ArticleCell reports2013
HIV-1 Nef responsiveness is determined by Env variable regions involved in trimer association and correlates with neutralization sensitivity.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it.
- HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016Pooled it
- Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5.Viruses · 2024Review
- SERINC5 counters retroviruses and non-retroviruses.Frontiers in cellular and infection microbiology · 2024Review
- HIV-1 restriction by SERINC5.Medical microbiology and immunology · 2023Review
- SERINC5 Restricts HIV-1 Infectivity by Promoting Conformational Changes and Accelerating Functional Inactivation of Env.Viruses · 2022Article
- The Emerging Role of the Serine Incorporator Protein Family in Regulating Viral Infection.Frontiers in cell and developmental biology · 2022Review
- HIV-1 entry: Duels between Env and host antiviral transmembrane proteins on the surface of virus particles.Current opinion in virology · 2021Review
- Influence of Different Glycoproteins and of the Virion Core on SERINC5 Antiviral Activity.Viruses · 2021Article
- Selective Disruption of SERINC5 Antagonism by Nef Impairs SIV Replication in Primary CD4Journal of virology · 2021Article
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- A Conserved Acidic-Cluster Motif in SERINC5 Confers Partial Resistance to Antagonism by HIV-1 Nef.Journal of virology · 2020Article
- Flow Cytometry Analysis of HIV-1 Env Conformations at the Surface of Infected Cells and Virions: Role of Nef, CD4, and SERINC5.Journal of virology · 2020Article
- Proteasomal degradation of human SERINC4: A potent host anti-HIV-1 factor that is antagonized by nef.Current research in virological science · 2020Article
- A bipartite structural organization defines the SERINC family of HIV-1 restriction factors.Nature structural & molecular biology · 2020Article
- Plasma Membrane-Associated Restriction Factors and Their Counteraction by HIV-1 Accessory Proteins.Cells · 2019Review
- CD4 Expression and Env Conformation Are Critical for HIV-1 Restriction by SERINC5.Journal of virology · 2019Article
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- Localization to detergent-resistant membranes and HIV-1 core entry inhibition correlate with HIV-1 restriction by SERINC5.Virology · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
HIV-1 Nef and the unrelated murine leukemia virus glycoGag similarly enhance the infectivity of HIV-1 virions. We now show that the effects of Nef and glycoGag are similarly determined by variable regions of HIV-1 gp120 that control Env trimer association and neutralization sensitivity. Whereas neutralization-sensitive X4-tropic Env proteins conferred high responsiveness to Nef and glycoGag, particles bearing neutralization-resistant R5-tropic Envs were considerably less affected. The profoundly different Nef/glycoGag responsiveness of a neutralization-resistant and a neutralization-sensitive R5-tropic Env could be switched by exchanging their gp120 V1/V2 regions, which also switches their neutralization sensitivity. Within V1/V2, the same determinants governed Nef/glycoGag responsiveness and neutralization sensitivity, indicating that these phenotypes are mechanistically linked. The V1/V2 and V3 regions, which form an apical trimer-association domain, together determined the Nef and glycoGag responsiveness of an X4-tropic Env. Our results suggest that Nef and glycoGag counteract the inactivation of Env spikes with relatively unstable apical trimer-association domains.
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