Evidence map›Paper›PMID 28407486›Full record

ArticleCell host & microbe2017

Transcriptional Elongation of HSV Immediate Early Genes by the Super Elongation Complex Drives Lytic Infection and Reactivation from Latency.

Roberto Alfonso-Dunn, Anne-Marie W Turner, Pierre M Jean Beltran, Jesse H Arbuckle, Hanna G Budayeva, Ileana M Cristea, Thomas M Kristie

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

7 authors at 2 institutions in 1 country.

Roberto Alfonso-DunnLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20814, USA.
Anne-Marie W TurnerLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20814, USA.
Pierre M Jean BeltranDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Jesse H ArbuckleLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20814, USA.
Hanna G BudayevaDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Ileana M CristeaDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Thomas M KristieLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20814, USA. Electronic address: tkristie@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USPrinceton University · US

Funding

Transcriptional control of herpes simplex virus lytic infection and latency-reactivation cyclesZIAAI000712 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KRISTIE, THOMAS M · 2009 to 2025
$13.0M
HCF-1, A Mammalian Factor Controlling HSV Gene ExpressionZIAAI000711 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KRISTIE, THOMAS M · 2009 to 2017
$5.4M
Mechanisms mediating immune response upon sensing of nuclear viral DNAR01GM114141 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 2015 to 2023
$2.6M
NIGMS NIH HHS R01 GM114141
6 · The paper itself

Abstract

The cellular transcriptional coactivator HCF-1 is required for initiation of herpes simplex virus (HSV) lytic infection and for reactivation from latency in sensory neurons. HCF-1 stabilizes the viral Immediate Early (IE) gene enhancer complex and mediates chromatin transitions to promote IE transcription initiation. In infected cells, HCF-1 was also found to be associated with a network of transcription elongation components including the super elongation complex (SEC). IE genes exhibit characteristics of genes controlled by transcriptional elongation, and the SEC-P-TEFb complex is specifically required to drive the levels of productive IE mRNAs. Significantly, compounds that enhance the levels of SEC-P-TEFb also potently stimulated HSV reactivation from latency both in a sensory ganglia model system and in vivo. Thus, transcriptional elongation of HSV IE genes is a key limiting parameter governing both the initiation of HSV infection and reactivation of latent genomes.

Indexed as

Gene Expression Regulation, ViralGenes, Immediate-EarlyTranscription Elongation, GeneticVirus ActivationAnimalsCell LineEpithelial CellsGanglia, SensoryHost Cell Factor C1HumansMiceSimplexvirusTranscription FactorsHCFC1 protein, humanHost Cell Factor C1Transcription Factorsherpes simplex virushost cell factor-1latencyP-TEFbsuper elongation complextranscriptional elongation

Identifiers

PMID28407486
PMCPMC5997188
OpenAlexW2605407832

What OpenQuestion holds

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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.