Winkler, Michael

[["dc.bibliographiccitation.firstpage","S210"],["dc.bibliographiccitation.issue","suppl 2"],["dc.bibliographiccitation.journal","Journal of Infectious Diseases"],["dc.bibliographiccitation.lastpage","S218"],["dc.bibliographiccitation.volume","212"],["dc.contributor.author","Wrensch, Florian"],["dc.contributor.author","Karsten, Christina B."],["dc.contributor.author","Gnirß, Kerstin"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Lu, Kai"],["dc.contributor.author","Takada, Ayato"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Simmons, Graham"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2022-10-06T13:35:09Z"],["dc.date.available","2022-10-06T13:35:09Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1093/infdis/jiv255"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116027"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1537-6613"],["dc.relation.issn","0022-1899"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Interferon-Induced Transmembrane Protein–Mediated Inhibition of Host Cell Entry of Ebolaviruses"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9178"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Journal of Virology"],["dc.bibliographiccitation.lastpage","9188"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Gnirß, Kerstin"],["dc.contributor.author","Zmora, Pawel"],["dc.contributor.author","Blazejewska, Paulina"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Lins, Anika"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Moldenhauer, Anna-Sophie"],["dc.contributor.author","Hofmann-Winkler, Heike"],["dc.contributor.author","Wolff, Thorsten"],["dc.contributor.editor","Lyles, D. S."],["dc.date.accessioned","2022-10-06T13:25:33Z"],["dc.date.available","2022-10-06T13:25:33Z"],["dc.date.issued","2015"],["dc.description.abstract","ABSTRACT\n The expression of the antiviral host cell factor tetherin is induced by interferon and can inhibit the release of enveloped viruses from infected cells. The Vpu protein of HIV-1 antagonizes the antiviral activity of tetherin, and tetherin antagonists with Vpu-like activity have been identified in other viruses. In contrast, it is incompletely understood whether tetherin inhibits influenza A virus (FLUAV) release and whether FLUAV encodes tetherin antagonists. Here, we show that release of several laboratory-adapted FLUAV strains and a seasonal FLUAV strain is inhibited by tetherin, while pandemic FLUAV A/Hamburg/4/2009 is resistant. Studies with a virus-like particle system and analysis of reassortant viruses provided evidence that the viral hemagglutinin (HA) is an important determinant of tetherin antagonism but requires the presence of its cognate neuraminidase (NA) to inhibit tetherin. Finally, tetherin antagonism by FLUAV was dependent on the virion context, since retrovirus release from tetherin-positive cells was not rescued, and correlated with an HA- and NA-dependent reduction in tetherin expression. In sum, our study identifies HA and NA proteins of certain pandemic FLUAV as tetherin antagonists, which has important implications for understanding FLUAV pathogenesis.\n \n IMPORTANCE\n Influenza A virus (FLUAV) infection is responsible for substantial global morbidity and mortality, and understanding how the virus evades the immune defenses of the host may uncover novel targets for antiviral intervention. Tetherin is an antiviral effector molecule of the innate immune system which can contribute to control of viral invasion. However, it has been unclear whether FLUAV is inhibited by tetherin and whether these viruses encode tetherin-antagonizing proteins. Our observation that several pandemic FLUAV strains can counteract tetherin via their HA and NA proteins identifies these proteins as novel tetherin antagonists and indicates that HA/NA-dependent inactivation of innate defenses may contribute to the efficient spread of pandemic FLUAV."],["dc.identifier.doi","10.1128/JVI.00615-15"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114866"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1098-5514"],["dc.relation.issn","0022-538X"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights.uri","https://journals.asm.org/non-commercial-tdm-license"],["dc.title","Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e43337"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Bertram, Stephanie"],["dc.contributor.author","Gnirß, Kerstin"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Gawanbacht, Ali"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Ehrhardt, Christina"],["dc.contributor.author","Ludwig, Stephan"],["dc.contributor.author","Kiene, Miriam"],["dc.contributor.author","Moldenhauer, Anna-Sophie"],["dc.contributor.author","Goedecke, Ulrike"],["dc.contributor.author","Karsten, Christina B."],["dc.contributor.author","Kühl, Annika"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2019-07-09T11:53:44Z"],["dc.date.available","2019-07-09T11:53:44Z"],["dc.date.issued","2012"],["dc.description.abstract","The interferon-induced host cell factor tetherin inhibits release of human immunodeficiency virus (HIV) from the plasma membrane of infected cells and is counteracted by the HIV-1 protein Vpu. Influenza A virus (FLUAV) also buds from the plasma membrane and is not inhibited by tetherin. Here, we investigated if FLUAV encodes a functional equivalent of Vpu for tetherin antagonism. We found that expression of the FLUAV protein NS1, which antagonizes the interferon (IFN) response, did not block the tetherin-mediated restriction of HIV release, which was rescued by Vpu. Similarly, tetherinmediated inhibition of HIV release was not rescued by FLUAV infection. In contrast, FLUAV infection induced tetherin expression on target cells in an IFN-dependent manner. These results suggest that FLUAV escapes the antiviral effects of tetherin without encoding a tetherin antagonist with Vpu-like activity."],["dc.identifier.doi","10.1371/journal.pone.0043337"],["dc.identifier.fs","588509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60484"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Influenza A Virus Does Not Encode a Tetherin Antagonist with Vpu-Like Activity and Induces IFN-Dependent Tetherin Expression in Infected Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]