Evidence map›Paper›PMID 41756862›Full record

ArticlebioRxiv : the preprint server for biology2026

Mechanisms of HIV Latency in Hematopoietic Progenitors: GFI1 as a Key Regulator.

Jackline A Onyango, Chen Li, Cuie Chen, W Miguel Disbennett, Maria C Virgilio, Mark M Painter, Valeri H Terry, Barkha Ramnani, Joshua D Welch, Kathleen L Collins

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Jackline A OnyangoDepartment of Biological Chemistry, University of Michigan, Ann Arbor, MI, USA.ORCID 0009-0004-2724-7238
Chen LiDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-1790-6664
Cuie ChenDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
W Miguel DisbennettPost-Baccalaureate Research Education Program (PREP), University of Michigan, Ann Arbor, MI, USA.
Maria C VirgilioDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-4940-188X
Mark M PainterGraduate Program in Immunology, University of Michigan, Ann Arbor, MI, USA.
Valeri H TerryDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Barkha RamnaniDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.ORCID 0009-0009-1040-9612
Joshua D WelchDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-5869-2391
Kathleen L CollinsDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Funding

Integrative Single-Cell Analysis of Transcriptome, Epigenome, and Lineage in HIV Latency and ActivationR01AI149669 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L., WELCH, JOSHUA · 2020 to 2024
$3.4M
Single-cell multi-omic analysis of opioid-mediated HIV disease pathogenesisR33DA059916 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Kathleen L. Collins, Joshua Welch · 2025 to 2026
$1.4M
NIAID NIH HHS R01 AI149669NIDA NIH HHS R33 DA059916
6 · The paper itself

Abstract

Durable control of HIV infection is challenged by persistent latent reservoirs, including hematopoietic stem and progenitor cells (HSPCs), which provide a unique niche for proviral silencing. Mechanisms of HIV latency in HSPCs remain poorly studied. Here, we utilized a dual-reporter HIV (89.6 VT1) and single-cell RNA sequencing to identify host factors governing latency in HSPCs. Transcriptomic profiling revealed elevated expression of several genes in latently infected cells, among them the transcriptional repressor GFI1. Functional studies showed that GFI1 suppresses HIV gene expression by binding a conserved sequence near the primer binding site within the long terminal repeat (LTR). Disruption of GFI1 DNA-binding or corepressor recruitment domains diminished its silencing effect. GFI1 also antagonized Tat and NF-κB-mediated activation, and reversal of GFI1-mediated suppression was most robust with combined HDAC inhibition and NF-κB activation. These findings position GFI1 as an important regulator of HIV latency in HSPCs.

Indexed as

GFI1HIV latencyHSPCsscRNA-seqtranscriptional repression

Identifiers

PMID41756862
PMCPMC12934941

What OpenQuestion holds

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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.