Evidence map›Paper›PMID 37991365›Full record

ArticleJournal of virology2023

HIV-2 inhibits HIV-1 gene expression via two independent mechanisms during cellular co-infection.

Vincent Yapo, Kinjal Majumder, Philip R Tedbury, Xin Wen, Yee T Ong, Marc C Johnson, Stefan G Sarafianos

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Current view on HIV-2 - epidemiology, diagnosis and treatment.Central European journal of public health · 2025
    Review
  5. Article
  6. 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

7 authors at 2 institutions in 1 country.

Vincent YapoCS Bond Life Sciences Center, University of Missouri, Columbia, Missouri, USA.ORCID 0009-0002-8829-6880
Kinjal MajumderCS Bond Life Sciences Center, University of Missouri, Columbia, Missouri, USA.
Philip R TedburyCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.
Xin WenCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.
Yee T OngCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.
Marc C JohnsonCS Bond Life Sciences Center, University of Missouri, Columbia, Missouri, USA.
Stefan G SarafianosCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.ORCID 0000-0002-5840-154X
Emory University · USUniversity of Missouri · US

Funding

Ultrapotent Inhibitors of Wild-type and Multi-drug Resistant HIVR37AI076119 · NIAID · EMORY UNIVERSITY · PI Stefan G Sarafianos · 2020 to 2026
$3.6M
Characterization of JT-4-173, a Potent Antiviral that Inhibits HIV-1 by a Novel Mechanism of ActionF31AI179424 · NIAID · EMORY UNIVERSITY · PI Xin Wen · 2023 to 2026
$196k
NIAID NIH HHS F31 AI179424NIAID NIH HHS R37 AI076119
6 · The paper itself

Abstract

importanceTwenty-five years after the first report that HIV-2 infection can reduce HIV-1-associated pathogenesis in dual-infected patients, the mechanisms are still not well understood. We explored these mechanisms in cell culture and showed first that these viruses can co-infect individual cells. Under specific conditions, HIV-2 inhibits HIV-1 through two distinct mechanisms, a broad-spectrum interferon response and an HIV-1-specific inhibition conferred by the HIV-2 TAR. The former could play a prominent role in dually infected individuals, whereas the latter targets HIV-1 promoter activity through competition for HIV-1 Tat binding when the same target cell is dually infected. That mechanism suppresses HIV-1 transcription by stalling RNA polymerase II complexes at the promoter through a minimal inhibitory region within the HIV-2 TAR. This work delineates the sequence of appearance and the modus operandi of each mechanism.

Indexed as

CoinfectionGene Expression Regulation, ViralHIV-1HIV-2HIV Long Terminal RepeatInterferonsRNA, Viraltat Gene Products, Human Immunodeficiency VirusBinding, CompetitiveHumansPeptide FragmentsPromoter Regions, GeneticRNA Polymerase IITranscription, GeneticInterferonsPeptide FragmentsRNA Polymerase IIRNA, Viraltat Gene Products, Human Immunodeficiency Virustat peptide (17-25), Human immunodeficiency virus 1dual infectionHIV-1HIV-2HIV-2 TARinterferon responseRNA polymerase II

Identifiers

PMID37991365
PMCPMC10734542
OpenAlexW4388909014

What OpenQuestion holds

Textmetadata
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.