Evidence map›Paper›PMID 37883416›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Nuclear interferon-stimulated gene product maintains heterochromatin on the herpes simplex viral genome to limit lytic infection.

Catherine N Sodroski, David M Knipe

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Expulsion of nuclear DNA to the cytoplasm after viral entry: A mechanism for activation of the cGAS pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  17. QnAs with David M. Knipe.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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

2 authors at 1 institution in 1 country.

Catherine N SodroskiDepartment of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
David M KnipeDepartment of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.ORCID 0000-0003-1554-6236
Harvard University · US

Funding

Nuclear Sensing of Herpesviral DNAR01AI106934 · NIAID · HARVARD MEDICAL SCHOOL · PI KNIPE, DAVID M. · 2014 to 2021
$3.8M
Nuclear Sensing of Herpesviral DNAR56AI106934 · NIAID · HARVARD MEDICAL SCHOOL · PI KNIPE, DAVID M. · 2024 to 2024
$587k
Incorporation of a histone variant into viral chromatin to promote herpes simplex virus replicationF31AI145062 · NIAID · HARVARD MEDICAL SCHOOL · PI SODROSKI, CATHERINE · 2019 to 2022
$105k
NIAID NIH HHS F31 AI145062NIAID NIH HHS R01 AI106934NIAID NIH HHS R56 AI106934
6 · The paper itself

Abstract

Interferons (IFN) are expressed in and secreted from cells in response to virus infection, and they induce the expression of a variety of genes called interferon-stimulated genes (ISGs) in infected and surrounding cells to block viral infection and limit spread. The mechanisms of action of a number of cytoplasmic ISGs have been well defined, but little is known about the mechanism of action of nuclear ISGs. Constitutive levels of nuclear interferon-inducible protein 16 (IFI16) serve to induce innate signaling and epigenetic silencing of herpes simplex virus (HSV), but only when the HSV infected cell protein 0 (ICP0) E3 ligase, which promotes IFI16 degradation, is inactivated. In this study, we found that following IFN induction, the pool of IFI16 within the infected cell remains high and can restrict wild-type viral gene expression and replication due to both the induced levels of IFI16 and the IFI16-mediated repression of ICP0 levels. Restriction of viral gene expression is achieved by IFI16 promoting the maintenance of heterochromatin on the viral genome, which silences it epigenetically. These results indicate that a nuclear ISG can restrict gene expression and replication of a nuclear DNA virus by maintaining or preventing the removal of repressive heterochromatin associated with the viral genome.

Indexed as

Herpes SimplexHerpesvirus 1, HumanGenome, ViralHeterochromatinHumansInterferonsNuclear ProteinsPhosphoproteinsUbiquitin-Protein LigasesVirus ReplicationHeterochromatinInterferonsNuclear ProteinsPhosphoproteinsUbiquitin-Protein Ligasesherpes simplex virusHSVICP0interferonlytic infection

Identifiers

PMID37883416
PMCPMC10636318
OpenAlexW4387952909

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.