Evidence map›Paper›PMID 21081904›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2011

HSV delivery of a ligand-regulated endogenous ion channel gene to sensory neurons results in pain control following channel activation.

James R Goss, Michael Cascio, William F Goins, Shaohua Huang, David M Krisky, Richard J Clarke, Jon W Johnson, Hitoshi Yokoyama, Naoki Yoshimura, Michael S Gold and 1 more

Abstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Gene Therapy Leaves a Vicious Cycle.Frontiers in oncology · 2019
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. 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

11 authors.

James R GossDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15219, USA.
Michael Cascio
William F Goins
Shaohua Huang
David M Krisky
Richard J Clarke
Jon W Johnson
Hitoshi Yokoyama
Naoki Yoshimura
Michael S Gold
Joseph C Glorioso

Funding

PRE-CLINICAL VECTOR PRODUCTIONP01DK044935 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GLORIOSO, JOSEPH C · 1993 to 2010
$11.8M
Mechanisms and Treatment of Dental PainR01DE018252 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOLD, MICHAEL S · 2009 to 2013
$2.4M
Determination of Glycine Receptor Structure Using FT-ESRR01NS053788 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAXENA, SUNIL K · 2007 to 2011
$1.5M
Inflammation-induced changes in spinal GABA-A receptor signalingR01NS063010 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOLD, MICHAEL S · 2009 to 2011
$1.1M
NIDCR NIH HHS R01 DE018252NIDDK NIH HHS P01 DK044935NINDS NIH HHS R01 NS053788NINDS NIH HHS R01 NS063010PHS HHS R01
6 · The paper itself

Abstract

Persistent pain remains a tremendous health problem due to both its prevalence and dearth of effective therapeutic interventions. To maximize pain relief while minimizing side effects, current gene therapy-based approaches have mostly exploited the expression of pain inhibitory products or interfered with pronociceptive ion channels. These methods do not enable control over the timing or duration of analgesia, nor titration to analgesic efficacy. Here, we describe a gene therapy strategy that potentially overcomes these limitations by providing exquisite control over therapy with efficacy in clinically relevant models of inflammatory pain. We utilize a herpes simplex viral (HSV) vector (vHGlyRα1) to express a ligand-regulated chloride ion channel, the glycine receptor (GlyR) in targeted sensory afferents; the subsequent exogenous addition of glycine provides the means for temporal and spatial control of afferent activity, and therefore pain. Use of an endogenous inhibitory receptor not normally present on sensory neurons both minimizes immunogenicity and maximizes therapeutic selectivity.

Indexed as

Genetic VectorsGene Transfer TechniquesPain ManagementReceptors, GlycineSensory Receptor CellsSimplexvirusAnimalsDisease Models, AnimalDose-Response Relationship, DrugFemaleGene Expression RegulationGene OrderGenetic TherapyGlycineHEK293 CellsHumansGlycineLigandsReceptors, Glycine

Identifiers

PMID21081904
PMCPMC3048176

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.