Evidence map›Paper›PMID 31919284›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

A promiscuous inflammasome sparks replication of a common tumor virus.

Eric M Burton, Raphaela Goldbach-Mansky, Sumita Bhaduri-McIntosh

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  12. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  13. Article
  14. Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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 3 institutions in 1 country.

Eric M BurtonDepartment of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794.
Raphaela Goldbach-ManskyTranslational Autoinflammatory Disease Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20852.
Sumita Bhaduri-McIntoshDivision of Infectious Disease, Department of Pediatrics, University of Florida, Gainesville, FL 32610; sbhadurimcintosh@ufl.edu.ORCID 0000-0003-2946-9497
National Institutes of Health · USStony Brook University · USUniversity of Florida · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Pathogenesis, and Outcome of Autoinflammatory Diseases, NOMID/CAPS, DIRA, CANDLE, SAVI, NLRC4-MAS, Stills-like Diseases, and other Undifferentiated Autoinflammatory DiseasesZIAAI001220 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GOLDBACH-MANSKY, RAPHAELA · 2017 to 2025
$22.3M
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
sxRNA-based Antiviral Approach targeting Epstein-Barr virusR41AI115834 · NIAID · HOCUSLOCUS, INC. · PI BHADURI-MCINTOSH, SUMITA · 2015 to 2015
$225k
NCATS NIH HHS UL1 TR001863NIAID NIH HHS R01 AI113134NIAID NIH HHS R41 AI115834NIAID NIH HHS T32 AI007539
6 · The paper itself

Abstract

Viruses activate inflammasomes but then subvert resulting inflammatory responses to avoid elimination. We asked whether viruses could instead use such activated or primed inflammasomes to directly aid their propagation and spread. Since herpesviruses are experts at coopting cellular functions, we investigated whether Epstein-Barr virus (EBV), an oncoherpesvirus, exploits inflammasomes to activate its replicative or lytic phase. Indeed, our experiments reveal that EBV exploits several inflammasome sensors to actually activate its replicative phase from quiescence/latency. In particular, TXNIP, a key inflammasome intermediary, causes assembly of the NLRP3 inflammasome, resulting in caspase-1-mediated depletion of the heterochromatin-inducing epigenetic repressor KAP1/TRIM28 in a subpopulation of cells. As a result, only TXNIP

Indexed as

B-LymphocytesCarrier ProteinsCaspase 1Cell LineGlucoseHerpesvirus 4, HumanHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinOncogenic VirusesTripartite Motif-Containing Protein 28Virus ReplicationCarrier ProteinsCaspase 1GlucoseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanTRIM28 protein, humanTripartite Motif-Containing Protein 28TXNIP protein, humandiabetesEpstein−Barr virusinflammasomeKAP1TXNIP

Identifiers

PMID31919284
PMCPMC6983388
OpenAlexW2998971367

What OpenQuestion 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 OpenQuestion graph.