Evidence map›Paper›PMID 28910400›Full record

ArticlePLoS pathogens2017

Exosome-mediated miR-146a transfer suppresses type I interferon response and facilitates EV71 infection.

Yuxuan Fu, Li Zhang, Fang Zhang, Ting Tang, Qi Zhou, Chunhong Feng, Yu Jin, Zhiwei Wu

Abstract 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 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
–field-weighted citation impact
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

88 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Does extracellular vesicle specificity truly exist?Cell communication and signaling : CCS · 2026
    Review
  6. Review
  7. Extracellular vesicles in viral disease management.Current research in microbial sciences · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Research progress on the mechanism of exosome-mediated virus infection.Frontiers in cellular and infection microbiology · 2024
    Review
  20. TLR4 signalling: the key to controlling EV71 replication and inflammatory response.Frontiers in cellular and infection microbiology · 2024
    Article

28 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.

Yuxuan FuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.
Li ZhangCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.
Fang ZhangCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.
Ting TangCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.
Qi ZhouNanjing Children's Hospital, Nanjing Medical University, Nanjing, PR China.
Chunhong FengCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.
Yu JinNanjing Children's Hospital, Nanjing Medical University, Nanjing, PR China.
Zhiwei WuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, PR China.ORCID http://orcid.org/0000-0002-0672-948X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes can transfer genetic materials between cells. Their roles in viral infections are beginning to be appreciated. Researches have shown that exosomes released from virus-infected cells contain a variety of viral and host cellular factors that are able to modulate recipient's cellular response and result in productive infection of the recipient host. Here, we showed that EV71 infection resulted in upregulated exosome secretion and differential packaging of the viral genomic RNA and miR-146a into exosomes. We provided evidence showing that miR-146a was preferentially enriched in exosomes while the viral RNA was not in infected cells. Moreover, the exosomes contained replication-competent EV71 RNA in complex with miR-146a, Ago2, and GW182 and could mediate EV71 transmission independent of virus-specific receptor. The exosomal viral RNA could be transferred to and replicate in a new target cell while the exosomal miR-146a suppressed type I interferon response in the target cell, thus facilitating the viral replication. Additionally, we found that the IFN-stimulated gene factors (ISGs), BST-2/tetherin, were involved in regulating EV71-induced upregulation of exosome secretion. Importantly, in vivo study showed that exosomal viral RNA exhibited differential tissue accumulation as compared to the free virus particles. Together, our findings provide evidence that exosomes secreted by EV71-infected cells selectively packaged high level miR-146a that can be functionally transferred to and facilitate exosomal EV71 RNA to replicate in the recipient cells by suppressing type I interferon response.

Indexed as

Enterovirus A, HumanAnimalsBiological TransportCoxsackievirus InfectionsExosomesHumansInterferon Type IMiceMicroRNAsRNA, ViralVirus ReplicationInterferon Type IMicroRNAsMIRN146 microRNA, humanMirn146 microRNA, mouseRNA, Viral

Identifiers

PMID28910400
PMCPMC5614653

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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.