Evidence map›Paper›PMID 27348612›Full record

ArticlePLoS pathogens2016

An Epstein-Barr Virus-Encoded Protein Complex Requires an Origin of Lytic Replication In Cis to Mediate Late Gene Transcription.

Reza Djavadian, Ya-Fang Chiu, Eric Johannsen

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025
    Article
  6. Arginine Metabolism SupportsbioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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

3 authors at 2 institutions in 2 countries.

Reza DjavadianDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America.
Ya-Fang ChiuDepartment of Oncology (McArdle Laboratory for Cancer Research), University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America.
Eric JohannsenDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America.
University of Wisconsin–Madison · USChang Gung University · TW

Funding

Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
Virology Training ProgramT32AI078985 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2009 to 2018
$3.3M
Epigenetic determinants of Epstein-Barr virus and cellular DNA in oral diseasesR01DE023939 · NIDCR · UNIVERSITY OF WISCONSIN-MADISON · PI JOHANNSEN, ERIC C, KENNEY, SHANNON CELESTE · 2013 to 2017
$2.9M
NCI NIH HHS P01 CA022443NIAID NIH HHS T32 AI078985NIDCR NIH HHS R01 DE023939
6 · The paper itself

Abstract

Epstein-Barr virus lytic replication is accomplished by an intricate cascade of gene expression that integrates viral DNA replication and structural protein synthesis. Most genes encoding structural proteins exhibit "true" late kinetics-their expression is strictly dependent on lytic DNA replication. Recently, the EBV BcRF1 gene was reported to encode a TATA box binding protein homolog, which preferentially recognizes the TATT sequence found in true late gene promoters. BcRF1 is one of seven EBV genes with homologs found in other β- and γ-, but not in α-herpesviruses. Using EBV BACmids, we systematically disrupted each of these "βγ" genes. We found that six of them, including BcRF1, exhibited an identical phenotype: intact viral DNA replication with loss of late gene expression. The proteins encoded by these six genes have been found by other investigators to form a viral protein complex that is essential for activation of TATT-containing reporters in EBV-negative 293 cells. Unexpectedly, in EBV infected 293 cells, we found that TATT reporter activation was weak and non-specific unless an EBV origin of lytic replication (OriLyt) was present in cis. Using two different replication-defective EBV genomes, we demonstrated that OriLyt-mediated DNA replication is required in cis for TATT reporter activation and for late gene expression from the EBV genome. We further demonstrate by fluorescence in situ hybridization that the late BcLF1 mRNA localizes to EBV DNA replication factories. These findings support a model in which EBV true late genes are only transcribed from newly replicated viral genomes.

Indexed as

DNA ReplicationDNA, ViralGene Expression Regulation, ViralGenes, ViralHEK293 CellsHerpesvirus 4, HumanHumansImmunoblottingIn Situ Hybridization, FluorescencePolymerase Chain ReactionReplication OriginTranscription, GeneticVirus ReplicationDNA, Viral

Identifiers

PMID27348612
PMCPMC4922670
OpenAlexW2467918292

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.