Evidence map›Paper›PMID 8795620›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996

Selective vulnerability of mouse CNS neurons to latent infection with a neuroattenuated herpes simplex virus-1.

S Kesari, V M Lee, S M Brown, J Q Trojanowski, N W Fraser

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. 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
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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Oncolytic Virotherapy in Solid Tumors: A Current Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
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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 3 countries.

S KesariWistar Institute, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
V M Lee
S M Brown
J Q Trojanowski
N W Fraser
University of Pennsylvania · USInstitute of Virology of the Slovak Academy of Sciences · SKThe Wistar Institute · US

Funding

Gene Transfer to Expression in Neurons In vivoR01NS029390 · NINDS · WISTAR INSTITUTE · PI FRASER, NIGEL WILLIAM · 1991 to 2013
$4.3M
HERPES VIRUS THERAPY FOR EXPERIMENTAL BRAIN TUMORSF30MH010915 · NIMH · WISTAR INSTITUTE · PI KESARI, SANTOSH · 1994 to 1998
–
INTERMEDIATE FILAMENT PROTEINS AS TUMOR MARKERSR01CA036245 · NCI · UNIVERSITY OF PENNSYLVANIA · PI TROJANOWSKI, JOHN Q. · 1985 to 1999
–
NEUROFILAMENT EXPRESSION AND TUMOR PROGRESSIONR37CA036245 · NCI · UNIVERSITY OF PENNSYLVANIA · PI TROJANOWSKI, JOHN Q. · 1987 to 1995
–
NCI NIH HHS CA-36245NIMH NIH HHS F30 MH010915NIMH NIH HHS MH10915NINDS NIH HHS NS29390NINDS NIH HHS R01 NS029390
6 · The paper itself

Abstract

Herpes simplex viruses that lack ICP34.5 are neuroattenuated and are presently being considered for cancer and gene therapy in the nervous system. Previously, we documented the focal presence of the latency-associated transcripts (LATs) in the hippocampi of immunocompromised mice after intracranial (IC) inoculation of an ICP34.5-deficient virus called strain 1716. To characterize further the biological properties of strain 1716 in the CNS of immunocompetent mice, we determined the extent of viral gene expression in different cell types and regions of the CNS after stereotactic IC inoculation of this virus. At survival times of > 30 d after inoculation, we found that (1) infectious virus was not detectable by titration and immunohistochemical studies; (2) neurons harbored virus as demonstrated by the detection of the LATs by in situ hybridization (ISH); (3) transcripts expressed during the lytic cycle of infection were not detected by ISH; and (4) subsets of neurons were selectively vulnerable to latent infection, depending on the site of inoculation. These results suggest that the absence of ICP34.5 does not abrogate latent infection of the CNS by strain 1716. Additional studies of strain 1716 in the model system described here will facilitate the elucidation of the mechanisms that regulate the selective vulnerability of CNS cells to latent viral infection and lead to the development of ICP34.5 mutant viruses as therapeutic vectors for CNS diseases.

Indexed as

Virus LatencyAnimalsBrainDisease SusceptibilityHerpes SimplexImmunocompetenceImmunohistochemistryIn Situ HybridizationMiceMice, Inbred BALB CNeuronsSimplexvirusTranscription, GeneticViral Proteinsgamma 34.5 protein, Human herpesvirus 1Viral Proteins

Identifiers

PMID8795620
PMCPMC6578968
OpenAlexW2121857951

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.