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SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination

View ORCID ProfileMarkus Hoffmann, Heike Hofmann-Winkler, View ORCID ProfileNadine Krüger, Amy Kempf, Inga Nehlmeier, Luise Graichen, Anzhalika Sidarovich, Anna-Sophie Moldenhauer, Martin S. Winkler, Sebastian Schulz, Hans-Martin Jäck, Metodi V. Stankov, Georg M. N. Behrens, View ORCID ProfileStefan Pöhlmann
doi: https://doi.org/10.1101/2021.05.04.442663
Markus Hoffmann
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
2Faculty of Biology and Psychology, Georg-August-University Göttingen, Wilhelmsplatz 1, 37073 Göttingen, Germany
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  • For correspondence: mhoffmann@dpz.eu spoehlmann@dpz.eu
Heike Hofmann-Winkler
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
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Nadine Krüger
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
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Amy Kempf
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
2Faculty of Biology and Psychology, Georg-August-University Göttingen, Wilhelmsplatz 1, 37073 Göttingen, Germany
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Inga Nehlmeier
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
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Luise Graichen
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
2Faculty of Biology and Psychology, Georg-August-University Göttingen, Wilhelmsplatz 1, 37073 Göttingen, Germany
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Anzhalika Sidarovich
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
2Faculty of Biology and Psychology, Georg-August-University Göttingen, Wilhelmsplatz 1, 37073 Göttingen, Germany
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Anna-Sophie Moldenhauer
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
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Martin S. Winkler
3Department of Anaesthesiology, University of Göttingen Medical Center, Göttingen, Georg-August University of Göttingen, Robert-Koch-Straße 40, 37075 Göttingen, Germany
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Sebastian Schulz
4Division of Molecular Immunology, Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nürnberg, Glückstraße 6, 91054 Erlangen, Germany
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Hans-Martin Jäck
4Division of Molecular Immunology, Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nürnberg, Glückstraße 6, 91054 Erlangen, Germany
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Metodi V. Stankov
5Department for Rheumatology and Immunology, Hannover Medical School, Carl-Neuberg-Str.1, 30625 Hannover, Germany
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Georg M. N. Behrens
5Department for Rheumatology and Immunology, Hannover Medical School, Carl-Neuberg-Str.1, 30625 Hannover, Germany
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Stefan Pöhlmann
1Infection Biology Unit, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
2Faculty of Biology and Psychology, Georg-August-University Göttingen, Wilhelmsplatz 1, 37073 Göttingen, Germany
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  • ORCID record for Stefan Pöhlmann
  • For correspondence: mhoffmann@dpz.eu spoehlmann@dpz.eu
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SUMMARY

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.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted May 05, 2021.
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SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination
Markus Hoffmann, Heike Hofmann-Winkler, Nadine Krüger, Amy Kempf, Inga Nehlmeier, Luise Graichen, Anzhalika Sidarovich, Anna-Sophie Moldenhauer, Martin S. Winkler, Sebastian Schulz, Hans-Martin Jäck, Metodi V. Stankov, Georg M. N. Behrens, Stefan Pöhlmann
bioRxiv 2021.05.04.442663; doi: https://doi.org/10.1101/2021.05.04.442663
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SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination
Markus Hoffmann, Heike Hofmann-Winkler, Nadine Krüger, Amy Kempf, Inga Nehlmeier, Luise Graichen, Anzhalika Sidarovich, Anna-Sophie Moldenhauer, Martin S. Winkler, Sebastian Schulz, Hans-Martin Jäck, Metodi V. Stankov, Georg M. N. Behrens, Stefan Pöhlmann
bioRxiv 2021.05.04.442663; doi: https://doi.org/10.1101/2021.05.04.442663

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