Evidence map›Paper›PMID 42410445›Full record

ReviewClinical epigenetics2026

Epstein-Barr Virus-host epigenetic interplay: mechanisms of regulation and therapeutic potential.

Sanaz Baghban Rahimi, Ahmad Hosseinzadeh Adli, Hossein Bannazadeh Baghi, Vahdat Poortahmasebi, Jamal Sarvari

Abstract readReview
In one paragraph

Review in Clinical epigenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Sanaz Baghban RahimiDepartment of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Ahmad Hosseinzadeh AdliDepartment of Microbiology and Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Hossein Bannazadeh BaghiDepartment of Microbiology and Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Vahdat PoortahmasebiDepartment of Microbiology and Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Jamal SarvariDepartment of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. sarvarij@sums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Epstein-Barr virus (EBV) has evolved complex mechanisms to manipulate the host immune system and epigenetic machinery, enabling it to establish lifelong latent infection within host cells. Emerging evidence strongly indicates that the EBV acts as a main epigenetic manipulator by silencing host regulatory genes, altering host chromatin landscapes and exploiting B-cell biology. Key mechanisms include viral-mediated recruitment of host DNA methyltransferases and histone-modifying enzymes; modulation of host non-coding RNAs and chromatin architectural factors; and targeted disruption of interferon signaling through RNA methylation and restructuring of host chromatin. These integrated processes allow EBV to maintain a lifelong infection in humans, evade both innate and adaptive immunity, and respond to reactivation signals. Understanding the virus-host epigenetic interplay offers new opportunities for therapeutic interventions targeting epigenetic regulators in EBV-associated diseases.

Indexed as

Epigenesis, GeneticEpstein-Barr Virus InfectionsHerpesvirus 4, HumanChromatinDNA MethylationHost-Pathogen InteractionsHumansChromatinEpigeneticEpstein–Barr virusTherapeutic potential

Identifiers

PMID42410445
PMCPMC13617722

What Socratic 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 Socratic graph.