Evidence map›Paper›PMID 29046460›Full record

ArticleJournal of virology2018

Myeloid Dendritic Cells Repress Human Cytomegalovirus Gene Expression and Spread by Releasing Interferon-Unrelated Soluble Antiviral Factors.

Bahram Kasmapour, Tobias Kubsch, Ulfert Rand, Britta Eiz-Vesper, Martin Messerle, Florian W R Vondran, Bettina Wiegmann, Axel Haverich, Luka Cicin-Sain

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. 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
1.0field-weighted citation impact, top 22% 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.

  1. Article
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  10. Cytomegalovirus inhibition of extrinsic apoptosis determines fitness and resistance to cytotoxic CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Review
  12. Article
  13. Tuning the Orchestra: HCMV vs. Innate Immunity.Frontiers in microbiology · 2020
    Review
  14. Article
  15. Article
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

9 authors at 2 institutions in 1 country.

Bahram KasmapourImmune Ageing and Chronic Infections Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Tobias KubschImmune Ageing and Chronic Infections Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Ulfert RandImmune Ageing and Chronic Infections Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Britta Eiz-VesperInstitute for Transfusion Medicine, Hannover Medical School, Hannover, Germany.
Martin MesserleInstitute of Virology, Hannover Medical School, Hannover, Germany.ORCID http://orcid.org/0000-0002-1227-3933
Florian W R VondranDepartment of General, Visceral and Transplant Surgery, Hannover Medical School, Hannover, Germany.
Bettina WiegmannDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Axel HaverichDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Luka Cicin-SainImmune Ageing and Chronic Infections Group, Helmholtz Centre for Infection Research, Braunschweig, Germany lcs09@helmholtz-hzi.de.ORCID http://orcid.org/0000-0003-3978-778X
Medizinische Hochschule Hannover · DEHelmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytomegalovirus (CMV) is a betaherpesvirus that latently infects most adult humans worldwide and is a major cause of morbidity and mortality in immunocompromised hosts. Latent human CMV (HCMV) is believed to reside in precursors of myeloid-lineage leukocytes and monocytes, which give rise to macrophages and dendritic cells (DC). We report here that human monocyte-derived DC (mo-DC) suppress HCMV infection in coculture with infected fibroblast target cells in a manner dependent on the effector-to-target ratio. Intriguingly, optimal activation of mo-DC was achieved under coculture conditions and not by direct infection with HCMV, implying that mo-DC may recognize unique molecular patterns on, or within, infected fibroblasts. We show that HCMV is controlled by secreted factors that act by priming defenses in target cells rather than by direct viral neutralization, but we excluded a role for interferons (IFNs) in this control. The expression of lytic viral genes in infected cells and the progression of infection were significantly slowed, but this effect was reversible, indicating that the control of infection depended on the transient induction of antiviral effector molecules in target cells. Using immediate early or late-phase reporter HCMVs, we show that soluble factors secreted in the cocultures suppress HCMV replication at both stages of the infection and that their antiviral effects are robust and comparable in numerous batches of mo-DC as well as in primary fibroblasts and stromal cells.

Indexed as

Gene ExpressionAntiviral AgentsCoculture TechniquesCytomegalovirusDendritic CellsFibroblastsGenes, ViralHumansImmunity, InnateInterferonsMicroscopy, VideoMyeloid CellsSolubilityVirus ActivationVirus LatencyAntiviral AgentsInterferonsantiviral agentscytomegalovirusdendritic cellsfluorescent image analysisvideo microscopy

Identifiers

PMID29046460
PMCPMC5730771
OpenAlexW2766485027

What OpenQuestion holds

Textmetadata
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.