Evidence map›Paper›PMID 32232535›Full record

ReviewSeminars in immunopathology2020

Epigenetic lifestyle of Epstein-Barr virus.

Alexander Buschle, Wolfgang Hammerschmidt

Abstract readReview
In one paragraph

Review in Seminars in immunopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing 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

74 citing papers in PubMed.

  1. Article
  2. Article
  3. Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025
    Article
  16. Arginine Metabolism SupportsbioRxiv : the preprint server for biology · 2025
    Article
  17. Article
  18. Review
  19. Article
  20. Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025
    Article

14 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

2 authors.

Alexander BuschleResearch Unit Gene Vectors, Helmholtz Zentrum München, German Research Center for Environmental Health and German Centre for Infection Research (DZIF), Partner site Munich, Marchioninistr. 25, D-81377, Munich, Germany.ORCID 0000-0001-6126-514X
Wolfgang HammerschmidtResearch Unit Gene Vectors, Helmholtz Zentrum München, German Research Center for Environmental Health and German Centre for Infection Research (DZIF), Partner site Munich, Marchioninistr. 25, D-81377, Munich, Germany. hammerschmidt@helmholtz-muenchen.de.ORCID 0000-0002-4659-0427

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is a model of herpesvirus latency and epigenetic changes. The virus preferentially infects human B-lymphocytes (and also other cell types) but does not turn them straight into virus factories. Instead, it establishes a strictly latent infection in them and concomitantly induces the activation and proliferation of infected B cells. How the virus establishes latency in its target cells is only partially understood, but its latent state has been studied intensively by many. During latency, several copies of the viral genome are maintained as minichromosomes in the nucleus. In latently infected cells, most viral genes are epigenetically repressed by cellular chromatin constituents and DNA methylation, but certain EBV genes are spared and remain expressed to support the latent state of the virus in its host cell. Latency is not a dead end, but the virus can escape from this state and reactivate. Reactivation is a coordinated process that requires the removal of repressive chromatin components and a gain in accessibility for viral and cellular factors and machines to support the entire transcriptional program of EBV's ensuing lytic phase. We have a detailed picture of the initiating events of EBV's lytic phase, which are orchestrated by a single viral protein - BZLF1. Its induced expression can lead to the expression of all lytic viral proteins, but initially it fosters the non-licensed amplification of viral DNA that is incorporated into preformed capsids. In the virions, the viral DNA is free of histones and lacks methylated cytosine residues which are lost during lytic DNA amplification. This review provides an overview of EBV's dynamic epigenetic changes, which are an integral part of its ingenious lifestyle in human host cells.

Indexed as

Epstein-Barr Virus InfectionsHerpesvirus 4, HumanEpigenesis, GeneticGene Expression Regulation, ViralHumansLife StyleVirus LatencyChromatinHerpesvirusInfectionLatencyReactivation

Identifiers

PMID32232535
PMCPMC7174264

What OpenQuestion holds

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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.