Evidence map›Paper›PMID 16160155›Full record

ArticleJournal of virology2005

A herpes simplex virus type 1 mutant expressing a baculovirus inhibitor of apoptosis gene in place of latency-associated transcript has a wild-type reactivation phenotype in the mouse.

Ling Jin, Guey-Chuen Perng, Kevin R Mott, Nelson Osorio, Julia Naito, David J Brick, Dale Carpenter, Clinton Jones, Steven L Wechsler

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 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

43 citing papers in PubMed, 59 citations in OpenAlex.

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  17. Covert Infection of Insects by Baculoviruses.Frontiers in microbiology · 2017
    Review
  18. Article
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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

9 authors at 2 institutions in 1 country.

Ling JinDepartment of Ophthalmology, University of California, Irvine, School of Medicine, 92697, USA.
Guey-Chuen Perng
Kevin R Mott
Nelson Osorio
Julia Naito
David J Brick
Dale Carpenter
Clinton Jones
Steven L Wechsler
University of California, Irvine · USUniversity of Nebraska–Lincoln · US

Funding

VIRAL SHUTOFF OF HOST TRANSCRIPTION--PBCV-1 INFECTEDP20RR015635 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 2000 to 2009
$22.1M
Corneal HSV-1: LAT's Anti-Apoptosis Activity and LatencyR01EY013191 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI WECHSLER, STEVEN L · 2001 to 2013
$6.9M
CORNEAL HSV-1: A NOVEL VIRULENCE/REACTIVATION GENER01EY012823 · NEI · UNIVERSITY OF CALIFORNIA IRVINE · PI WECHSLER, STEVEN L · 2000 to 2004
$2.4M
NCRR NIH HHS P20 RR015635NCRR NIH HHS P20RR15635NEI NIH HHS EY12823NEI NIH HHS EY13191NEI NIH HHS R01 EY012823NEI NIH HHS R01 EY013191
6 · The paper itself

Abstract

The latency-associated transcript (LAT) is essential for the wild-type herpes simplex virus type 1 (HSV-1) high-reactivation phenotype since LAT- mutants have a low-reactivation phenotype. We previously reported that LAT can decrease apoptosis and proposed that this activity is involved in LAT's ability to enhance the HSV-1 reactivation phenotype. The first 20% of the primary 8.3-kb LAT transcript is sufficient for enhancing the reactivation phenotype and for decreasing apoptosis, supporting this proposal. For this study, we constructed an HSV-1 LAT- mutant that expresses the baculovirus antiapoptosis gene product cpIAP under control of the LAT promoter and in place of the LAT region mentioned above. Mice were ocularly infected with this mutant, designated dLAT-cpIAP, and the reactivation phenotype was determined using the trigeminal ganglion explant model. dLAT-cpIAP had a reactivation phenotype similar to that of wild-type virus and significantly higher than that of (i) the LAT- mutant dLAT2903; (ii) dLAT1.5, a control virus containing the same LAT deletion as dLAT-cpIAP, but with no insertion of foreign DNA, thereby controlling for potential readthrough transcription past the cpIAP insert; and (iii) dLAT-EGFP, a control virus identical to dLAT-cpIAP except that it contained the enhanced green fluorescent protein open reading frame (ORF) in place of the cpIAP ORF, thereby controlling for expression of a random foreign gene instead of the cpIAP gene. These results show that an antiapoptosis gene with no sequence similarity to LAT can efficiently substitute for the LAT function involved in enhancing the in vitro-induced HSV-1 reactivation phenotype in the mouse.

Indexed as

Virus ActivationAnimalsApoptosisBaculoviridaeCell LineFemaleGene DeletionHerpes SimplexHerpesvirus 1, HumanInhibitor of Apoptosis ProteinsMiceMicroRNAsPhenotypeProteinsRabbitsRecombination, GeneticInhibitor of Apoptosis Proteinslatency associated transcript, herpes simplex virus-1MicroRNAsProteinsViral Proteins

Identifiers

PMID16160155
PMCPMC1211541
OpenAlexW2037781454

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.