Evidence map›Paper›PMID 41676118›Full record

ArticleiMetaOmics2024

Commentary on LRAs targeting NF-κB with epigenetic and mutational impacts on HIV latency.

Shaoming Chen

Abstract read
In one paragraph

Article in iMetaOmics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

1 author.

Shaoming ChenRheast LLC Houston Texas USA.ORCID 0000-0002-1988-6329

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) latency is controlled by factors like nuclear factor kappa B (NF-κB), which binds to the long terminal repeat of the HIV genome to start viral gene expression. The primary cellular form of NF-κB is a heterodimer comprising the DNA-binding subunit p50 and the transactivator p65. Phosphorylation of IkappaB kinase (IκB) is driven by the IκB kinase complex, whose core is formed by the NF-κB essential modulator. However, epigenetic changes like DNA methylation and histone modifications can suppress this activation. Recent studies show that HIV reservoirs are diverse, with complex interactions between viral and host factors affecting latency-reversing agent (LRA) effectiveness. Mutations in the NF-κB binding sites, converting them to GA-binding protein sites, complicate latency reversal by altering responses to LRAs.

Identifiers

PMID41676118
PMCPMC12806263

What OpenQuestion holds

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LicenceCC BY
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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.