ which sensor starts SARS-CoV-2 IFN in epithelium
Limits the claim's scope: a different population, assay, or outcome.
TIR-domain architecture participates in innate association/signaling logic.
TIR-domain association findings add receptor-proximal innate signaling context to nucleic-acid sensor → IFN pathways.
Scope note — TIR-domain study ≠ MDA5 SARS-CoV-2 screen
Limits the claim's scope: a different population, assay, or outcome.
Which sensor fires in one epithelial infection model does not settle interferon effector strategies across all viruses or tissues.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Which sensor fires in one epithelial infection model does not settle interferon effector strategies across all viruses or tissues.
Study at a glance
- Design
- Animal / in-vitro — Lung epithelial infection + RNA-sensor/TF screens
- N
- N=16 · 16 putative sensors screened
- Population
- Lung epithelial cells infected with SARS-CoV-2
- Outcome
- Sensors/TFs governing IFN induction
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Which sensor starts IFN against SARS-CoV-2 in lung cells?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
16 sensors screened.
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.
Delayed IFN in lung epithelium.
Here, we find that SARS-CoV-2 replication induces a delayed interferon (IFN) response in lung epithelial cells.
Key findings
Delayed IFN; MDA5 and LGP2 primary sensors; viral intermediates activate MDA5 pathway; IRF3, IRF5, NF-κB/p65 key TFs.
Methodology
Infected lung epithelial cells and screened candidate RNA sensors and transcription factors for IFN induction.
Limitations
In-vitro epithelial circuits may differ from whole-lung immune networks in patients.
Related papers in this topic
Same topic cluster — not a recommendation engine.