Evidence map›Paper›PMID 11836395›Full record

ArticleJournal of virology2002

Expression of herpes simplex virus ICP0 inhibits the induction of interferon-stimulated genes by viral infection.

Kasey M Eidson, William E Hobbs, Brian J Manning, Paul Carlson, Neal A DeLuca

Abstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

120 citing papers in PubMed, 177 citations in OpenAlex.

  1. Article
  2. IFN-κ directs antiviral immunity in human skin.bioRxiv : the preprint server for biology · 2026
    Article
  3. 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
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Histone deacetylase 4 promotes type I interferon signaling, restricts DNA viruses, and is degraded via vaccinia virus protein C6.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Article
  16. Article
  17. Review
  18. Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019
    Review
  19. Article
  20. Article

60 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Kasey M EidsonDepartment of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
William E Hobbs
Brian J Manning
Paul Carlson
Neal A DeLuca
University of Pittsburgh · US

Funding

Virus-cell Interactions Affecting HSV Gene ExpressionR01AI030612 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Neal A. DeLuca · 1992 to 2026
$9.3M
Virus-cell interactions affecting HSV gene expressionR56AI030612 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DELUCA, NEAL A. · 2021 to 2021
$618k
INNATE IMMUNITYR13AI044812 · NIAID · NEW YORK ACADEMY OF MEDICINE · PI FLEISCHMAN, ALAN R. · 1999 to 1999
–
NIAID NIH HHS AI 30612NIAID NIH HHS AI 44812NIAID NIH HHS R01 AI030612NIAID NIH HHS R56 AI030612
6 · The paper itself

Abstract

The herpes simplex virus type 1 (HSV-1) mutant d109 does not express any of the immediate-early (IE) proteins and persists in cells for a prolonged length of time. As has been shown by Nicholl et al. (J. Gen. Virol. 81:2215-2218, 2000) and Mossman et al. (J. Virol. 75:750-758, 2001) using other mutants defective for IE gene expression, infection with d109 induced the expression of a number of interferon-stimulated genes. Induction of these genes was significantly greater at multiplicities of infection (MOI) of 10 PFU/cell or greater, and the resulting antiviral effect was only seen at MOIs greater than 10 PFU/cell. Using mutants defective for sets of IE genes established that the lack of ICP0 expression was necessary for high levels of interferon-stimulated gene expression in HEL cells. The induction of interferon-stimulated genes by d109 could also be inhibited by infection with an E1-:E3-:E4- adenovirus expressing levels of ICP0 that are comparable to those expressed within the first hour of wild-type virus infection. Lastly, the addition of the proteasome inhibitor MG132 to cells infected with a mutant that expresses ICP0, d106, also resulted in the induction of interferon-stimulated genes. Thus, ICP0 may function through the proteasome very early in HSV infection to inhibit a cellular antiviral response induced by the virion.

Indexed as

AnimalsAntiviral AgentsCells, CulturedChlorocebus aethiopsFibroblastsGene ExpressionGene Expression RegulationHerpes SimplexHerpesvirus 1, HumanHumansImmediate-Early ProteinsInterferonsLungOligonucleotide Array Sequence AnalysisUbiquitin-Protein LigasesVero CellsAntiviral AgentsImmediate-Early ProteinsInterferonsUbiquitin-Protein LigasesVmw110 protein, Human herpesvirus 1

Identifiers

PMID11836395
PMCPMC153810
OpenAlexW2142756909

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.