SARS-CoV-2 variant B.1.617 is resistant to bamlanivimab and evades antibodies induced by infection and vaccination
Author(s) -
Markus Hoffmann,
Heike Hofmann-Winkler,
Nadine Krüger,
Amy Kempf,
Inga Nehlmeier,
Luise Graichen,
Prerna Arora,
Anzhalika Sidarovich,
Anna-Sophie Moldenhauer,
Martin Sebastian Winkler,
Sebastian Schulz,
HansMartin Jäck,
Metodi V. Stankov,
Georg M. N. Behrens,
Stefan Pöhlmann
Publication year - 2021
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2021.109415
Subject(s) - antibody , virology , vaccination , spike protein , biology , receptor , covid-19 , coronavirus , b cell , immunology , pandemic , medicine , disease , genetics , infectious disease (medical specialty)
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 and a 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 analyze whether B.1.617 is more adept in entering cells and/or evades antibody responses. B.1.617 enters two out of eight cell lines tested with roughly 50% increased efficiency and is equally inhibited by two entry inhibitors. In contrast, B.1.617 is resistant against Bamlanivimab, an antibody used for COVID-19 treatment. B.1.617 evades antibodies induced by infection or vaccination, although less so than the B.1.351 variant. Collectively, our study reveals that antibody evasion of B.1.617 may contribute to the rapid spread of this variant.
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