ArticleViruses2014
Analysis of determinants in filovirus glycoproteins required for tetherin antagonism.
Article in Viruses, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Marburg Virus Glycoprotein Is a Remarkable Virulent Factor Linked to Hemorrhagic Pathology: Evidence from Multimodal Experimental Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Interferon-Induced HERC5 Inhibits Ebola Virus Particle Production and Is Antagonized by Ebola Glycoprotein.Cells · 2021Article
- Viral Membrane Fusion and the Transmembrane Domain.Viruses · 2020Review
- BST2/Tetherin Overexpression Modulates Morbillivirus Glycoprotein Production to Inhibit Cell-Cell Fusion.Viruses · 2019Article
- Tetherin Inhibits Nipah Virus but Not Ebola Virus Replication in Fruit Bat Cells.Journal of virology · 2019Article
- Review
- Recent advances in marburgvirus research.F1000Research · 2019Review
- A GXXXA Motif in the Transmembrane Domain of the Ebola Virus Glycoprotein Is Required for Tetherin Antagonism.Journal of virology · 2018Article
- BST-2 controls T cell proliferation and exhaustion by shaping the early distribution of a persistent viral infection.PLoS pathogens · 2018Article
- Cooperation of the Ebola Virus Proteins VP40 and GPJournal of virology · 2017Article
- The lifecycle of the Ebola virus in host cells.Oncotarget · 2017Review
- The Tetherin Antagonism of the Ebola Virus Glycoprotein Requires an Intact Receptor-Binding Domain and Can Be Blocked by GP1-Specific Antibodies.Journal of virology · 2016Article
- Potent in vitro antiviral activity of Cistus incanus extract against HIV and Filoviruses targets viral envelope proteins.Scientific reports · 2016Article
- Article
- Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase.Journal of virology · 2015Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The host cell protein tetherin can restrict the release of enveloped viruses from infected cells. The HIV-1 protein Vpu counteracts tetherin by removing it from the site of viral budding, the plasma membrane, and this process depends on specific interactions between the transmembrane domains of Vpu and tetherin. In contrast, the glycoproteins (GPs) of two filoviruses, Ebola and Marburg virus, antagonize tetherin without reducing surface expression, and the domains in GP required for tetherin counteraction are unknown. Here, we show that filovirus GPs depend on the presence of their authentic transmembrane domains for virus-cell fusion and tetherin antagonism. However, conserved residues within the transmembrane domain were dispensable for membrane fusion and tetherin counteraction. Moreover, the insertion of the transmembrane domain into a heterologous viral GP, Lassa virus GPC, was not sufficient to confer tetherin antagonism to the recipient. Finally, mutation of conserved residues within the fusion peptide of Ebola virus GP inhibited virus-cell fusion but did not ablate tetherin counteraction, indicating that the fusion peptide and the ability of GP to drive host cell entry are not required for tetherin counteraction. These results suggest that the transmembrane domains of filoviral GPs contribute to tetherin antagonism but are not the sole determinants.
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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.