Evidence map›Paper›PMID 28100608›Full record

ArticleJournal of virology2017

Herpes Simplex Virus 1 UL24 Abrogates the DNA Sensing Signal Pathway by Inhibiting NF-κB Activation.

Haiyan Xu, Chenhe Su, Angela Pearson, Christopher H Mody, Chunfu Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 115 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Comparative Review of the Conserved UL24 Protein Family in Herpesviruses.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Microbial infections in burn patients.Acute and critical care · 2024
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

20 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 3 institutions in 2 countries.

Haiyan XuSoochow University, Institutes of Biology and Medical Sciences, Suzhou, China.
Chenhe SuSoochow University, Institutes of Biology and Medical Sciences, Suzhou, China.
Angela PearsonUniversité INRS, INRS-Institut Armand-Frappier, Laval, Québec, Canada.
Christopher H ModyDepartment of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, AB, Canada.ORCID http://orcid.org/0000-0001-7264-3679
Chunfu ZhengSoochow University, Institutes of Biology and Medical Sciences, Suzhou, China zheng.alan@hotmail.com.
Soochow University · CNUniversity of Calgary · CAInstitut National de la Recherche Scientifique · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclic GMP-AMP synthase (cGAS) is a newly identified DNA sensor that recognizes foreign DNA, including the genome of herpes simplex virus 1 (HSV-1). Upon binding of viral DNA, cGAS produces cyclic GMP-AMP, which interacts with and activates stimulator of interferon genes (STING) to trigger the transcription of antiviral genes such as type I interferons (IFNs), and the production of inflammatory cytokines. HSV-1 UL24 is widely conserved among members of the herpesviruses family and is essential for efficient viral replication. In this study, we found that ectopically expressed UL24 could inhibit cGAS-STING-mediated promoter activation of IFN-β and interleukin-6 (IL-6), and UL24 also inhibited interferon-stimulatory DNA-mediated IFN-β and IL-6 production during HSV-1 infection. Furthermore, UL24 selectively blocked nuclear factor κB (NF-κB) but not IFN-regulatory factor 3 promoter activation. Coimmunoprecipitation analysis demonstrated that UL24 bound to the endogenous NF-κB subunits p65 and p50 in HSV-1-infected cells, and UL24 was also found to bind the Rel homology domains (RHDs) of these subunits. Furthermore, UL24 reduced the tumor necrosis factor alpha (TNF-α)-mediated nuclear translocation of p65 and p50. Finally, mutational analysis revealed that the region spanning amino acids (aa) 74 to 134 of UL24 [UL24(74-134)] is responsible for inhibiting cGAS-STING-mediated NF-κB promoter activity. For the first time, UL24 was shown to play an important role in immune evasion during HSV-1 infection.

Indexed as

Signal TransductionActive Transport, Cell NucleusAnimalsChlorocebus aethiopsGene Expression Regulation, ViralHEK293 CellsHeLa CellsHerpesvirus 1, HumanHost-Pathogen InteractionsHumansInterferon-betaInterleukin-6NF-kappa B p50 SubunitPromoter Regions, GeneticProtein BindingProtein Interaction Domains and MotifsIL6 protein, humanInterferon-betaInterleukin-6NF-kappa B p50 SubunitRELA protein, humanTranscription Factor RelAUL24 protein, Human herpesvirus 1Viral ProteinsDNA sensorHSV-1NF-κBp65UL24

Identifiers

PMID28100608
PMCPMC5355614
OpenAlexW2577626296

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.