Evidence map›Paper›PMID 28249048›Full record

ArticlePLoS pathogens2017

Chloroquine triggers Epstein-Barr virus replication through phosphorylation of KAP1/TRIM28 in Burkitt lymphoma cells.

Xiaofan Li, Eric M Burton, Sumita Bhaduri-McIntosh

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.4field-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

53 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Insights into the protein domains of C-VI TRIM subfamily in viral infection.Frontiers in cellular and infection microbiology · 2025
    Review
  10. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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 1 institution in 1 country.

Xiaofan LiDivision of Infectious Diseases, Department of Pediatrics, Stony Brook University School of Medicine, Stony Brook, NY, United States of America.
Eric M BurtonDepartment of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY, United States of America.ORCID 0000-0002-2432-2288
Sumita Bhaduri-McIntoshDivision of Infectious Diseases, Department of Pediatrics, Stony Brook University School of Medicine, Stony Brook, NY, United States of America.ORCID 0000-0003-2946-9497
Stony Brook University · US

Funding

MOLECULAR AND CELL BIOLOGY OF INFECTIOUS DISEASEST32AI007539 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI KONOPKA, JAMES B · 1998 to 2023
$3.6M
Host determinants of Epstein-Barr virus lytic cycle activationR01AI113134 · NIAID · UNIVERSITY OF FLORIDA · PI BHADURI-MCINTOSH, SUMITA · 2014 to 2018
$1.9M
NIAID NIH HHS R01 AI113134NIAID NIH HHS T32 AI007539
6 · The paper itself

Abstract

Trials to reintroduce chloroquine into regions of Africa where P. falciparum has regained susceptibility to chloroquine are underway. However, there are long-standing concerns about whether chloroquine increases lytic-replication of Epstein-Barr virus (EBV), thereby contributing to the development of endemic Burkitt lymphoma. We report that chloroquine indeed drives EBV replication by linking the DNA repair machinery to chromatin remodeling-mediated transcriptional repression. Specifically, chloroquine utilizes ataxia telangiectasia mutated (ATM) to phosphorylate the universal transcriptional corepressor Krüppel-associated Box-associated protein 1/tripartite motif-containing protein 28 (KAP1/TRIM28) at serine 824 -a mechanism that typically facilitates repair of double-strand breaks in heterochromatin, to instead activate EBV. Notably, activation of ATM occurs in the absence of detectable DNA damage. These findings i) clarify chloroquine's effect on EBV replication, ii) should energize field investigations into the connection between chloroquine and endemic Burkitt lymphoma and iii) provide a unique context in which ATM modifies KAP1 to regulate persistence of a herpesvirus in humans.

Indexed as

AntimalarialsAtaxia Telangiectasia Mutated ProteinsBurkitt LymphomaCell Line, TumorChloroquineFlow CytometryFluorescent Antibody TechniqueHerpesvirus 4, HumanHumansImmunoblottingImmunoprecipitationPhosphorylationPolymerase Chain ReactionRepressor ProteinsRNA, Small InterferingTransfectionAntimalarialsAtaxia Telangiectasia Mutated ProteinsChloroquineRepressor ProteinsRNA, Small InterferingTRIM28 protein, humanTripartite Motif-Containing Protein 28

Identifiers

PMID28249048
PMCPMC5348047
OpenAlexW2593244834

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.