Evidence map›Paper›PMID 16051826›Full record

ArticleJournal of virology2005

Gamma interferon can block herpes simplex virus type 1 reactivation from latency, even in the presence of late gene expression.

Vilma Decman, Paul R Kinchington, Stephen A K Harvey, Robert L Hendricks

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
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  14. Persistent Herpes Simplex Virus Type 1 Infection of Enteric Neurons Triggers CD8Frontiers in cellular and infection microbiology · 2021
    Article
  15. Article
  16. Article
  17. Herpes Simplex Virus 1-Specific CD8Journal of virology · 2020
    Article
  18. Article
  19. Review
  20. Review

24 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

4 authors at 2 institutions in 2 countries.

Vilma DecmanUniversity of Pittsburgh, Department of Ophthalmology, 203 Lothrop Street, Pittsburgh, PA 15213, USA.
Paul R Kinchington
Stephen A K Harvey
Robert L Hendricks
Institute of Immunology · HRUniversity of Pittsburgh · US

Funding

Virus Production and Manipulation of Protein/Gene Expression ModuleP30EY008098 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Ethan A Rossi · 1989 to 2026
$17.8M
ROLE OF CYTOTOXIC LYMPHOCYTES IN HSV-1 CORNEAL LESIONSR01EY005945 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HENDRICKS, ROBERT L · 1986 to 2017
$8.3M
Gene Expression in HSV-1 Latency After Corneal InfectionR01EY015291 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KINCHINGTON, PAUL R. · 2004 to 2013
$2.9M
NEI NIH HHS EY005945NEI NIH HHS EY008098NEI NIH HHS EY015291NEI NIH HHS P30 EY008098NEI NIH HHS R01 EY005945NEI NIH HHS R01 EY015291
6 · The paper itself

Abstract

Herpes simplex virus type 1 (HSV-1)-specific CD8+ T cells and the cytokine gamma interferon (IFN-gamma) are persistently present in trigeminal ganglia (TG) harboring latent HSV-1. We define "latency" as the retention of functional viral genomes in sensory neurons without the production of infectious virions and "reactivation" as a multistep process leading from latency to virion assembly. CD8+ T cells can block HSV-1 reactivation in ex vivo mouse TG cultures and appear to be the sole source of IFN-gamma in these cultures. Here we demonstrate that IFN-gamma alone can block HSV-1 reactivation in some latently infected neurons, and we identify points of intervention in the life cycle of the reactivating virus. Cell suspensions of TG that were latently infected with recombinant RE HSV-1 expressing enhanced green fluorescent protein from the promoter for infected cell protein 0 (ICP0) or glycoprotein C (gC) were depleted of endogenous CD8+ or CD45+ cells and cultured in the presence or absence of IFN-gamma. Our results demonstrate that IFN-gamma acts on latently infected neurons to inhibit (i) HSV-1 reactivation, (ii) ICP0 promoter activity, (iii) gC promoter activity, and (iv) reactivation in neurons in which the ICP0 or gC promoter is active. Interestingly, we detected transcripts for ICP0, ICP4, and gH in neurons that expressed the ICP0 promoter but were prevented by IFN-gamma from reactivation and virion formation. Thus, the IFN-gamma blockade of HSV-1 reactivation from latency in neurons is associated with an inhibition of the expression of the ICP0 gene (required for reactivation) and a blockade of a step that occurs after the expression of at least some viral structural genes.

Indexed as

AnimalsAntiviral AgentsFemaleHerpesvirus 1, HumanImmediate-Early ProteinsInterferon-gammaMiceMice, Inbred BALB CPromoter Regions, GeneticUbiquitin-Protein LigasesVirus ActivationVirus LatencyVirus ReplicationAntiviral AgentsImmediate-Early ProteinsInterferon-gammaUbiquitin-Protein LigasesVmw110 protein, Human herpesvirus 1

Identifiers

PMID16051826
PMCPMC1182646
OpenAlexW2131585285

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.