The glycoprotein of vesicular stomatitis virus promotes release of virus-like particles from tetherin-positive cells.
In: PLoS ONE, Jg. 12 (2017-12-07), Heft 12, S. 1-19
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Zugriff:
Vesicular stomatitis virus (VSV) release from infected cells is inhibited by the interferon (IFN)-inducible antiviral host cell factor tetherin (BST-2, CD317). However, several viruses encode tetherin antagonists and it is at present unknown whether residual VSV spread in tetherin-positive cells is also promoted by a virus-encoded tetherin antagonist. Here, we show that the viral glycoprotein (VSV-G) antagonizes tetherin in transfected cells, although with reduced efficiency as compared to the HIV-1 Vpu protein. Tetherin antagonism did not involve alteration of tetherin expression and was partially dependent on a GXXXG motif in the transmembrane domain of VSV-G. However, mutation of the GXXXG motif did not modulate tetherin sensitivity of infectious VSV. These results identify VSV-G as a tetherin antagonist in transfected cells but fail to provide evidence for a contribution of tetherin antagonism to viral spread. [ABSTRACT FROM AUTHOR]
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Titel: |
The glycoprotein of vesicular stomatitis virus promotes release of virus-like particles from tetherin-positive cells.
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Autor/in / Beteiligte Person: | Brinkmann, Constantin ; Hoffmann, Markus ; Lübke, Anastasia ; Nehlmeier, Inga ; Krämer-Kühl, Annika ; Winkler, Michael ; Pöhlmann, Stefan |
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Zeitschrift: | PLoS ONE, Jg. 12 (2017-12-07), Heft 12, S. 1-19 |
Veröffentlichung: | 2017 |
Medientyp: | academicJournal |
ISSN: | 1932-6203 (print) |
DOI: | 10.1371/journal.pone.0189073 |
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