Evidence map›Paper›PMID 20668090›Full record

ArticleJournal of virology2010

Cellular microRNAs 200b and 429 regulate the Epstein-Barr virus switch between latency and lytic replication.

Amy L Ellis-Connell, Tawin Iempridee, Iris Xu, Janet E Mertz

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.6field-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

60 citing papers in PubMed, 87 citations in OpenAlex.

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  14. miRNAs: The Key Regulator of COVID-19 Disease.International journal of cell biology · 2022
    Review
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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

4 authors at 1 institution in 1 country.

Amy L Ellis-ConnellMcArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA.
Tawin Iempridee
Iris Xu
Janet E Mertz
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
BAYESIAN MODELING AND DATA INTEGRATION IN INFECTIOUS DISEASE PHYLODYNAMICSR01AI107034 · NIAID · UNIVERSITY OF WASHINGTON · PI MININ, VOLODYMYR · 2013 to 2017
$1.7M
NCI NIH HHS P01 CA022443NCI NIH HHS P01 CA22443NCI NIH HHS P30 CA014520NCI NIH HHS P30 CA14520NCI NIH HHS T32 CA009135NCI NIH HHS T32 CA09135NIAID NIH HHS R01 AI107034
6 · The paper itself

Abstract

We previously showed that the cellular proteins ZEB1 and ZEB2/SIP1 both play key roles in regulating the latent-lytic switch of Epstein-Barr Virus (EBV) by repressing BZLF1 gene expression. We investigated here the effects of cellular microRNA (miRNA) 200 (miR200) family members on the EBV infection status of cells. We show that miR200b and miR429, but not miR200a, can induce EBV-positive cells into lytic replication by downregulating expression of ZEB1 and ZEB2, leading to production of infectious virus. The levels of miR200 family members in EBV-infected cells strongly negatively correlated with the levels of the ZEBs (e.g., -0.89 [P < 0.001] for miR429 versus ZEB1) and positively correlated with the degree of EBV lytic gene expression (e.g., 0.73 [P < 0.01] for miR429 versus BZLF1). The addition of either miR200b or miR429 to EBV-positive cells led to EBV lytic reactivation in a ZEB-dependent manner; inhibition of these miRNAs led to decreased EBV lytic gene expression. The degree of latent infection by an EBV mutant defective in the primary ZEB-binding site of the EBV BZLF1 promoter was not affected by the addition of these miRNAs. Furthermore, EBV infection of primary blood B cells led to downregulation of these miRNAs and upregulation of ZEB levels. Thus, we conclude that miRNAs 200b and 429 are key regulators via their effects on expression of ZEB1 and ZEB2 of the switch between latent and lytic infection by EBV and, therefore, potential targets for development of new lytic induction therapeutics with which to treat patients with EBV-associated malignancies.

Indexed as

Base SequenceCell LineDNA, ViralDown-RegulationEpstein-Barr Virus InfectionsGenes, ViralHerpesvirus 4, HumanHomeodomain ProteinsHost-Pathogen InteractionsHumansMicroRNAsModels, BiologicalPromoter Regions, GeneticRepressor ProteinsTrans-ActivatorsTranscription FactorsBZLF1 protein, Herpesvirus 4, HumanDNA, ViralHomeodomain ProteinsMicroRNAsMIRN200 microRNA, humanMIRN429 microRNA, humanRepressor ProteinsTrans-ActivatorsTranscription FactorsZEB1 protein, humanZEB2 protein, humanZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2

Identifiers

PMID20668090
PMCPMC2937814
OpenAlexW2120350608

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.