Evidence map›Paper›PMID 34551301›Full record

ArticleCell reports2021

An additional NF-κB site allows HIV-1 subtype C to evade restriction by nuclear PYHIN proteins.

Matteo Bosso, Christina M Stürzel, Dorota Kmiec, Smitha Srinivasachar Badarinarayan, Elisabeth Braun, Jumpei Ito, Kei Sato, Beatrice H Hahn, Konstantin M J Sparrer, Daniel Sauter and 1 more

Abstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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

11 authors.

Matteo BossoInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Christina M StürzelInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Dorota KmiecInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany; Department of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE5 9RS, UK.
Smitha Srinivasachar BadarinarayanInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany; Institute for Medical Virology and Epidemiology of Viral Diseases, University Hospital Tübingen, 72076 Tübingen, Germany.
Elisabeth BraunInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Jumpei ItoDivision of Systems Virology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Tokyo 1088639, Japan.
Kei SatoDivision of Systems Virology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Tokyo 1088639, Japan.
Beatrice H HahnDepartments of Medicine and Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6076, USA.
Konstantin M J SparrerInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Daniel SauterInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany; Institute for Medical Virology and Epidemiology of Viral Diseases, University Hospital Tübingen, 72076 Tübingen, Germany.
Frank KirchhoffInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany. Electronic address: frank.kirchhoff@uni-ulm.de.

Funding

Virus & Reservoirs CoreP30AI045008 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DAVID S METZGER · 1999 to 2026
$78.6M
BEAT-HIV: Delaney Collaboratory to Cure HIV-1 Infection by Combination ImmunotherapyUM1AI164570 · NIAID · WISTAR INSTITUTE · PI Luis J Montaner, James L. Riley · 2021 to 2026
$34.7M
Characterizing the viral and host effector mechanisms that govern HIV-1 reboundR01AI162646 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI BAR, KATHARINE JUNE, HAHN, BEATRICE H · 2021 to 2025
$4.1M
NIAID NIH HHS P30 AI045008NIAID NIH HHS R01 AI162646NIAID NIH HHS UM1 AI164570
6 · The paper itself

Abstract

Subtype C is the most prevalent clade of human immunodeficiency virus type 1 (HIV-1) worldwide. The reasons for this are poorly understood. Here, we demonstrate that a characteristic additional third nuclear factor κB (NF-κB) binding site in the long terminal repeat (LTR) promoter allows subtype C HIV-1 strains to evade restriction by nuclear PYHIN proteins, which sequester the transcription factor Sp1. Further, other LTR alterations are responsible for rare PYHIN resistance of subtype B viruses. Resistance-conferring mutations generally reduce the dependency of HIV-1 on Sp1 for virus production and render LTR transcription highly responsive to stimulation by NF-κB/p65. A third NF-κB binding site increases infectious virus yield in primary CD4

Indexed as

Binding SitesCD4-Positive T-LymphocytesDisease SusceptibilityGenotypeHEK293 CellsHIV-1HIV InfectionsHumansNF-kappa BNuclear ProteinsPhosphoproteinsSp1 Transcription FactorTerminal Repeat SequencesVirus ReplicationIFI16 protein, humanNF-kappa BNuclear ProteinsPhosphoproteinsPYHIN1 protein, humanSP1 protein, humanSp1 Transcription FactorGamma Interferon Inducible Protein 16HIV-1 subtypesinnate immunitynuclear factor-κBPYHIN proteinsspecificity protein 1

Identifiers

PMID34551301
PMCPMC8505707

What OpenQuestion holds

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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.