Evidence map›Paper›PMID 31243131›Full record

ArticleJournal of virology2019

Alternate NF-κB-Independent Signaling Reactivation of Latent HIV-1 Provirus.

Chiara Acchioni, Anna Lisa Remoli, Giulia Marsili, Marta Acchioni, Ilenia Nardolillo, Roberto Orsatti, Stefania Farcomeni, Enrico Palermo, Edvige Perrotti, Maria Letizia Barreca and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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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

17 authors at 5 institutions in 2 countries.

Chiara AcchioniDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Anna Lisa RemoliDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Giulia MarsiliDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Marta AcchioniDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Ilenia NardolilloDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Roberto OrsattiDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Stefania FarcomeniNational HIV/AIDS Research Center, Istituto Superiore di Sanità, Rome, Italy.
Enrico PalermoIstituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Edvige PerrottiDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Maria Letizia BarrecaDepartment of Pharmaceutical Sciences, Università degli Studi di Perugia, Perugia, Italy.
Stefano SabatiniDepartment of Pharmaceutical Sciences, Università degli Studi di Perugia, Perugia, Italy.
Silvia SandiniDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Cristina ParolinDepartment of Molecular Medicine, University of Padua, Padua, Italy.
Rongtuan LinDepartment of Medicine, Lady Davis Institute-Jewish General Hospital, McGill University, Montreal, Québec, Canada.
Alessandra BorsettiNational HIV/AIDS Research Center, Istituto Superiore di Sanità, Rome, Italy.
John HiscottIstituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Marco SgarbantiDepartment of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy marco.sgarbanti@iss.it.ORCID 0000-0002-0433-5110
Istituto Superiore di Sanità · ITIstituto Pasteur · ITUniversity of Perugia · ITJewish General Hospital · CAUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current combination antiretroviral therapies (cART) are unable to eradicate HIV-1 from infected individuals because of the establishment of proviral latency in long-lived cellular reservoirs. The shock-and-kill approach aims to reactivate viral replication from the latent state (shock) using latency-reversing agents (LRAs), followed by the elimination of reactivated virus-producing cells (kill) by specific therapeutics. The NF-κB RelA/p50 heterodimer has been characterized as an essential component of reactivation of the latent HIV-1 long terminal repeat (LTR). Nevertheless, prolonged NF-κB activation contributes to the development of various autoimmune, inflammatory, and malignant disorders. In the present study, we established a cellular model of HIV-1 latency in J-Lat CD4

Indexed as

Anti-Retroviral AgentsCD4-Positive T-LymphocytesGene Expression Regulation, ViralHIV-1HIV InfectionsHIV SeropositivityHumansJurkat CellsNF-kappa BNF-KappaB Inhibitor alphaProvirusesReceptors, ImmunologicSignal TransductionTranscription Factor RelAVirus ActivationVirus LatencyAnti-Retroviral AgentsNF-kappa BNF-KappaB Inhibitor alphap50 natural killer cell receptorReceptors, ImmunologicRELA protein, humanTranscription Factor RelAaspirinc-JunHIV-1LRANF-κBshock and kill

Identifiers

PMID31243131
PMCPMC6714815
OpenAlexW2955990171

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.