Evidence map›Paper›PMID 32097085›Full record

ArticleAutophagy2021

HIV-1 Nef counteracts autophagy restriction by enhancing the association between BECN1 and its inhibitor BCL2 in a PRKN-dependent manner.

Sergio Castro-Gonzalez, Yuhang Shi, Marta Colomer-Lluch, Ying Song, Kaitlyn Mowery, Sharilyn Almodovar, Anju Bansal, Frank Kirchhoff, Konstantin Sparrer, Chengyu Liang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 55 citations in OpenAlex.

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  12. Inflammasomes and autophagy in cancer: unlocking targeted therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  13. Article
  14. DAPK3 is Essential for DBP-Induced Autophagy of Mouse Leydig Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Article
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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 at 6 institutions in 3 countries.

Sergio Castro-GonzalezBiological Sciences, College of Arts and Sciences, Texas Tech University, Lubbock, TX, USA.
Yuhang ShiBiological Sciences, College of Arts and Sciences, Texas Tech University, Lubbock, TX, USA.
Marta Colomer-LluchIrsiCaixa AIDS Research Institute, Germans Trias i Pujol Research Institute, Badalona, Spain.
Ying SongMolecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Kaitlyn MoweryBiological Sciences, College of Arts and Sciences, Texas Tech University, Lubbock, TX, USA.
Sharilyn AlmodovarImmunology and Molecular Microbiology, Texas Tech Health Sciences Center, Lubbock, TX, USA.
Anju BansalMedicine, Infectious Diseases, University of Alabama at Birmingham, Birmingham, AL, USA.
Frank KirchhoffInstitute of Molecular Virology, University of Ulm, Ulm, Germany.
Konstantin SparrerInstitute of Molecular Virology, University of Ulm, Ulm, Germany.ORCID 0000-0002-8682-1779
Chengyu LiangMolecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Ruth Serra-MorenoBiological Sciences, College of Arts and Sciences, Texas Tech University, Lubbock, TX, USA.
Texas Tech University · USUniversität Ulm · DEUniversity of Southern California · USIrsiCaixa · ESTexas Tech University Health Sciences Center · USUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is an auto-digestive pro-survival pathway activated in response to stress to target cargo for lysosomal degradation. In recent years, autophagy has become prominent as an innate antiviral defense mechanism through multiple processes, such as targeting virions and viral components for elimination. These exciting findings have encouraged studies on the ability of autophagy to restrict HIV. However, the role of autophagy in HIV infection remains unclear. Whereas some reports indicate that autophagy is detrimental for HIV, others have claimed that HIV deliberately activates this pathway to increase its infectivity. Moreover, these contrasting findings seem to depend on the cell type investigated. Here, we show that autophagy poses a hurdle for HIV replication, significantly reducing virion production. However, HIV-1 uses its accessory protein Nef to counteract this restriction. Previous studies have indicated that Nef affects autophagy maturation by preventing the fusion between autophagosomes and lysosomes. Here, we uncover that Nef additionally blocks autophagy initiation by enhancing the association between BECN1 and its inhibitor BCL2, and this activity depends on the cellular E3 ligase PRKN. Remarkably, the ability of Nef to counteract the autophagy block is more frequently observed in pandemic HIV-1 and its simian precursor SIV

Indexed as

Apoptosis Regulatory ProteinsAutophagosomesAutophagyBeclin-1HIV-1HIV InfectionsHumansLysosomesProto-Oncogene Proteins c-bcl-2Apoptosis Regulatory ProteinsBCL2 protein, humanBeclin-1BECN1 protein, humanProto-Oncogene Proteins c-bcl-2AutophagyBCL2BECN1GagHIVNefPRKN

Identifiers

PMID32097085
PMCPMC8007141
OpenAlexW3007073470

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.