Evidence map›Paper›PMID 34960613›Full record

ReviewViruses2021

Molecular Basis of Epstein-Barr Virus Latency Establishment and Lytic Reactivation.

Takayuki Murata, Atsuko Sugimoto, Tomoki Inagaki, Yusuke Yanagi, Takahiro Watanabe, Yoshitaka Sato, Hiroshi Kimura

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
9.3field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 164 citations in OpenAlex.

  1. Review
  2. Review
  3. A tonsil organoid model reveals Epstein-Barr virus-infected germinal center B cell states during primary infection.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026
    Article
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  18. Review
  19. Review
  20. Review

55 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 2 institutions in 2 countries.

Takayuki MurataDepartment of Virology and Parasitology, Fujita Health University School of Medicine, Toyoake 470-1192, Japan.ORCID 0000-0001-7228-0839
Atsuko SugimotoDepartment of Virology and Parasitology, Fujita Health University School of Medicine, Toyoake 470-1192, Japan.
Tomoki InagakiDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yusuke YanagiDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Takahiro WatanabeDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yoshitaka SatoDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-8541-6413
Hiroshi KimuraDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0001-8063-5660
Nagoya University · JPFujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of cancer. Like other herpesviruses, it establishes an asymptomatic, life-long latent infection, with occasional reactivation and shedding of progeny viruses. During latency, EBV expresses a small number of viral genes, and exists as an episome in the host-cell nucleus. Expression patterns of latency genes are dependent on the cell type, time after infection, and milieu of the cell (e.g., germinal center or peripheral blood). Upon lytic induction, expression of the viral immediate-early genes, BZLF1 and BRLF1, are induced, followed by early gene expression, viral DNA replication, late gene expression, and maturation and egress of progeny virions. Furthermore, EBV reactivation involves more than just progeny production. The EBV life cycle is regulated by signal transduction, transcription factors, promoter sequences, epigenetics, and the 3D structure of the genome. In this article, the molecular basis of EBV latency establishment and reactivation is summarized.

Indexed as

Epstein-Barr Virus InfectionsHerpesvirus 4, HumanHumansImmediate-Early ProteinsTrans-ActivatorsVirus ActivationVirus LatencyBRLF1 protein, Human herpesvirus 4BZLF1 protein, Herpesvirus 4, HumanImmediate-Early ProteinsTrans-ActivatorsEBVepigeneticslatencyoncogenesisreactivationtranscription

Identifiers

PMID34960613
PMCPMC8706188
OpenAlexW3217565827

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.