Evidence map›Paper›PMID 28837697›Full record

ArticlePLoS pathogens2017

Herpesviruses shape tumour microenvironment through exosomal transfer of viral microRNAs.

Ohad Yogev, Stephen Henderson, Matthew John Hayes, Sara Sofia Marelli, Yifat Ofir-Birin, Neta Regev-Rudzki, Javier Herrero, Tariq Enver

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 91 citations in OpenAlex.

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  15. Extracellular Vesicles: The Invisible Heroes and Villains of COVID-19 Central Neuropathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
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  17. Exosomal transmission of viruses, a two-edged biological sword.Cell communication and signaling : CCS · 2023
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  20. Article

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

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

8 authors at 3 institutions in 2 countries.

Ohad YogevUCL Cancer Institute, Research Department of Cancer Biology, Paul O'Gorman Building, University College London, London, England, United Kingdom.
Stephen HendersonUCL Cancer Institute, Bill Lyons Informatics Centre, Paul O'Gorman Building, University College London, London, England, United Kingdom.ORCID http://orcid.org/0000-0002-9032-3828
Matthew John HayesUCL Institute of Ophthalmology, EM-Unit, Bath Street, London, England, United Kingdom.
Sara Sofia MarelliUCL Cancer Institute, Research Department of Cancer Biology, Paul O'Gorman Building, University College London, London, England, United Kingdom.
Yifat Ofir-BirinFaculty of Biochemistry, Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.
Neta Regev-RudzkiFaculty of Biochemistry, Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.
Javier HerreroUCL Cancer Institute, Bill Lyons Informatics Centre, Paul O'Gorman Building, University College London, London, England, United Kingdom.ORCID http://orcid.org/0000-0001-7313-717X
Tariq EnverUCL Cancer Institute, Research Department of Cancer Biology, Paul O'Gorman Building, University College London, London, England, United Kingdom.ORCID http://orcid.org/0000-0002-0866-6443
CRUK Lung Cancer Centre of Excellence · GBWeizmann Institute of Science · ILUniversity College Hospital · GB

Funding

Cancer Research UK 12796Cancer Research UK 13100
6 · The paper itself

Abstract

Metabolic changes within the cell and its niche affect cell fate and are involved in many diseases and disorders including cancer and viral infections. Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma (KS). KSHV latently infected cells express only a subset of viral genes, mainly located within the latency-associated region, among them 12 microRNAs. Notably, these miRNAs are responsible for inducing the Warburg effect in infected cells. Here we identify a novel mechanism enabling KSHV to manipulate the metabolic nature of the tumour microenvironment. We demonstrate that KSHV infected cells specifically transfer the virus-encoded microRNAs to surrounding cells via exosomes. This flow of genetic information results in a metabolic shift toward aerobic glycolysis in the surrounding non-infected cells. Importantly, this exosome-mediated metabolic reprogramming of neighbouring cells supports the growth of infected cells, thereby contributing to viral fitness. Finally, our data show that this miRNA transfer-based regulation of cell metabolism is a general mechanism used by other herpesviruses, such as EBV, as well as for the transfer of non-viral onco-miRs. This exosome-based crosstalk provides viruses with a mechanism for non-infectious transfer of genetic material without production of new viral particles, which might expose them to the immune system. We suggest that viruses and cancer cells use this mechanism to shape a specific metabolic niche that will contribute to their fitness.

Indexed as

Blotting, WesternCell LineExomeHerpesviridae InfectionsHerpesvirus 8, HumanHumansMicroRNAsMicroscopy, Electron, TransmissionPolymerase Chain ReactionRNA, ViralSarcoma, KaposiTumor MicroenvironmentVirulenceMicroRNAsRNA, Viral

Identifiers

PMID28837697
PMCPMC5570218
OpenAlexW2749141135

What OpenQuestion holds

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LicenceCC BY
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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.