Evidence map›Paper›PMID 31501540›Full record

ArticleNature microbiology2019

Epstein-Barr virus ncRNA from a nasopharyngeal carcinoma induces an inflammatory response that promotes virus production.

Zhe Li, Ming-Han Tsai, Anatoliy Shumilov, Francesco Baccianti, Sai Wah Tsao, Remy Poirey, Henri-Jacques Delecluse

Abstract read
PubMed Publisher
In one paragraph

Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026
    Review
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  8. Impact ofBiomolecules & biomedicine · 2024
    Article
  9. Article
  10. Diagnostic Value of DynamicDiagnostics (Basel, Switzerland) · 2023
    Article
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  14. Article
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  16. Article
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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

7 authors at 3 institutions in 3 countries.

Zhe Li *Unit F100, DKFZ, Heidelberg, Germany.
Ming-Han Tsai *Unit F100, DKFZ, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-5563-3057
Anatoliy ShumilovUnit F100, DKFZ, Heidelberg, Germany.
Francesco BacciantiUnit F100, DKFZ, Heidelberg, Germany.
Sai Wah TsaoSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Remy PoireyUnit F100, DKFZ, Heidelberg, Germany.
Henri-Jacques DelecluseUnit F100, DKFZ, Heidelberg, Germany. h.delecluse@dkfz-heidelberg.de.ORCID http://orcid.org/0000-0002-1744-6274
Heidelberg University · DENational Yang Ming Chiao Tung University · TWUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Epstein-Barr virus M81 strain, isolated from a nasopharyngeal carcinoma, induces potent spontaneous virus production in infected B cells. We found that the M81 non-coding Epstein-Barr-encoded RNA EBER2, which carries polymorphisms that are mainly restricted to viruses found in endemic nasopharyngeal carcinomas, markedly stimulated this process. M81 EBER2 increased CXCL8 expression, and this chemokine enhanced spontaneous lytic replication levels in M81-infected B cells. Both events resulted from the endocytosis of extracellular vesicles containing EBER2 that were generated by neighbouring M81-infected B cells, thereby generating a paracrine loop. These effects were strictly dependent on a functional Toll-like receptor 7 (TLR7), a sensor of single-stranded RNA located in the endosome of these cells. These unique properties of M81 EBER2 could be ascribed to its unusually high expression level and to the ability of its single-stranded region to activate TLR7; both of these properties were dependent on M81-specific polymorphisms. Thus, M81 induced chronic inflammation in its target cells and this resulted in increased virus production. These observations provide a mechanistic molecular link between M81 virus replication-a central viral function and a cancer risk factor-and the production of a chemokine involved in inflammation and carcinogenesis.

Indexed as

Virus ReplicationB-LymphocytesChemokinesEpstein-Barr Virus InfectionsHEK293 CellsHerpesvirus 4, HumanHost-Pathogen InteractionsHumansInterleukin-8Nasopharyngeal CarcinomaNasopharyngeal NeoplasmsOncogenic VirusesRNA, UntranslatedRNA, ViralToll-Like Receptor 7Virus CultivationChemokinesCXCL8 protein, humanEpstein-Barr virus encoded RNA 2Interleukin-8RNA, UntranslatedRNA, ViralTLR7 protein, humanToll-Like Receptor 7

Identifiers

PMID31501540
OpenAlexW2972529803

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.