Evidence map›Paper›PMID 20874010›Full record

ReviewJournal of neurovirology2010

Varicella-zoster virus human ganglionic latency: a current summary.

Peter G E Kennedy, Randall J Cohrs

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neurovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Rare complication of varicella-zoster virus infection: a case report of vernet syndrome in clinical and radiological evidence.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2025
    Article
  4. Article
  5. Article
  6. Varicella Zoster Virus Neuronal Latency and Reactivation Modeled in Vitro.Current topics in microbiology and immunology · 2023
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Bilateral herpes zoster in a patient with end-stage kidney disease.International medical case reports journal · 2017
    Article
  15. Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV).Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 2 institutions in 2 countries.

Peter G E KennedyDepartment of Neurology, Glasgow University, Southern General Hospital, Glasgow, Scotland, UK. P.G.Kennedy@clinmed.gla.ac.uk
Randall J Cohrs
Southern General Hospital · GBUniversity of Colorado Denver · US

Funding

VARICELLA ZOSTER VIRUS VASCULOPATHY: CHANGING CLINICAL PRACTICEP01AG032958 · NIA · UNIVERSITY OF COLORADO DENVER · PI COHRS, RANDALL J. · 2009 to 2023
$30.3M
Chief Scientist OfficeNIA NIH HHS AG032958
6 · The paper itself

Abstract

Varicella-zoster virus (VZV) is a ubiquitous human herpes virus typically acquired in childhood when it causes varicella (chickenpox), following which the virus establishes a latent infection in trigeminal and dorsal root ganglia that lasts for the life of the individual. VZV subsequently reactivates, spontaneously or after specific triggering factors, to cause herpes zoster (shingles), which may be complicated by postherpetic neuralgia and several other neurological complications including vasculopathy. Our understanding of VZV latency lags behind our knowledge of herpes simplex virus type 1 (HSV-1) latency primarily due to the difficulty in propagating the virus to high titers in a cell-free state, and the lack of a suitable small-animal model for studying virus latency and reactivation. It is now established beyond doubt that latent VZV is predominantly located in human ganglionic neurons. Virus gene transcription during latency is epigenetically regulated, and appears to be restricted to expression of at least six genes, with expression of gene 63 being the hallmark of latency. However, viral gene transcription may be more extensive than previously thought. There is also evidence for several VZV genes being expressed at the protein level, including VZV gene 63-encoded protein, but recent evidence suggests that this may not be a common event. The nature and extent of the chronic inflammatory response in latently infected ganglia is also of current interest. There remain several questions concerning the VZV latency process that still need to be resolved unambiguously and it is likely that this will require the use of newly developed molecular technologies, such as GeXPS multiplex polymerase chain reaction (PCR) for virus transcriptional analysis and ChIP-seq to study the epigenetic of latent virus genome ( Liu et al, 2010 , BMC Biol 8: 56).

Indexed as

EpigenomicsChickenpoxDNA, ViralGanglia, SpinalGene Expression Regulation, ViralGenes, ViralHerpesvirus 3, HumanHerpes ZosterHumansNeuralgia, PostherpeticNeuronsSequence Analysis, DNAVirus LatencyDNA, Viral

Identifiers

PMID20874010
OpenAlexW2133803184

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.