Evidence map›Paper›PMID 38409141›Full record

ArticleNature communications2024

Human cytomegalovirus exploits STING signaling and counteracts IFN/ISG induction to facilitate infection of dendritic cells.

Bibiana Costa, Jennifer Becker, Tobias Krammer, Felix Mulenge, Verónica Durán, Andreas Pavlou, Olivia Luise Gern, Xiaojing Chu, Yang Li, Luka Čičin-Šain and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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

16 authors at 5 institutions in 2 countries.

Bibiana Costa *Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0009-0002-6126-6075
Jennifer Becker *Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0000-0002-0122-3922
Tobias KrammerHelmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz-Centre for Infection Research (HZI), Würzburg, Germany.ORCID 0000-0002-7638-9476
Felix MulengeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0000-0002-5056-2461
Verónica DuránInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Andreas PavlouInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Olivia Luise GernInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0000-0001-6638-2206
Xiaojing ChuDepartment of Computational Biology for Individualised Medicine, Centre for Individualised Infection Medicine (CiiM) & TWINCORE, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0000-0002-9882-2912
Yang LiDepartment of Computational Biology for Individualised Medicine, Centre for Individualised Infection Medicine (CiiM) & TWINCORE, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.ORCID 0000-0003-4022-7341
Luka Čičin-ŠainInstitute for Immune Aging and Chronic Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany.ORCID 0000-0003-3978-778X
Britta Eiz-VesperInstitute for Transfusion Medicine and Transplant Engineering, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-8378-3298
Martin MesserleInstitute of Virology, Hannover Medical School, Hannover, Germany.ORCID 0000-0002-1227-3933
Lars DölkenInstitute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany.ORCID 0000-0002-4651-3544
Antoine-Emmanuel SalibaHelmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz-Centre for Infection Research (HZI), Würzburg, Germany.ORCID 0000-0001-8539-2784
Florian ErhardInstitute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany. florian.erhard@informatik.regensburg.de.ORCID 0000-0002-3574-6983
Ulrich KalinkeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany. ulrich.kalinke@twincore.de.ORCID 0000-0003-0503-9564
Medizinische Hochschule Hannover · DEHelmholtz Centre for Infection Research · DEUniversity of Würzburg · DEOTH Regensburg · DERadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is a widespread pathogen that in immunocompromised hosts can cause life-threatening disease. Studying HCMV-exposed monocyte-derived dendritic cells by single-cell RNA sequencing, we observe that most cells are entered by the virus, whereas less than 30% of them initiate viral gene expression. Increased viral gene expression is associated with activation of the stimulator of interferon genes (STING) that usually induces anti-viral interferon responses, and with the induction of several pro- (RHOB, HSP1A1, DNAJB1) and anti-viral (RNF213, TNFSF10, IFI16) genes. Upon progression of infection, interferon-beta but not interferon-lambda transcription is inhibited. Similarly, interferon-stimulated gene expression is initially induced and then shut off, thus further promoting productive infection. Monocyte-derived dendritic cells are composed of 3 subsets, with one being especially susceptible to HCMV. In conclusion, HCMV permissiveness of monocyte-derived dendritic cells depends on complex interactions between virus sensing, regulation of the interferon response, and viral gene expression.

Indexed as

CytomegalovirusInterferonsAdenosine TriphosphatasesAntiviral AgentsDendritic CellsHSP40 Heat-Shock ProteinsHumansSignal TransductionUbiquitin-Protein LigasesAdenosine TriphosphatasesAntiviral AgentsDNAJB1 protein, humanHSP40 Heat-Shock ProteinsInterferonsRNF213 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID38409141
PMCPMC10897438
OpenAlexW4392156857

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.