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Reduced sensitivity of infectious SARS-CoV-2 variant B.1.617.2 to monoclonal antibodies and sera from convalescent and vaccinated individuals

Delphine Planas; David Veyer; Artem Baidaliuk; Isabelle Staropoli; Florence Guivel-Benhassine; Maaran Rajah; Cyril Planchais; Francoise Porrot; Nicolas Robillard; Julien Puech; Matthieu Prot; Floriane Gallais; Pierre Gantner; Aurelie Velay; Julien Le Guen; Najibi Kassis-Chikhani; Dhiaeddine Edriss; Laurent Belec; Aymeric Seve; Helene Pere; Laura Courtellemenont; Laurent Hocqueloux; Samira Fafi-Kremer; Thierry Prazuck; Hugo Mouquet; Timothee Bruel; Etienne Simon-Loriere; Felix Rey; Olivier Schwartz.
Preprint en Inglés | PREPRINT-BIORXIV | ID: ppbiorxiv-445838
The SARS-CoV-2 B.1.617 lineage emerged in October 2020 in India1-6. It has since then become dominant in some indian regions and further spread to many countries. The lineage includes three main subtypes (B1.617.1, B.1617.2 and B.1.617.3), which harbour diverse Spike mutations in the N-terminal domain (NTD) and the receptor binding domain (RBD) which may increase their immune evasion potential. B.1.617.2 is believed to spread faster than the other versions. Here, we isolated infectious B.1.617.2 from a traveller returning from India. We examined its sensitivity to monoclonal antibodies (mAbs) and to antibodies present in sera from COVID-19 convalescent individuals or vaccine recipients, in comparison to other viral lineages. B.1.617.2 was resistant to neutralization by some anti-NTD and anti-RBD mAbs, including Bamlanivimab, which were impaired in binding to the B.1.617.2 Spike. Sera from convalescent patients collected up to 12 months post symptoms and from Pfizer Comirnaty vaccine recipients were 3 to 6 fold less potent against B.1.617.2, relative to B.1.1.7. Sera from individuals having received one dose of AstraZeneca Vaxzevria barely inhibited B.1.617.2. Thus, B.1.617.2 spread is associated with an escape to antibodies targeting non-RBD and RBD Spike epitopes.