Pöhlmann, Stefan

[["dc.bibliographiccitation.artnumber","e0265453"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Arora, Prerna"],["dc.contributor.author","Sidarovich, Anzhalika"],["dc.contributor.author","Graichen, Luise"],["dc.contributor.author","Hörnich, Bojan"],["dc.contributor.author","Hahn, Alexander"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.editor","Bogyo, Matthew"],["dc.date.accessioned","2022-04-01T10:02:01Z"],["dc.date.available","2022-04-01T10:02:01Z"],["dc.date.issued","2022"],["dc.description.abstract","Several SARS-CoV-2 variants emerged that harbor mutations in the surface unit of the viral spike (S) protein that enhance infectivity and transmissibility. Here, we analyzed whether ten naturally-occurring mutations found within the extended loop harboring the S1/S2 cleavage site of the S protein, a determinant of SARS-CoV-2 cell tropism and pathogenicity, impact S protein processing and function. None of the mutations increased but several decreased S protein cleavage at the S1/S2 site, including S686G and P681H, the latter of which is found in variants of concern B.1.1.7 (Alpha variant) and B.1.1.529 (Omicron variant). None of the mutations reduced ACE2 binding and cell-cell fusion although several modulated the efficiency of host cell entry. The effects of mutation S686G on viral entry were cell-type dependent and could be linked to the availability of cathepsin L for S protein activation. These results show that polymorphisms at the S1/S2 site can modulate S protein processing and host cell entry."],["dc.identifier.doi","10.1371/journal.pone.0265453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105803"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1932-6203"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Functional analysis of polymorphisms at the S1/S2 site of SARS-CoV-2 spike protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]