Evidence map›Paper›PMID 35022513›Full record

ArticleCommunications biology2022

SARS-CoV-2 infection induces a pro-inflammatory cytokine response through cGAS-STING and NF-κB.

Christopher J Neufeldt, Berati Cerikan, Mirko Cortese, Jamie Frankish, Ji-Young Lee, Agnieszka Plociennikowska, Florian Heigwer, Vibhu Prasad, Sebastian Joecks, Sandy S Burkart and 12 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 2 pooled it
18.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

196 citing papers in PubMed, 2 syntheses or guidelines pooled it, 254 citations in OpenAlex.

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136 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 4 institutions in 2 countries.

Christopher J Neufeldt *Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany. christopher.john.neufeldt@emory.edu.ORCID http://orcid.org/0000-0002-4551-1811
Berati Cerikan *Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Mirko CorteseDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Jamie FrankishBioMed X Institute, BioMed X GmbH, Heidelberg, Germany.
Ji-Young LeeDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Agnieszka PlociennikowskaDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Florian HeigwerDivision of Signaling and Functional Genomics, German Cancer Research Center, and Department of Cell and Molecular Biology, Heidelberg University, Medical Faculty Mannheim, Mannheim, Germany.ORCID http://orcid.org/0000-0002-8230-1485
Vibhu PrasadDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-7450-607X
Sebastian JoecksDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Sandy S BurkartResearch Group "Dynamics of Early Viral Infection and the Innate Antiviral Response", Division Virus-Associated Carcinogenesis, German Cancer Research Center, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-1096-0550
David Y ZanderDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9235-6191
Baskaran SubramanianSpring Bank Pharmaceuticals, Inc., 35 Corporate Drive, Hopkinton, MA, 01748, USA.
Rayomand GimiSpring Bank Pharmaceuticals, Inc., 35 Corporate Drive, Hopkinton, MA, 01748, USA.
Seetharamaiyer PadmanabhanSpring Bank Pharmaceuticals, Inc., 35 Corporate Drive, Hopkinton, MA, 01748, USA.
Radhakrishnan IyerSpring Bank Pharmaceuticals, Inc., 35 Corporate Drive, Hopkinton, MA, 01748, USA.
Mathieu GendarmeBioMed X Institute, BioMed X GmbH, Heidelberg, Germany.
Bachir El DebsBioMed X Institute, BioMed X GmbH, Heidelberg, Germany.
Niels HalamaDivision of Translational Immunotherapy, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0003-0344-6027
Uta MerleDepartment of Internal Medicine IV, University Hospital Heidelberg, Heidelberg, Germany.
Michael BoutrosDivision of Signaling and Functional Genomics, German Cancer Research Center, and Department of Cell and Molecular Biology, Heidelberg University, Medical Faculty Mannheim, Mannheim, Germany.
Marco BinderResearch Group "Dynamics of Early Viral Infection and the Innate Antiviral Response", Division Virus-Associated Carcinogenesis, German Cancer Research Center, Heidelberg, Germany.
Ralf BartenschlagerDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany. ralf.bartenschlager@med.uni-heidelberg.de.ORCID http://orcid.org/0000-0001-5601-9307
German Cancer Research Center · DEHeidelberg University · DESpring Bank Pharmaceuticals (United States) · USBioMed X Institute · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 240245660Deutsche Forschungsgemeinschaft (German Research Foundation) 272983813Deutsche Forschungsgemeinschaft (German Research Foundation) BI1693/1-2Deutsche Forschungsgemeinschaft (German Research Foundation) BI1693/2-1Deutsche Forschungsgemeinschaft (German Research Foundation) TRR 179Deutsches Krebsforschungszentrum (German Cancer Research Center) fightCOVID@DKFZDeutsches Zentrum für Infektionsforschung (German Center for Infection Research) 8029705705Helmholtz Association COVIPA
6 · The paper itself

Abstract

SARS-CoV-2 is a novel virus that has rapidly spread, causing a global pandemic. In the majority of infected patients, SARS-CoV-2 leads to mild disease; however, in a significant proportion of infections, individuals develop severe symptoms that can lead to long-lasting lung damage or death. These severe cases are often associated with high levels of pro-inflammatory cytokines and low antiviral responses, which can cause systemic complications. Here, we have evaluated transcriptional and cytokine secretion profiles and detected a distinct upregulation of inflammatory cytokines in infected cell cultures and samples taken from infected patients. Building on these observations, we found a specific activation of NF-κB and a block of IRF3 nuclear translocation in SARS-CoV-2 infected cells. This NF-κB response was mediated by cGAS-STING activation and could be attenuated through several STING-targeting drugs. Our results show that SARS-CoV-2 directs a cGAS-STING mediated, NF-κB-driven inflammatory immune response in human epithelial cells that likely contributes to inflammatory responses seen in patients and could be therapeutically targeted to suppress severe disease symptoms.

Indexed as

Cytokine Release SyndromeCOVID-19Cyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHumansInflammation MediatorsMembrane ProteinsNF-kappa BNucleotidyltransferasesSARS-CoV-2Signal TransductionSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseInflammation MediatorsMembrane ProteinsNF-kappa BNucleotidyltransferasesSTING1 protein, humanSTING Protein

Identifiers

PMID35022513
PMCPMC8755718
OpenAlexW4224987978

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.