ArticleViruses2016
Mutation of Glycosylation Sites in BST-2 Leads to Its Accumulation at Intracellular CD63-Positive Vesicles without Affecting Its Antiviral Activity against Multivesicular Body-Targeted HIV-1 and Hepatitis B Virus.
Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
- Human BST2 inhibits rabies virus release independently of cysteine-linked dimerization and asparagine-linked glycosylation.PloS one · 2023Article
- Genetic and Molecular Characterization of the Immortalized Murine Hepatic Stellate Cell Line GRX.Cells · 2022Article
- Review
- Glycosylation Modulates Plasma Membrane Trafficking of CD24 in Breast Cancer Cells.International journal of molecular sciences · 2021Article
- Increased BST-2 expression by HBV infection promotes HBV-associated HCC tumorigenesis.Journal of gastrointestinal oncology · 2021Article
- The N-glycosylation of Equine Tetherin Affects Antiviral Activity by Regulating Its Subcellular Localization.Viruses · 2020Article
- ATP1B3 cooperates with BST-2 to promote hepatitis B virus restriction.Journal of medical virology · 2020Article
- High-Mannose But Not Complex-Type Glycosylation of Tetherin Is Required for Restriction of HIV-1 Release.Viruses · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BST-2/tetherin blocks the release of various enveloped viruses including HIV-1 with a "physical tethering" model. The detailed contribution of N-linked glycosylation to this model is controversial. Here, we confirmed that mutation of glycosylation sites exerted an effect of post-translational mis-trafficking, leading to an accumulation of BST-2 at intracellular CD63-positive vesicles. BST-2 with this phenotype potently inhibited the release of multivesicular body-targeted HIV-1 and hepatitis B virus, without affecting the co-localization of BST-2 with EEA1 and LAMP1. These results suggest that N-linked glycosylation of human BST-2 is dispensable for intracellular virion retention and imply that this recently discovered intracellular tethering function may be evolutionarily distinguished from the canonical antiviral function of BST-2 by tethering nascent virions at the cell surface.
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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.