ArticleScientific reports2018
PYRE insertion within HIV-1 subtype C p6-Gag functions as an ALIX-dependent late domain.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Review
- Cytotoxic Lymphocytes Target HIV-1 Gag Through Granzyme M-Mediated Cleavage.Frontiers in immunology · 2021Article
- Role of the ESCRT Pathway in Laccase Trafficking and Virulence of Cryptococcus neoformans.Infection and immunity · 2020Article
- Article
- HIV-1 Subtype C with PYxE Insertion Has Enhanced Binding of Gag-p6 to Host Cell Protein ALIX and Increased Replication Fitness.Journal of virology · 2019Article
- Dendritic Cells, the Double Agent in the War Against HIV-1.Frontiers in immunology · 2019Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ALG-2 interacting protein X (ALIX) links HIV-1 Gag to the components of ESCRT-III. HIV-1 engages the ALIX via its nucleocapsid and LYPXnL motif in p6. Overexpression of ALIX corrects the release defect of PTAP deleted HIV-1 via LYPXnL/ALIX pathway. However, HIV-1 subtype C lacks the LYPXnL motif and hence cannot employ LYPXnL/ALIX mechanism. Though the preferential occurrences of PYXE insertion in HIV-1 C p6 is predicted to restore the ALIX binding site there is no functional proof to support these observations. In this study we show that HIV-1 construct with subtype C p6 having PTAP deletion and PYRE insertion (pNL-INp6ΔPTAP/PYRE) could respond to ALIX overexpression. Notably, conserved Phenyl alanine residue (F676) in ALIX was critical for ALIX mediated release of pNL-INp6ΔPTAP/PYRE implying the critical role of this hydrophobic patch in ALIX recruitment. In addition, we show that Nedd4-1 could also correct the release defect of pNL-INp6ΔPTAP/PYRE. Moreover, Nedd4-1 was more robust compared to ALIX in its ability to stimulate the release of pNL-INp6ΔPTAP/PYRE. Replication kinetic data highlights the positive effect of PYRE insertion on virus replication. In summary, our data reveals the functional role of PYRE insertion towards the cooperative mechanism of ALIX/Nedd4-1 in virus release in the absence of PTAP/Tsg101 pathway.
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