Evidence map›Paper›PMID 31584995›Full record

ArticlePLoS pathogens2019

Stable integrant-specific differences in bimodal HIV-1 expression patterns revealed by high-throughput analysis.

David F Read, Edmond Atindaana, Kalyani Pyaram, Feng Yang, Sarah Emery, Anna Cheong, Katherine R Nakama, Cleo Burnett, Erin T Larragoite, Emilie Battivelli and 5 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 7 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

15 authors at 4 institutions in 2 countries.

David F ReadDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-8464-6081
Edmond AtindaanaDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0003-2355-5730
Kalyani PyaramDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0003-2744-7470
Feng YangDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Sarah EmeryDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Anna CheongDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-0192-071X
Katherine R NakamaDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Cleo BurnettDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-6754-0787
Erin T LarragoiteDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Emilie BattivelliDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Eric VerdinDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.ORCID 0000-0003-3703-3183
Vicente PlanellesDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0000-0002-5318-2982
Cheong-Hee ChangDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0001-8725-852X
Alice TelesnitskyDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0001-9878-5931
Jeffrey M KiddDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-9631-1465
University of Michigan · USBuck Institute for Research on Aging · USUniversity of Utah · USUniversity of Ghana · GH

Funding

First-in-human study of two anti-SARS CoV-2 antibodies in health volunteersUM1AI126620 · NIAID · WISTAR INSTITUTE · PI MONTANER, LUIS J, RILEY, JAMES L. · 2016 to 2021
$24.5M
The Center for HIV RNA Studies (CRNA)U54AI150470 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHIU, WAH · 2019 to 2021
$15.1M
Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
High throughput analysis of latency/reactivation with barcoded provirusesR33AI116190 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, CHEONG-HEE, KIDD, JEFFREY M · 2016 to 2018
$1.4M
High throughput analysis of latency/reactivation with barcoded provirusesR21AI116190 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, CHEONG-HEE, KIDD, JEFFREY M · 2014 to 2015
$427k
NIAID NIH HHS R21 AI116190NIAID NIH HHS R33 AI116190NIAID NIH HHS T32 AI055434NIAID NIH HHS U54 AI150470NIAID NIH HHS UM1 AI126620
6 · The paper itself

Abstract

HIV-1 gene expression is regulated by host and viral factors that interact with viral motifs and is influenced by proviral integration sites. Here, expression variation among integrants was followed for hundreds of individual proviral clones within polyclonal populations throughout successive rounds of virus and cultured cell replication, with limited findings using CD4+ cells from donor blood consistent with observations in immortalized cells. Tracking clonal behavior by proviral "zip codes" indicated that mutational inactivation during reverse transcription was rare, while clonal expansion and proviral expression states varied widely. By sorting for provirus expression using a GFP reporter in the nef open reading frame, distinct clone-specific variation in on/off proportions were observed that spanned three orders of magnitude. Tracking GFP phenotypes over time revealed that as cells divided, their progeny alternated between HIV transcriptional activity and non-activity. Despite these phenotypic oscillations, the overall GFP+ population within each clone was remarkably stable, with clones maintaining clone-specific equilibrium mixtures of GFP+ and GFP- cells. Integration sites were analyzed for correlations between genomic features and the epigenetic phenomena described here. Integrants inserted in the sense orientation of genes were more frequently found to be GFP negative than those in the antisense orientation, and clones with high GFP+ proportions were more distal to repressive H3K9me3 peaks than low GFP+ clones. Clones with low frequencies of GFP positivity appeared to expand more rapidly than clones for which most cells were GFP+, even though the tested proviruses were Vpr-. Thus, much of the increase in the GFP- population in these polyclonal pools over time reflected differential clonal expansion. Together, these results underscore the temporal and quantitative variability in HIV-1 gene expression among proviral clones that are conferred in the absence of metabolic or cell-type dependent variability, and shed light on cell-intrinsic layers of regulation that affect HIV-1 population dynamics.

Indexed as

Virus ReplicationCD4-Positive T-LymphocytesHigh-Throughput Screening AssaysHIV-1HIV InfectionsHumansJurkat CellsProvirusesTransduction, GeneticVirus Integration

Identifiers

PMID31584995
PMCPMC6795456
OpenAlexW2978032880

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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.