PT  - JOURNAL ARTICLE
AU  - Markus Hoffmann
AU  - Prerna Arora
AU  - Rüdiger Groß
AU  - Alina Seidel
AU  - Bojan Hörnich
AU  - Alexander Hahn
AU  - Nadine Krüger
AU  - Luise Graichen
AU  - Heike Hofmann-Winkler
AU  - Amy Kempf
AU  - Martin Sebastian Winkler
AU  - Sebastian Schulz
AU  - Hans-Martin Jäck
AU  - Bernd Jahrsdörfer
AU  - Hubert Schrezenmeier
AU  - Martin Müller
AU  - Alexander Kleger
AU  - Jan Münch
AU  - Stefan Pöhlmann
TI  - SARS-CoV-2 variants B.1.351 and B.1.1.248: Escape from therapeutic antibodies and antibodies induced by infection and vaccination
AID  - 10.1101/2021.02.11.430787
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.02.11.430787
4099  - http://biorxiv.org/content/early/2021/02/11/2021.02.11.430787.short
4100  - http://biorxiv.org/content/early/2021/02/11/2021.02.11.430787.full
AB  - The global spread of SARS-CoV-2/COVID-19 is devastating health systems and economies worldwide. Recombinant or vaccine-induced neutralizing antibodies are used to combat the COVID-19 pandemic. However, recently emerged SARS-CoV-2 variants B.1.1.7 (UK), B.1.351 (South Africa) and B.1.1.248 (Brazil) harbor mutations in the viral spike (S) protein that may alter virus-host cell interactions and confer resistance to inhibitors and antibodies. Here, using pseudoparticles, we show that entry of UK, South Africa and Brazil variant into human cells is susceptible to blockade by entry inhibitors. In contrast, entry of the South Africa and Brazil variant was partially (Casirivimab) or fully (Bamlanivimab) resistant to antibodies used for COVID-19 treatment and was less efficiently inhibited by serum/plasma from convalescent or BNT162b2 vaccinated individuals. These results suggest that SARS-CoV-2 may escape antibody responses, which has important implications for efforts to contain the pandemic.Competing Interest StatementThe authors have declared no competing interest.