ArticlePLoS pathogens2016
The Race against Protease Activation Defines the Role of ESCRTs in HIV Budding.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Real-Time Imaging of HIV-1 Protease Activation and Substrate Cleavage in Single Virions Assembling on the Plasma Membrane.Viruses · 2026Article
- Cryo-ET reveals distinct Gag lattice architectures in virus-like particles and immature HIV-1.Structure (London, England : 1993) · 2026Article
- Evasion of CARD8 activation during HIV-1 assembly.Science advances · 2025Article
- Article
- Mechanism and Kinetics of HIV-1 Protease Activation.Viruses · 2024Review
- Premature Activation of the HIV-1 Protease Is Influenced by Polymorphisms in the Hinge Region.Viruses · 2024Article
- Structure of the HIV immature lattice allows for essential lattice remodeling within budded virions.eLife · 2023Article
- Mutation of Phenylalanine 23 of Newcastle Disease Virus Matrix Protein Inhibits Virus Release by Disrupting the Interaction between the FPIV L-Domain and Charged Multivesicular Body Protein 4B.Microbiology spectrum · 2023Article
- The HIV-1 Viral Protease Is Activated during Assembly and Budding Prior to Particle Release.Journal of virology · 2022Article
- Perturbing HIV-1 Ribosomal Frameshifting Frequency Reveals aJournal of virology · 2022Article
- Embedding of HIV Egress within Cortical F-Actin.Pathogens (Basel, Switzerland) · 2022Article
- Article
- Article
- Gag-Gag Interactions Are Insufficient to Fully Stabilize and Order the Immature HIV Gag Lattice.Viruses · 2021Article
- Review
- Review
- Application of Advanced Light Microscopy to the Study of HIV and Its Interactions with the Host.Viruses · 2021Review
- HIV-1 Gag release from yeast reveals ESCRT interaction with the Gag N-terminal protein region.The Journal of biological chemistry · 2020Article
- Nanoscale flow cytometry reveals interpatient variability in HIV protease activity that correlates with viral infectivity and identifies drug-resistant viruses.Scientific reports · 2020Article
- Budding of a Retrovirus: Some Assemblies Required.Viruses · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HIV virions assemble on the plasma membrane and bud out of infected cells using interactions with endosomal sorting complexes required for transport (ESCRTs). HIV protease activation is essential for maturation and infectivity of progeny virions, however, the precise timing of protease activation and its relationship to budding has not been well defined. We show that compromised interactions with ESCRTs result in delayed budding of virions from host cells. Specifically, we show that Gag mutants with compromised interactions with ALIX and Tsg101, two early ESCRT factors, have an average budding delay of ~75 minutes and ~10 hours, respectively. Virions with inactive proteases incorporated the full Gag-Pol and had ~60 minutes delay in budding. We demonstrate that during budding delay, activated proteases release critical HIV enzymes back to host cytosol leading to production of non-infectious progeny virions. To explain the molecular mechanism of the observed budding delay, we modulated the Pol size artificially and show that virion release delays are size-dependent and also show size-dependency in requirements for Tsg101 and ALIX. We highlight the sensitivity of HIV to budding "on-time" and suggest that budding delay is a potent mechanism for inhibition of infectious retroviral release.
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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.