Evidence map›Paper›PMID 18952891›Full record

ArticleBlood2009

HSV ICP0 recruits USP7 to modulate TLR-mediated innate response.

Sandrine Daubeuf, Divyendu Singh, Yaohong Tan, Hongiu Liu, Howard J Federoff, William J Bowers, Khaled Tolba

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

90 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. USP7 at PML Nuclear Bodies: A Protein Interaction Network Perspective.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. The Small Molecule Compound Eupalinolide B Alleviates Neuropathic Pain by Regulating the USP7/Keap1/Nrf2 Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  7. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  8. Review
  9. Article
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  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

30 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

7 authors at 5 institutions in 2 countries.

Sandrine DaubeufInstitut de Pharmacologie et de Biologie Structurale, Centre National de Recherche Scientifique (CNRS), Unité Mixte de Recherche 5089, Toulouse, France.
Divyendu Singh
Yaohong Tan
Hongiu Liu
Howard J Federoff
William J Bowers
Khaled Tolba
University of Miami · USGeorgetown University Medical Center · USInstitut de Pharmacologie et de Biologie Structurale · FRSylvester Comprehensive Cancer Center · USUniversity of Rochester · US

Funding

NCI NIH HHS R01 CA08798-05
6 · The paper itself

Abstract

Pattern recognition receptors represent the first line of defense against invading pathogens. Herpes simplex virus (HSV) encodes multiple ligands detected by these receptors, yet persists in the majority of infected individuals indicating a breakdown in host defense against the virus. Here we identify a novel mechanism through which HSV immediate-early protein ICP0 inhibits TLR-dependent inflammatory response by blocking NF-kappaB and JNK activation downstream of TLR signal activation. This process depends on ICP0-mediated translocation of USP7 (HAUSP) from the nucleus to cytoplasm. We show that nuclear USP7 migrates to the cytoplasm in response to TLR engagement, a process that contributes to termination of TLR response. Cytoplasmic USP7 binds to and deubiquitinates TRAF6 and IKKgamma, thus terminating TLR-mediated NF-kappaB and JNK activation. These findings suggest that USP7 is part of a negative feedback loop regulating TLR signaling and that ICP0 exploits this physiologic process to attenuate innate response to HSV. ICP0 inhibition of the TLR response serves to uncouple the innate and adaptive immune response, thereby playing a key role in HSV pathogenesis and persistence.

Indexed as

Cells, CulturedHerpes SimplexHumansI-kappa B KinaseImmediate-Early ProteinsImmunity, InnateNF-kappa BProtein BindingProtein Processing, Post-TranslationalProtein TransportTNF Receptor-Associated Factor 6Toll-Like ReceptorsUbiquitinUbiquitin-Protein LigasesUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseI-kappa B KinaseImmediate-Early ProteinsNF-kappa BTNF Receptor-Associated Factor 6Toll-Like ReceptorsUbiquitinUbiquitin-Protein LigasesUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseUSP7 protein, humanVmw110 protein, Human herpesvirus 1

Identifiers

PMID18952891
PMCPMC3401030
OpenAlexW2168837438

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.