Evidence map›Paper›PMID 29549786›Full record

ArticleVirology2018

Tat controls transcriptional persistence of unintegrated HIV genome in primary human macrophages.

Beatrix Meltzer, Deemah Dabbagh, Jia Guo, Fatah Kashanchi, Mudit Tyagi, Yuntao Wu

Open access · hybridAbstract read
In one paragraph

Article in Virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Beatrix MeltzerNational Center for Biodefense and Infectious Diseases, George Mason University, Manassas, USA.
Deemah DabbaghNational Center for Biodefense and Infectious Diseases, George Mason University, Manassas, USA.
Jia GuoNational Center for Biodefense and Infectious Diseases, George Mason University, Manassas, USA.
Fatah KashanchiLaboratory of Molecular Virology, George Mason University, Manassas, USA.
Mudit TyagiNational Center for Biodefense and Infectious Diseases, George Mason University, Manassas, USA.
Yuntao WuNational Center for Biodefense and Infectious Diseases, George Mason University, Manassas, USA. Electronic address: ywu8@gmu.edu.
George Mason University · US

Funding

HIV1 INHIBITION USING TAT PEPTIDE DERIVATIVESR01AI043894 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KASHANCHI, FATAH · 1999 to 2015
$4.4M
Validation of the Rev-dependent vector for targeting SIV macrophage reservoirsR01MH102144 · NIMH · GEORGE MASON UNIVERSITY · PI WU, YUNTAO · 2014 to 2018
$3.3M
Characterization of cocaine induced signaling pathways that enhances HIV transcriptionR01DA041746 · NIDA · THOMAS JEFFERSON UNIVERSITY · PI TYAGI, MUDIT · 2017 to 2023
$2.3M
HIV neuropathogenesis related to exosomes containing HIV non-coding RNAsR01NS099029 · NINDS · GEORGE MASON UNIVERSITY · PI KASHANCHI, FATAH · 2016 to 2020
$1.9M
Cocaine enhances HIV replication by inducing transcriptionally active chromatin sR21DA033924 · NIDA · GEORGE WASHINGTON UNIVERSITY · PI TYAGI, MUDIT · 2013 to 2014
$436k
Effect of chromatin remodelers/modifiers on HIV-1 Tat activated transcriptionR21AI074410 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI KASHANCHI, FATAH · 2009 to 2010
$432k
HIV-1 TAR derived miRNA: Implications for Latency and PathogenesisR21AI078859 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI KASHANCHI, FATAH · 2009 to 2010
$400k
Development of a novel HIV-1 nuclear localization assayR03AI110174 · NIAID · GEORGE MASON UNIVERSITY · PI WU, YUNTAO · 2014 to 2015
$142k
NIAID NIH HHS R01 AI043894NIAID NIH HHS R03 AI110174NIAID NIH HHS R21 AI074410NIAID NIH HHS R21 AI078859NIDA NIH HHS R01 DA041746NIDA NIH HHS R21 DA033924NIMH NIH HHS R01 MH102144NINDS NIH HHS R01 NS099029
6 · The paper itself

Abstract

In HIV infected macrophages, a large population of viral genomes persists as the unintegrated form (uDNA) that is transcriptionally active. However, how this transcriptional activity is controlled remains unclear. In this report, we investigated whether Tat, the viral transactivator of transcription, is involved in uDNA transcription. We demonstrate that de novo Tat activity is generated from uDNA, and this uDNA-derived Tat (uTat) transactivates the uDNA LTR. In addition, uTat is required for the transcriptional persistence of uDNA that is assembled into repressive episomal minichromatin. In the absence of uTat, uDNA minichromatin is gradually silenced, but remains highly inducible by HDAC inhibitors (HDACi). Therefore, functionally, uTat antagonizes uDNA minichromatin repression to maintain persistent viral transcription in macrophages. uTat-mediated viral persistence may establish a viral reservoir in macrophages where uDNA were found to persist.

Indexed as

Transcription, GeneticCells, CulturedDNA, ViralHIVHumansMacrophagestat Gene Products, Human Immunodeficiency VirusDNA, Viraltat Gene Products, Human Immunodeficiency VirusHDACiHIVMacrophagePersistenceReservoirTatTranscriptionUnintegrated HIV DNA

Identifiers

PMID29549786
PMCPMC6021179
OpenAlexW2791057374

What OpenQuestion holds

Textmetadata
LicenceTDM
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.