Evidence map›Paper›PMID 37295842›Full record

ArticleGenome research2023

Integration site-dependent HIV-1 promoter activity shapes host chromatin conformation.

Jack A Collora, Ya-Chi Ho

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
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  10. Article
  11. Review
  12. Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  13. Article
  14. Review
  15. HIV-1 control in vivo is related to the number but not the fraction of infected cells with viral unspliced RNA.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Transcription of HIV-1 at sites of intact latent provirus integration.bioRxiv : the preprint server for biology · 2024
    Article
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

2 authors at 1 institution in 1 country.

Jack A ColloraDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut 06519, USA jacollora@gmail.com ya-chi.ho@yale.edu.
Ya-Chi HoDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut 06519, USA jacollora@gmail.com ya-chi.ho@yale.edu.
Yale University · US

Funding

BEAT-HIV: Delaney Collaboratory to Cure HIV-1 Infection by Combination ImmunotherapyUM1AI164570 · NIAID · WISTAR INSTITUTE · PI Luis J Montaner, James L. Riley · 2021 to 2026
$34.7M
CHEETAH Center for the Structural Biology of HIV Infection, Restriction, and Viral DynamicsU54AI170856 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI WESLEY I. SUNDQUIST · 2022 to 2026
$34.4M
REACH: Research Enterprise to Advance a Cure for HIVUM1AI164565 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Marina Caskey, R. Brad Jones · 2021 to 2026
$32.9M
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 Y-SCORCH Data Generation Center at Yale for Single-Cell Opioid Responses in the Context of HIVUM1DA051410 · NIDA · YALE UNIVERSITY · PI GERSTEIN, MARK BENDER, KLUGER, YUVAL · 2020 to 2025
$15.3M
Virus TransmissionP50AI150464 · NIAID · UNIVERSITY OF UTAH · PI SUNDQUIST, WESLEY I. · 2019 to 2021
$14.9M
High-Definition Characterization of the Persistence and Perturbation of the HIV Reservoir: Project 3P01AI169768 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Jonathan Li · 2022 to 2026
$10.1M
M-SCORCH: Methamphetamine use disorder data generation center for Single Cell Opioid Responses in the Context of HIVU01DA053628 · NIDA · YALE UNIVERSITY · PI HO, YA-CHI, SESTAN, NENAD · 2021 to 2025
$9.5M
The HUSH complex in HIV-1 latencyR37AI147868 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI JEREMY LUBAN · 2019 to 2026
$6.4M
Role of clonal expansion in HIV-1 persistenceR01AI141009 · NIAID · YALE UNIVERSITY · PI Ya-Chi Ho · 2018 to 2026
$5.3M
T cell-targeted lentiviral vectors with Cas9/RNP for the in vivo gene therapy of HIV-AIDSR01AI145164 · NIAID · YALE UNIVERSITY · PI KUMAR, PRITI · 2019 to 2024
$3.7M
Predoctoral Training Program in VirologyT32AI055403 · NIAID · YALE UNIVERSITY · PI KUMAR, PRITI, MOTHES, WALTHER H · 2003 to 2024
$3.6M
NIAID NIH HHS P01 AI169768NIAID NIH HHS P50 AI150464NIAID NIH HHS R01 AI141009NIAID NIH HHS R01 AI145164NIAID NIH HHS R01 AI174863NIAID NIH HHS R37 AI147868NIAID NIH HHS T32 AI055403NIAID NIH HHS U54 AI170856NIAID NIH HHS UM1 AI126620NIAID NIH HHS UM1 AI164565NIAID NIH HHS UM1 AI164570NIDA NIH HHS R01 DA051906NIDA NIH HHS R33 DA047037NIDA NIH HHS R61 DA047037NIDA NIH HHS U01 DA053628NIDA NIH HHS UM1 DA051410
6 · The paper itself

Abstract

HIV-1 integration introduces ectopic transcription factor binding sites into host chromatin. We postulate that the integrated provirus serves as an ectopic enhancer that recruits additional transcription factors to the integration locus, increases chromatin accessibility, changes 3D chromatin interactions, and enhances both retroviral and host gene expression. We used four well-characterized HIV-1-infected cell line clones having unique integration sites and low to high levels of HIV-1 expression. Using single-cell DOGMA-seq, which captured the heterogeneity of HIV-1 expression and host chromatin accessibility, we found that HIV-1 transcription correlated with HIV-1 accessibility and host chromatin accessibility. HIV-1 integration increased local host chromatin accessibility within an ∼5- to 30-kb distance. CRISPRa- and CRISPRi-mediated HIV-1 promoter activation and inhibition confirmed integration site-dependent HIV-1-driven changes of host chromatin accessibility. HIV-1 did not drive chromatin confirmation changes at the genomic level (by Hi-C) or the enhancer connectome (by H3K27ac HiChIP). Using 4C-seq to interrogate HIV-1-chromatin interactions, we found that HIV-1 interacted with host chromatin ∼100-300 kb from the integration site. By identifying chromatin regions having both increased transcription factor activity (by ATAC-seq) and HIV-1-chromatin interaction (by 4C-seq), we identified enrichment of ETS, RUNT, and ZNF-family transcription factor binding that may mediate HIV-1-host chromatin interactions. Our study has found that HIV-1 promoter activity increases host chromatin accessibility, and HIV-1 interacted with host chromatin within the existing chromatin boundaries in an integration site-dependent manner.

Indexed as

ChromatinHIV-1Promoter Regions, GeneticRegulatory Sequences, Nucleic AcidTranscription FactorsChromatinTranscription Factors

Identifiers

PMID37295842
PMCPMC10519397
OpenAlexW4379977950

What OpenQuestion holds

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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.