Evidence map›Paper›PMID 40936906›Full record

ReviewFrontiers in immunology2025

The role of Tat in HIV latency and reactivation.

David M Margolis, Edward P Browne

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
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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

2 authors.

David M MargolisDepartments of Medicine, Microbiology and Immunology, UNC HIV Cure Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Edward P BrowneDepartments of Medicine, Microbiology and Immunology, UNC HIV Cure Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV persists during therapy due the existence of a latently infected reservoir in which viral gene expression is silenced. This reservoir thus represents the primary barrier to a cure for HIV. To eliminate latently infected cells from people with HIV (PWH) on antiretroviral therapy (ART), small molecules that reverse HIV latency (Latency reversing agents - LRAs) have been previously developed and tested, but these lack specificity for HIV and are typically inefficient at promoting broad reservoir reactivation. As such, more potent and selective tools for latency reversal are needed. Recently, delivery of mRNA encoding the viral protein Tat, which promotes transcriptional elongation, has attracted interest as a possible HIV-specific approach to inducing latency reversal. This review will cover the evidence that Tat plays a key role in both establishment of HIV latency and latency reversal, as well as recent developments in which Tat mRNA delivery has been used to enhance latency reversal approaches. Delivery of Tat to infected cells represents a promising avenue to bypass the limitations of small molecule LRAs and achieve broad reactivation of the clinical reservoir.

Indexed as

HIV-1HIV Infectionstat Gene Products, Human Immunodeficiency VirusVirus ActivationVirus LatencyAnimalsHumansRNA, MessengerRNA, Messengertat Gene Products, Human Immunodeficiency VirusclearanceHIVlatencypersistenceTat

Identifiers

PMID40936906
PMCPMC12420295

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.