ArticleProceedings of the National Academy of Sciences of the United States of America2007
Dynamin 2 is required for the enhancement of HIV-1 infectivity by Nef.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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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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Who cites it
87 citing papers in PubMed, 123 citations in OpenAlex.
- HIV-1 Nef Uses a Conserved Pocket to Recruit the N-Terminal Cytoplasmic Tail of Serinc3.Viruses · 2025Article
- Extracellular vesicle isolation methods identify distinct HIV-1 particles released from chronically infected T-cells.Journal of extracellular vesicles · 2024Article
- Kinetic investigation reveals an HIV-1 Nef-dependent increase in AP-2 recruitment and productivity at endocytic sites.Molecular biology of the cell · 2024Article
- Human Immunodeficiency Virus 1 Preferentially Fuses with pH-Neutral Endocytic Vesicles in Cell Lines and Human Primary CD4+ T-Cells.ACS nano · 2023Article
- HIV-1 Vpr induces ciTRAN to prevent transcriptional repression of the provirus.Science advances · 2023Article
- Article
- Targeted protein degradation as an antiviral approach.Antiviral research · 2023Article
- Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells.Virology · 2023Article
- SERINC5 restricts influenza virus infectivity.PLoS pathogens · 2022Article
- Effect of High-Energy Milling on the Dissolution of Anti-HIV Drug Efavirenz in Different Solvents.ACS omega · 2021Article
- Selective Disruption of SERINC5 Antagonism by Nef Impairs SIV Replication in Primary CD4Journal of virology · 2021Article
- Nef Obtained from Individuals with HIV-1 Vary in Their Ability to Antagonize SERINC3- and SERINC5-Mediated HIV-1 Restriction.Viruses · 2021Article
- Nef homodimers down-regulate SERINC5 by AP-2-mediated endocytosis to promote HIV-1 infectivity.The Journal of biological chemistry · 2020Article
- Impaired ability of Nef to counteract SERINC5 is associated with reduced plasma viremia in HIV-infected individuals.Scientific reports · 2020Article
- Platelets Endocytose Viral Particles and Are Activated via TLR (Toll-Like Receptor) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- HIV-1 Nef dimers short-circuit immune receptor signaling by activating Tec-family kinases at the host cell membrane.The Journal of biological chemistry · 2020Article
- A Conserved Acidic-Cluster Motif in SERINC5 Confers Partial Resistance to Antagonism by HIV-1 Nef.Journal of virology · 2020Article
- Toward a Macaque Model of HIV-1 Infection: Roadblocks, Progress, and Future Strategies.Frontiers in microbiology · 2020Review
- How HIV Nef Proteins Hijack Membrane Traffic To Promote Infection.Journal of virology · 2019Review
- Plasma Membrane-Associated Restriction Factors and Their Counteraction by HIV-1 Accessory Proteins.Cells · 2019Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Nef is a virulence factor of HIV-1 and other primate lentiviruses that is crucial for rapid progression to AIDS. In cell culture, Nef increases the infectivity of HIV-1 progeny virions by an unknown mechanism. We now show that dynamin 2 (Dyn2), a key regulator of vesicular trafficking, is a binding partner of Nef that is required for its ability to increase viral infectivity. Dominant-negative Dyn2 or the depletion of Dyn2 by small interfering RNA potently inhibited the effect of Nef on HIV-1 infectivity. Furthermore, in Dyn2-depleted cells, this function of Nef could be rescued by ectopically expressed Dyn2 but not by Dyn1, a closely related isoform that does not bind Nef. The infectivity enhancement by Nef also depended on clathrin, because it was diminished in clathrin-depleted cells and profoundly inhibited in cells expressing the clathrin-binding domain of AP180, which blocks clathrin-coated pit formation but not clathrin-independent endocytosis. Together, these findings imply that the infectivity enhancement activity of Nef depends on Dyn2- and clathrin-mediated membrane invagination events.
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Registered trials
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.