Evidence map›Paper›PMID 9227860›Full record

ReviewClinical microbiology reviews1997

Experimental investigation of herpes simplex virus latency.

E K Wagner, D C Bloom

Open access · greenAbstract readReview
In one paragraph

Review in Clinical microbiology reviews, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 275 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. MicroRNAs: Harbingers and shapers of periodontal inflammation.Seminars in cell & developmental biology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Herpes Simplex Virus 1 Strains 17Journal of virology · 2020
    Article
  14. Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020
    Review
  15. Article
  16. Article
  17. MicroRNA Involvement in Signaling Pathways During Viral Infection.Frontiers in cell and developmental biology · 2020
    Review
  18. Article
  19. Review
  20. [Mechanisms of herpes simplex virus latency and reactivation].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019
    Review

77 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

2 authors at 1 institution in 1 country.

E K WagnerDepartment of Molecular Biology and Biochemistry, University of California, Irvine 92697-3900, USA. Ewagner@uci.edu
D C Bloom
University of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical manifestations of herpes simplex virus infection generally involve a mild and localized primary infection followed by asymptomatic (latent) infection interrupted sporadically by periods of recrudescence (reactivation) where virus replication and associated cytopathologic findings are manifest at the site of initial infection. During the latent phase of infection, viral genomes, but not infectious virus itself, can be detected in sensory and autonomic neurons. The process of latent infection and reactivation has been subject to continuing investigation in animal models and, more recently, in cultured cells. The initiation and maintenance of latent infection in neurons are apparently passive phenomena in that no virus gene products need be expressed or are required. Despite this, a single latency-associated transcript (LAT) encoded by DNA encompassing about 6% of the viral genome is expressed during latent infection in a minority of neurons containing viral DNA. This transcript is spliced, and the intron derived from this splicing is stably maintained in the nucleus of neurons expressing it. Reactivation, which can be induced by stress and assayed in several animal models, is facilitated by the expression of LAT. Although the mechanism of action of LAT-mediated facilitation of reactivation is not clear, all available evidence argues against its involving the expression of a protein. Rather, the most consistent models of action involve LAT expression playing a cis-acting role in a very early stage of the reactivation process.

Indexed as

AnimalsDisease Models, AnimalEncephalitisGene Expression Regulation, ViralHerpes SimplexHerpesvirus 3, HumanHumansIn Situ Hybridization, FluorescenceMiceNeuronsPromoter Regions, GeneticRabbitsSimplexvirusVirus ActivationVirus Latency

Identifiers

PMID9227860
PMCPMC172928
OpenAlexW2163424373

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.