Evidence map›Paper›PMID 15507638›Full record

ArticleJournal of virology2004

The herpes simplex virus type 1 latency-associated transcript (LAT) enhancer/rcr is hyperacetylated during latency independently of LAT transcription.

Nicole J Kubat, Antonio L Amelio, Nicole V Giordani, David C Bloom

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

87 citing papers in PubMed, 135 citations in OpenAlex.

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  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

27 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 1 country.

Nicole J KubatDepartment of Molecular Genetics and Microbiology, Box 100266, University of Florida College of Medicine, Gainesville, FL 32610-0266, USA.
Antonio L Amelio
Nicole V Giordani
David C Bloom
Florida College · USUniversity of Florida · US

Funding

Molecular Genetics of HSV ReactivationR01AI048633 · NIAID · UNIVERSITY OF FLORIDA · PI BLOOM, DAVID C. · 2001 to 2023
$7.2M
BASIC MICROBIOLOGY &INFECTIOUS DISEASEST32AI007110 · NIAID · UNIVERSITY OF FLORIDA · PI Stephanie M Karst · 1985 to 2026
$4.3M
NIAID NIH HHS AI 07110NIAID NIH HHS AI 48633NIAID NIH HHS R01 AI048633NIAID NIH HHS T32 AI007110
6 · The paper itself

Abstract

During herpes simplex virus type 1 (HSV-1) latency, only one region of the viral genome is actively transcribed: the region encoding the latency-associated transcript (LAT). A previous study demonstrated that during latency the LAT promoter is hyperacetylated at histone H3 (K9, K14) relative to lytic genes examined. In the present study, we examine the acetylation profile of regions downstream of the LAT promoter during a latent infection of murine dorsal root ganglia. These analyses revealed the following: (i) the region of the genome containing the 5' exon of the LAT primary transcript was at least as enriched in acetylated H3 as the LAT promoter, and (ii) the region of hyperacetylation does not extend to the ICP0 promoter. In order to assess the contribution of LAT transcription to the acetylation of the 5' exon region, the acetylation profile of KOS/29, a recombinant with a deletion of the LAT promoter, was examined. The region containing the 5' exon of KOS/29 was hyperacetylated relative to lytic gene regions in the absence of detectable LAT transcription. These results indicate that the region containing the 5' exon of LAT, known to contain enhancer activities and to be critical for induced reactivation (rcr), exists in a chromatin structure during latency that is distinct from other lytic gene regions. This result suggests a role for the 5' exon LAT enhancer region as a cis-acting regulator of transcription that maintains a transcriptionally permissive chromatin domain in the HSV-1 latent episome.

Indexed as

Transcription, GeneticVirus LatencyAcetylationAnimalsChromatinEnhancer Elements, GeneticExonsFemaleHistonesImmediate-Early ProteinsMiceMicroRNAsPromoter Regions, GeneticUbiquitin-Protein LigasesViral ProteinsVirus ActivationChromatinHistonesImmediate-Early Proteinslatency associated transcript, herpes simplex virus-1MicroRNAsUbiquitin-Protein LigasesViral ProteinsVmw110 protein, Human herpesvirus 1

Identifiers

PMID15507638
PMCPMC525101
OpenAlexW2153945899

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.