Cell ReportsMolecular BiologyPeer-reviewed journal article
SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination
Markus HoffmanniD, Heike Hofmann-Winkler, Nadine KrügeriD, Amy Madeleine Kempf, Inga NehlmeieriD, Luise Graichen, Prerna AroraiD, Anzhalika SidarovichiD, Anna-Sophie Moldenhauer, Martin Sebastian WinkleriD, Sebastian R. SchulziD, Hans‐Martin JäckiD, Metodi V. StankoviD, Georg M. N. BehrensiD, Stefan PöhlmanniD
Abstract
The emergence of SARS-CoV-2 variants threatens efforts to contain the COVID-19 pandemic. The number of COVID-19 cases and deaths in India has risen steeply in recent weeks and a novel SARS-CoV-2 variant, B.1.617, is believed to be responsible for many of these cases. The spike protein of B.1.617 harbors two mutations in the receptor binding domain, which interacts with the ACE2 receptor and constitutes the main target of neutralizing antibodies. Therefore, we analyzed whether B.1.617 is more adept in entering cells and/or evades antibody responses. B.1.617 entered two out of eight cell lines tested with slightly increased efficiency and was blocked by entry inhibitors. In contrast, B.1.617 was resistant against Bamlanivimab, an antibody used for COVID-19 treatment. Finally, B.1.617 evaded antibodies induced by infection or vaccination, although with moderate efficiency. Collectively, our study reveals that antibody evasion of B.1.617 may contribute to the rapid spread of this variant.
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