Evidence map›Paper›PMID 28904192›Full record

ArticleJournal of virology2017

Role of Herpes Simplex Virus 1 γ34.5 in the Regulation of IRF3 Signaling.

Richard Manivanh, Jesse Mehrbach, David M Knipe, David A Leib

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 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.1field-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

49 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  9. Article
  10. Herpes Simplex Virus Neurovirulence Across the Human Lifespan.The Journal of infectious diseases · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Personalizing Oncolytic Immunovirotherapy Approaches.Molecular diagnosis & therapy · 2024
    Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Richard ManivanhDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Jesse MehrbachDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
David M KnipeDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.
David A LeibDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA david.a.leib@dartmouth.edu.
Dartmouth College · USHarvard University · US

Funding

Understanding the role of RNA-binding protein mutations in cancerP20GM113132 · NIGMS · DARTMOUTH COLLEGE · PI MADDEN, DEAN R · 2016 to 2025
$25.9M
VIral and host mechanisms that tilt the HSV lytic/latent balanceP01AI098681 · NIAID · HARVARD MEDICAL SCHOOL · PI PESOLA, JEAN M · 2013 to 2023
$19.2M
VIRAL & HOST FACTORS IN HERPETIC REACTIVATIONR01EY009083 · NEI · WASHINGTON UNIVERSITY · PI David A Leib · 1992 to 2026
$10.3M
IMMUNOBIOLOGY OF MYELOID AND LYMPHOID CELLST32AI007363 · NIAID · DARTMOUTH COLLEGE · PI Claudia V Jakubzick · 1990 to 2026
$9.5M
Nuclear Sensing of Herpesviral DNAR01AI106934 · NIAID · HARVARD MEDICAL SCHOOL · PI KNIPE, DAVID M. · 2014 to 2021
$3.8M
NEI NIH HHS R01 EY009083NIAID NIH HHS P01 AI098681NIAID NIH HHS R01 AI106934NIAID NIH HHS T32 AI007363NIGMS NIH HHS P20 GM113132
6 · The paper itself

Abstract

During viral infection, pattern recognition receptors (PRRs) and their associated adaptors recruit TANK-binding kinase 1 (TBK1) to activate interferon regulatory factor 3 (IRF3), resulting in production of type I interferons (IFNs). ICP0 and ICP34.5 are among the proteins encoded by herpes simplex virus 1 (HSV-1) that modulate type I IFN signaling. We constructed a recombinant virus (ΔXX) that lacks amino acids 87 to 106, a portion of the previously described TBK1-binding domain of the γ34.5 gene (D. Verpooten, Y. Ma, S. Hou, Z. Yan, and B. He, J Biol Chem 284:1097-1105, 2009, https://doi.org/10.1074/JBC.M805905200). These 20 residues are outside the γ34.5 beclin1-binding domain (BBD) that interacts with beclin1 and regulates autophagy. Unexpectedly, ΔXX showed no deficit in replication

Indexed as

Host-Pathogen InteractionsSignal TransductionAnimalsBeclin-1Chlorocebus aethiopsFibroblastsHerpesvirus 1, HumanHumansImmunity, InnateInterferon-betaInterferon Regulatory Factor-3InterferonsMicePhosphorylationProtein Serine-Threonine KinasesVero CellsBeclin-1gamma 34.5 protein, Human herpesvirus 1Interferon-betaInterferon Regulatory Factor-3InterferonsProtein Serine-Threonine KinasesTbk1 protein, mouseViral Proteinsherpes simplex virusICP0ICP34.5innate immunityinterferonsIRF3recombinant virusesRL1TBK1viral pathogenesis

Identifiers

PMID28904192
PMCPMC5686731
OpenAlexW2755779087

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.