Evidence map›Paper›PMID 27491954›Full record

ArticleScientific reports2016

The Expression of Human Cytomegalovirus MicroRNA MiR-UL148D during Latent Infection in Primary Myeloid Cells Inhibits Activin A-triggered Secretion of IL-6.

Betty Lau, Emma Poole, Benjamin Krishna, Immaculada Sellart, Mark R Wills, Eain Murphy, John Sinclair

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 81 citations in OpenAlex.

  1. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Viral miRNA regulation of host gene expression.Seminars in cell & developmental biology · 2023
    Review
  8. Review
  9. Deletion of the non-adjacent genesFrontiers in immunology · 2023
    Article
  10. Review
  11. Hematopoietic stem cells and betaherpesvirus latency.Frontiers in cellular and infection microbiology · 2023
    Review
  12. Abundance ofFrontiers in immunology · 2023
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Human Cytomegalovirus miR-UL70-3p Downregulates the HInternational journal of molecular sciences · 2021
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Betty LauDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
Emma PooleDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
Benjamin KrishnaDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
Immaculada SellartDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
Mark R WillsDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
Eain MurphyDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, United States of America.
John SinclairDepartment of Medicine, University of Cambridge, Cambridge CB2 2QQ, United Kingdom.
University of Cambridge · GBCleveland Clinic Lerner College of Medicine · US

Funding

Mechanisms of Human Cytomegalovirus LatencyR01AI101080 · NIAID · EVRYS BIO, LLC · PI MURPHY, EAIN A · 2013 to 2016
$1.6M
Medical Research Council G0701279Medical Research Council MR/K021087/1NIAID NIH HHS R01 AI101080
6 · The paper itself

Abstract

The successful establishment and maintenance of human cytomegalovirus (HCMV) latency is dependent on the expression of a subset of viral genes. Whilst the exact spectrum and functions of these genes are far from clear, inroads have been made for protein-coding genes. In contrast, little is known about the expression of non-coding RNAs. Here we show that HCMV encoded miRNAs are expressed de novo during latent infection of primary myeloid cells. Furthermore, we demonstrate that miR-UL148D, one of the most highly expressed viral miRNAs during latent infection, directly targets the cellular receptor ACVR1B of the activin signalling axis. Consistent with this, we observed upregulation of ACVR1B expression during latent infection with a miR-UL148D deletion virus (ΔmiR-UL148D). Importantly, we observed that monocytes latently infected with ΔmiR-UL148D are more responsive to activin A stimulation, as demonstrated by their increased secretion of IL-6. Collectively, our data indicates miR-UL148D inhibits ACVR1B expression in latently infected cells to limit proinflammatory cytokine secretion, perhaps as an immune evasion strategy or to postpone cytokine-induced reactivation until conditions are more favourable. This is the first demonstration of an HCMV miRNA function during latency in primary myeloid cells, implicating that small RNA species may contribute significantly to latent infection.

Indexed as

Activin Receptors, Type IActivinsCells, CulturedCytokinesCytomegalovirusGene Expression RegulationHumansInterleukin-6MicroRNAsMonocytesMyeloid CellsUp-RegulationVirus Latencyactivin AActivin Receptors, Type IActivinsACVR1B protein, humanCytokinesIL6 protein, humanInterleukin-6MicroRNAsmiR-UL-148D , human cytomegalovirus

Identifiers

PMID27491954
PMCPMC4974560
OpenAlexW2499902457

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.