Evidence map›Paper›PMID 31682228›Full record

ArticleeLife2019

IFI16, a nuclear innate immune DNA sensor, mediates epigenetic silencing of herpesvirus genomes by its association with H3K9 methyltransferases SUV39H1 and GLP.

Arunava Roy, Anandita Ghosh, Binod Kumar, Bala Chandran

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 54 citations in OpenAlex.

  1. Epigenetic regulation of transgenes.Journal of biotechnology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. mViruses · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. The Role of Protein Methyltransferases in Immunity.Molecules (Basel, Switzerland) · 2024
    Review
  12. Review
  13. Nuclear interferon-stimulated gene product maintains heterochromatin on the herpes simplex viral genome to limit lytic infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. NAT10-dependent NNature communications · 2023
    Article
  15. Review
  16. RNF213 modulates γ-herpesvirus infection and reactivation via targeting the viral Replication and Transcription Activator.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Article
  18. Review
  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

4 authors at 2 institutions in 1 country.

Arunava RoyDepartment of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, United States.ORCID 0000-0002-8486-0539
Anandita GhoshDepartment of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, United States.
Binod KumarDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, United States.
Bala ChandranDepartment of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, United States.ORCID 0000-0002-5319-8714
University of South Florida · USRosalind Franklin University of Medicine and Science · US

Funding

KSHV interactions with host nuclear innate response componentsR01CA180758 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI CHANDRAN, BALA · 2014 to 2023
$3.4M
NCI NIH HHS R01 CA180758Public Health Institute CA 180758University of South Florida Start-up fund
6 · The paper itself

Abstract

IFI16, an innate immune DNA sensor, recognizes the nuclear episomal herpes viral genomes and induces the inflammasome and interferon-β responses. IFI16 also regulates cellular transcription and act as a DNA virus restriction factor. IFI16 knockdown disrupted the latency of Kaposi's sarcoma associated herpesvirus (KSHV) and induced lytic transcripts. However, the mechanism of IFI16's transcription regulation is unknown. Here, we show that IFI16 is in complex with the H3K9 methyltransferase SUV39H1 and GLP and recruits them to the KSHV genome during de novo infection and latency. The resulting depositions of H3K9me2/me3 serve as a docking site for the heterochromatin-inducing HP1α protein leading into the IFI16-dependent epigenetic modifications and silencing of KSHV lytic genes. These studies suggest that IFI16's interaction with H3K9MTases is one of the potential mechanisms by which IFI16 regulates transcription and establish an important paradigm of an innate immune sensor's involvement in epigenetic silencing of foreign DNA.

Indexed as

Epigenesis, GeneticImmunity, InnateAutoantigensCell LineChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA, ViralGene SilencingGenes, ViralGolgi Matrix ProteinsHerpesvirus 8, HumanHumansMethyltransferasesNuclear ProteinsPhosphoproteinsProtein BindingAutoantigensCBX5 protein, humanChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA, ViralGOLGA6A protein, humanGolgi Matrix ProteinsIFI16 protein, humanMethyltransferasesNuclear ProteinsPhosphoproteinsRepressor ProteinsSUV39H1 protein, humanchromosomesepigenetic silencinggene expressionhost methyltransferasesIFI16IFI16 and KSHV gene silencinginfectious diseaseinnate sensingKSHV epigeneticsKSHV latencymicrobiologyvirus

Identifiers

PMID31682228
PMCPMC6855800
OpenAlexW2986656182

What Socratic 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 Socratic graph.