ArticleJournal of molecular biology2015
Elucidating the mechanism by which compensatory mutations rescue an HIV-1 matrix mutant defective for gag membrane targeting and envelope glycoprotein incorporation.
Article in Journal of molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016Pooled it
- Different mechanisms for human rhinovirus survival in the presence of deleterious amino acid substitutions at virion protein-protein or RNA-protein interfaces.Journal of virology · 2026Article
- Reconstructing a Missing Link of HIV-1 Assembly: HIV-1 Envelope-Matrix Interactions in a Native Viral Context.bioRxiv : the preprint server for biology · 2026Article
- The Assembly of HTLV-1-How Does It Differ from HIV-1?Viruses · 2024Review
- Second site reversion of HIV-1 envelope protein baseplate mutations maps to the matrix protein.Journal of virology · 2024Article
- KIF16B Mediates Anterograde Transport and Modulates Lysosomal Degradation of the HIV-1 Envelope Glycoprotein.Journal of virology · 2023Article
- Advances in HIV-1 Assembly.Viruses · 2022Review
- Elucidating the Basis for Permissivity of the MT-4 T-Cell Line to Replication of an HIV-1 Mutant Lacking the gp41 Cytoplasmic Tail.Journal of virology · 2020Article
- Mechanisms of PI(4,5)P2 Enrichment in HIV-1 Viral Membranes.Journal of molecular biology · 2020Article
- Review
- HIV-1 Matrix Trimerization-Impaired Mutants Are Rescued by Matrix Substitutions That Enhance Envelope Glycoprotein Incorporation.Journal of virology · 2019Article
- Analysis of HIV-1 Matrix-Envelope Cytoplasmic Tail Interactions.Journal of virology · 2019Article
- Sequence Determinants in Gammaretroviral Env Cytoplasmic Tails Dictate Virus-Specific Pseudotyping Compatibility.Journal of virology · 2019Article
- H1N1 influenza virus epitopes classified by monoclonal antibodies.Experimental and therapeutic medicine · 2018Article
- Article
- Synchronized HIV assembly by tunable PIPeLife · 2017Article
- Trimer Enhancement Mutation Effects on HIV-1 Matrix Protein Binding Activities.Journal of virology · 2016Article
- Application of virus-like particles (VLP) to NMR characterization of viral membrane protein interactions.Journal of biomolecular NMR · 2016Article
- Equine Infectious Anemia Virus Gag Assembly and Export Are Directed by Matrix Protein through trans-Golgi Networks and Cellular Vesicles.Journal of virology · 2016Article
- Biochemical evidence of a role for matrix trimerization in HIV-1 envelope glycoprotein incorporation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The matrix (MA) domain of the human immunodeficiency virus (HIV) 1 Gag is responsible for Gag targeting to the plasma membrane where virions assemble. MA also plays a role in the incorporation of the viral envelope (Env) glycoproteins and can influence particle infectivity post-maturation and post-entry. A highly basic region of MA targets Gag to the plasma membrane via specific binding to phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2]. This binding also triggers exposure of an amino-terminal myristate moiety, which anchors Gag to the membrane. An MA mutant deficient for PI(4,5)P2 binding, 29KE/31KE, has been shown to mislocalize within the cell, leading to particle assembly in a multivesicular body compartment and defective release of cell-free particles in HeLa and 293T cells. Despite the defect in virus production in these cells, release of the 29KE/31KE mutant is not significantly reduced in primary T cells, macrophages and Jurkat T cells. 29KE/31KE virions also display an infectivity defect associated with impaired Env incorporation, irrespective of the producer cell line. Here we examine the properties of 29KE/31KE by analyzing compensatory mutations obtained by a viral adaptation strategy. The MA mutant 16EK restores virus release through enhanced membrane binding. 16EK also influences the infectivity defect, in combination with an additional MA mutant, 62QR. Additionally, the 29KE/31KE MA mutant displays a defect in proteolytic cleavage of the murine leukemia virus Env cytoplasmic tail in pseudotyped virions. Our findings elucidate the mechanism whereby an MA mutant defective in PI(4,5)P2 binding can be rescued and highlight the ability of MA to influence Env glycoprotein function.
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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.