Evidence map›Paper›PMID 31249303›Full record

ArticleNature communications2019

STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Pia-Katharina Tegtmeyer, Julia Spanier, Katharina Borst, Jennifer Becker, André Riedl, Christoph Hirche, Luca Ghita, Jennifer Skerra, Kira Baumann, Stefan Lienenklaus and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

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  11. Immune surveillance of cytomegalovirus in tissues.Cellular & molecular immunology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Pia-Katharina TegtmeyerTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Julia SpanierTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.ORCID http://orcid.org/0000-0002-8797-3563
Katharina BorstTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Jennifer BeckerTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
André RiedlFaculty of Medicine, Medical Center, Institute for Virology, University of Freiburg, 79106, Freiburg, Germany.
Christoph HircheTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Luca GhitaTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Jennifer SkerraTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Kira BaumannTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.
Stefan LienenklausTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.ORCID http://orcid.org/0000-0003-4790-3445
Marius DoeringTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany.ORCID http://orcid.org/0000-0002-5278-8376
Zsolt RuzsicsFaculty of Medicine, Medical Center, Institute for Virology, University of Freiburg, 79106, Freiburg, Germany.
Ulrich KalinkeTWINCORE-Centre for Experimental and Clinical Infection Research, a joint venture between the Hanover Medical School and the Helmholtz Centre for Infection Research, Institute for Experimental Infection Research, 30625, Hanover, Germany. Ulrich.Kalinke@twincore.de.ORCID http://orcid.org/0000-0003-0503-9564
Helmholtz Centre for Infection Research · DEUniversity of Freiburg · DEMedizinische Hochschule Hannover · DEInserm · FR

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 406922110Deutsche Forschungsgemeinschaft (German Research Foundation) SFB854Deutsche Forschungsgemeinschaft (German Research Foundation) SFB900Helmholtz Association VH-VI-424Helmholtz Association ZT-0027
6 · The paper itself

Abstract

Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.

Indexed as

AnimalsFemaleHepatocytesHerpesviridae InfectionsHost-Pathogen InteractionsInterferon-betaKupffer CellsLiverMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMuromegalovirusMyeloid CellsRodent DiseasesInterferon-betaMembrane ProteinsSting1 protein, mouseSTING ProteinToll-Like Receptors

Identifiers

PMID31249303
PMCPMC6597531
OpenAlexW2955263887

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.