Evidence map›Paper›PMID 21379335›Full record

ArticlePLoS pathogens2011

A viral microRNA cluster strongly potentiates the transforming properties of a human herpesvirus.

Regina Feederle, Sarah D Linnstaedt, Helmut Bannert, Helge Lips, Maja Bencun, Bryan R Cullen, Henri-Jacques Delecluse

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 150 citations in OpenAlex.

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  13. The Epstein-Barr virus noncoding RNA EBER2 transactivates the UCHL1 deubiquitinase to accelerate cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  20. Epstein-Barr virus-encoded miR-BART5-5p upregulates PD-L1 through PIAS3/pSTAT3 modulation, worsening clinical outcomes of PD-L1-positive gastric carcinomas.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020
    Article

42 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

7 authors at 3 institutions in 3 countries.

Regina FeederleDepartment of Virus Associated Tumours, German Cancer Research Center, Heidelberg, Germany.
Sarah D Linnstaedt
Helmut Bannert
Helge Lips
Maja Bencun
Bryan R Cullen
Henri-Jacques Delecluse
German Cancer Research Center · DEDuke University Hospital · USHeidelberg University · DE

Funding

Ruth L. Kirschstein National Research Service Award (NRSA)- T32T32AI007392 · NIAID · DUKE UNIVERSITY · PI Amy Lynn Corneli, Guido Ferrari · 1990 to 2026
$9.8M
Role and mechanism of action of Gamma herpesvirus microRNAsR01AI067968 · NIAID · DUKE UNIVERSITY · PI CULLEN, BRYAN R. · 2006 to 2016
$3.6M
NIAID NIH HHS R01 AI067968NIAID NIH HHS R01-AI067968NIAID NIH HHS T32 AI007392NIAID NIH HHS T32-AI007392
6 · The paper itself

Abstract

Epstein-Barr virus (EBV), an oncogenic human herpesvirus, induces cell proliferation after infection of resting B lymphocytes, its reservoir in vivo. The viral latent proteins are necessary for permanent B cell growth, but it is unknown whether they are sufficient. EBV was recently found to encode microRNAs (miRNAs) that are expressed in infected B cells and in some EBV-associated lymphomas. EBV miRNAs are grouped into two clusters located either adjacent to the BHRF1 gene or in introns contained within the viral BART transcripts. To understand the role of the BHRF1 miRNA cluster, we have constructed a virus mutant that lacks all its three members (Δ123) and a revertant virus. Here we show that the B cell transforming capacity of the Δ123 EBV mutant is reduced by more than 20-fold, relative to wild type or revertant viruses. B cells exposed to the knock-out virus displayed slower growth, and exhibited a two-fold reduction in the percentage of cells entering the cell cycle S phase. Furthermore, they displayed higher latent gene expression levels and latent protein production than their wild type counterparts. Therefore, the BHRF1 miRNAs accelerate B cell expansion at lower latent gene expression levels. Thus, this miRNA cluster simultaneously enhances expansion of the virus reservoir and reduces the viral antigenic load, two features that have the potential to facilitate persistence of the virus in the infected host. Thus, the EBV BHRF1 miRNAs may represent new therapeutic targets for the treatment of some EBV-associated lymphomas.

Indexed as

Cell Transformation, ViralBlotting, WesternB-LymphocytesCell CycleCells, CulturedEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHumansKidneyLungLymphomaMicroRNAsMutationReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRNA, ViralBHRF1 protein, Human herpesvirus 4MicroRNAsRNA, MessengerRNA, ViralViral Proteins

Identifiers

PMID21379335
PMCPMC3040666
OpenAlexW2063830630

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.