The cGAS–STING pathway drives type I IFN immunopathology in COVID-19
Open accessAbstract
COVID-19, which is caused by infection with SARS-CoV-2, is characterized by lung pathology and extrapulmonary complications 1,2 . Type I interferons (IFNs) have an essential role in the pathogenesis of COVID-19 (refs 3–5 ). Although rapid induction of type I IFNs limits virus propagation, a sustained increase in the levels of type I IFNs in the late phase of the infection is associated with aberrant inflammation and poor clinical outcome 5–17 . Here we show that the cyclic GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway, which controls immunity to cytosolic DNA, is a critical driver of aberrant type I IFN responses in COVID-19 (ref. 18 ). Profiling COVID-19 skin manifestations, we uncover a STING-dependent type I IFN signature that is primarily mediated by macrophages adjacent to areas of endothelial cell damage. Moreover, cGAS–STING activity was detected in lung samples from patients with COVID-19 with prominent tissue destruction, and was associated with type I IFN responses. A lung-on-chip model revealed that, in addition to macrophages, infection with SARS-CoV-2 activates cGAS–STING signalling in endothelial cells through mitochondrial DNA release, which leads to cell death and type I IFN production. In mice, pharmacological inhibition of STING reduces severe lung inflammation induced by SARS-CoV-2 and improves disease outcome. Collectively, our study establishes a mechanistic basis of pathological type I IFN responses in COVID-19 and reveals a principle for the development of host-directed therapeutics.
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Targeting the cGAS-STING axis with the small-molecule STING inhibitor H-151 had a SASP-suppressing, senomorphic effect and led to reduced lung pathology and prolonged survival in a human ACE2-transgenic mouse model of COVID-19.
“Targeting of the cGAS–STING axis, which induces type I interferons and other SASP factors, with the small-molecule STING inhibitor H-151 had a SASP-suppressing, senomorphic effect28,121,128,129 and led to reduced lung pathology and prolonged survival in a human ACE2-transgenic mouse model of COVID-19 (ref.59).”
From COVID-19 and cellular senescence (2023) · cites this paper as [59]
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- Authors
- Domizio, J. D., Gulen, M. F., Saidoune, F., Thacker, V. V., Yatim, A., Sharma, K., Nass, T., Guenova, E., Schaller, M., Conrad, C., Goepfert, C., de Leval, L., Garnier, C. V., Berezowska, S., Dubois, A., Gilliet, M., & Ablasser, A.
- Affiliations
- École Polytechnique Fédérale de Lausanne (CH)
- Centre Hospitalier Universitaire Vaudois (CH)
- University of Tübingen (DE)
- University of Bern (CH)
- Corresponding author
- Gilliet, Michel
- Ablasser, Andrea
- ORCID
- Venue
- Nature
- Published
- 2022-01-19
- Volume
- 603
- Issue
- 7899
- Pages
- 145-151
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC8891013
- OpenAlex
- W4205252391
- Cited by
- 538
- References
- 60
- Citations by year
- 2026: 63 · 2025: 98 · 2024: 136 · 2023: 141 · 2022: 98 · 2021: 1
- FWCI
- 45.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Nature (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (publishedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- BORIS (University Library Bern) (submittedVersion, cc-by)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- IRIS (submittedVersion, cc-by)
- Open Access CRIS of the University of Bern
- Funders
- Novartis Foundation
- Fondation Acteria
- European Commission (HORIZON2020, COVID-19)
- Novartis Stiftung für Medizinisch-Biologische Forschung
- Fondation Leenaards
- Université de Lausanne
- Centre Hospitalier Universitaire Vaudois
- H2020 European Research Council (804933)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Keywords
- COVID-19 pandemic, SARS-CoV-2, cGAS-STING pathway, type I interferon, immunopathology, cytosolic DNA sensing, macrophages, endothelial cells, mitochondrial DNA release, lung inflammation, STING inhibition, host-directed therapeutics, cutaneous manifestations
- MeSH terms
- COVID-19, SARS-CoV-2, STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Cells, Cultured, Disease Models, Animal, DNA, Mitochondrial, Female, Gene Expression Regulation, Humans, Immunity, Innate, Interferon Type I, Lung, Macrophages, Membrane Proteins, Mice, Inbred C57BL, Nucleotidyltransferases, Pneumonia, Skin, Signal Transduction, Disease Progression, Endothelial Cells, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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