Evidence map›Paper›PMID 26488441›Full record

ArticleeLife2015

HIV Tat controls RNA Polymerase II and the epigenetic landscape to transcriptionally reprogram target immune cells.

Jonathan E Reeder, Youn-Tae Kwak, Ryan P McNamara, Christian V Forst, Iván D'Orso

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 66 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

5 authors at 3 institutions in 1 country.

Jonathan E ReederDepartment of Biological Sciences, University of Texas at Dallas, Richardson, United States.
Youn-Tae KwakDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, United States.
Ryan P McNamaraDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, United States.
Christian V ForstDepartment of Genetics and Genomic Sciences, Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, United States.
Iván D'OrsoDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, United States.ORCID http://orcid.org/0000-0002-1409-2351
The University of Texas Southwestern Medical Center · USIcahn School of Medicine at Mount Sinai · USThe University of Texas at Dallas · US

Funding

MOLECULAR MICROBIOLOGY TRAINING GRANTT32AI007520 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Julie K Pfeiffer · 1997 to 2026
$7.0M
Transcriptional regulatory mechanisms shaping HIV proviral fateR01AI114362 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI D'ORSO, IVAN · 2015 to 2024
$4.6M
Transcriptional regulatory mechanisms shaping HIV proviral fateR37AI114362 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Ivan D'Orso · 2025 to 2026
$1.0M
Assembly of HIV -1 and Cellular Transcription Elongation ComplexesR00AI083087 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI D'ORSO, IVAN · 2011 to 2012
$514k
Studies of HIV and Host Transcriptional Control by TatR56AI106514 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI D'ORSO, IVAN · 2014 to 2014
$382k
NIAID NIH HHS R00 AI083087NIAID NIH HHS R00AI083087NIAID NIH HHS R01 AI114362NIAID NIH HHS R01AI114362NIAID NIH HHS R37 AI114362NIAID NIH HHS R56 AI106514NIAID NIH HHS R56AI106514NIAID NIH HHS T32 2T32AI007520-16NIAID NIH HHS T32 AI007520
6 · The paper itself

Abstract

HIV encodes Tat, a small protein that facilitates viral transcription by binding an RNA structure (trans-activating RNA [TAR]) formed on nascent viral pre-messenger RNAs. Besides this well-characterized mechanism, Tat appears to modulate cellular transcription, but the target genes and molecular mechanisms remain poorly understood. We report here that Tat uses unexpected regulatory mechanisms to reprogram target immune cells to promote viral replication and rewire pathways beneficial for the virus. Tat functions through master transcriptional regulators bound at promoters and enhancers, rather than through cellular 'TAR-like' motifs, to both activate and repress gene sets sharing common functional annotations. Despite the complexity of transcriptional regulatory mechanisms in the cell, Tat precisely controls RNA polymerase II recruitment and pause release to fine-tune the initiation and elongation steps in target genes. We propose that a virus with a limited coding capacity has optimized its genome by evolving a small but 'multitasking' protein to simultaneously control viral and cellular transcription.

Indexed as

Epigenesis, GeneticHost-Pathogen InteractionsTranscription, GeneticCD4-Positive T-LymphocytesCells, CulturedGene Expression RegulationHIVHumansRNA Polymerase IItat Gene Products, Human Immunodeficiency VirusRNA Polymerase IItat Gene Products, Human Immunodeficiency ViruschromatinchromosomesepigeneticsgeneshumanRNA polymerase IItranscriptiontranscription factors

Identifiers

PMID26488441
PMCPMC4733046
OpenAlexW2213362727

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.