Evidence map›Paper›PMID 30871003›Full record

ArticleViruses2019

Interferon-Independent Upregulation of Interferon-Stimulated Genes during Human Cytomegalovirus Infection is Dependent on IRF3 Expression.

Caroline L Ashley, Allison Abendroth, Brian P McSharry, Barry Slobedman

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Dual regulation of antiviral IFN response byJournal of pharmaceutical analysis · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. CD8Viruses · 2024
    Article
  20. iScience · 2024
    Article

11 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

4 authors at 1 institution in 1 country.

Caroline L AshleyDepartment of Infectious Diseases and Immunology, Charles Perkins Centre, University of Sydney, Camperdown, New South Wales 2050, Australia. cash7683@uni.sydney.edu.au.ORCID 0000-0001-8355-8891
Allison AbendrothDepartment of Infectious Diseases and Immunology, Charles Perkins Centre, University of Sydney, Camperdown, New South Wales 2050, Australia. allison.abendroth@sydney.edu.au.
Brian P McSharryDepartment of Infectious Diseases and Immunology, Charles Perkins Centre, University of Sydney, Camperdown, New South Wales 2050, Australia. brian.mcsharry@sydney.edu.au.
Barry SlobedmanDepartment of Infectious Diseases and Immunology, Charles Perkins Centre, University of Sydney, Camperdown, New South Wales 2050, Australia. barry.slobedman@sydney.edu.au.ORCID 0000-0002-9431-6094
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antiviral activity of type I interferons (IFNs) is primarily mediated by interferon-stimulated genes (ISGs). Induction of ISG transcription is achieved when type I IFNs bind to their cognate receptor and activate the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signaling pathways. Recently it has become clear that a number of viruses are capable of directly upregulating a subset of ISGs in the absence of type I IFN production. Using cells engineered to block either the response to, or production of type I IFN, the regulation of IFN-independent ISGs was examined in the context of human cytomegalovirus (HCMV) infection. Several ISGs, including IFIT1, IFIT2, IFIT3, Mx1, Mx2, CXCL10 and ISG15 were found to be upregulated transcriptionally following HCMV infection independently of type I IFN-initiated JAK-STAT signaling, but dependent on intact IRF3 signaling. ISG15 protein regulation mirrored that of its transcript with IFNβ neutralization failing to completely inhibit ISG15 expression post HCMV infection. In addition, no detectable ISG15 protein expression was observed following HCMV infection in IRF3 knockdown CRISPR/Cas-9 clones indicating that IFN-independent control of ISG expression during HCMV infection of human fibroblasts is absolutely dependent on IRF3 expression.

Indexed as

Immunity, InnateSignal TransductionCells, CulturedCytokinesCytomegalovirusFibroblastsGene Knockdown TechniquesHEK293 CellsHumansInterferon-betaInterferon Regulatory Factor-3InterferonsReal-Time Polymerase Chain ReactionUbiquitinsUp-RegulationCytokinesInterferon-betaInterferon Regulatory Factor-3InterferonsIRF3 protein, humanISG15 protein, humanUbiquitinshuman cytomegalovirusinterferoninterferon stimulated genesIRF3ISG15

Identifiers

PMID30871003
PMCPMC6466086
OpenAlexW2922286507

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.