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Nehls, J. ; Businger, R.* ; Hoffmann, M.* ; Brinkmann, C.* ; Fehrenbacher, B.* ; Schaller, M.* ; Maurer, B.* ; Schönfeld, C.* ; Kramer, D.* ; Hailfinger, S.* ; Pöhlmann, S.* ; Schindler, M.

Release of immunomodulatory Ebola virus glycoprotein-containingmicrovesicles is suppressed by tetherin in a species-specific manner.

Cell Rep. 26, 1841-1853.e6 (2019)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
The Ebola virus glycoprotein (EBOV-GP) forms GP-containing microvesicles, so-called virosomes, which are secreted from GP-expressing cells. However, determinants of GP-virosome release and their functionality are poorly understood. We characterized GP-mediated virosome formation and delineated the role of the antiviral factor tetherin (BST2, CD317) in this process. Residues in the EBOV-GP receptor-binding domain (RBD) promote GP-virosome secretion, while tetherin suppresses GP-virosomes by interactions involving the GP-transmembrane domain. Tetherin from multiple species interfered with GP-virosome release, and tetherin from the natural fruit bat reservoir showed the highest inhibitory activity. Moreover, analyses of GP from various ebo-lavirus strains, including the EBOV responsible for the West African epidemic, revealed the most efficient GP-virosome formation by highly pathogenic ebolaviruses. Finally, EBOV-GP-virosomes were immunomodulatory and acted as decoys for EBOV-neutralizing antibodies. Our results indicate that GP-virosome formation might be a determinant of EBOV immune evasion and pathogenicity, which is suppressed by tetherin.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Ebola Virus ; Antiviral Immune Response ; Exosome ; Glycoprotein ; Immune Evasion ; Immune Modulation ; Microvesicles ; Neutralizing Antibody ; Tetherin ; Virosome; Filovirus Glycoproteins; Hiv-1 Release; Cell-surface; Life-cycle; Protein; Entry; Infection; Binding; Pathogenesis; Restriction
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 26, Heft: 7, Seiten: 1841-1853.e6 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed