Circulating SARS-CoV-2 spike N439K variants maintain fitness while evading antibody-mediated immunity

Thomson, Emma C.; Rosen, Laura E.; Shepherd, James G.; Spreafico, Roberto; da Silva Filipe, Ana; Wojcechowskyj, Jason A.; Davis, Chris; Piccoli, Luca; Pascall, David J.; Dillen, Josh; Lytras, Spyros; Czudnochowski, Nadine; Shah, Rajiv; Meury, Marcel; Jesudason, Natasha; De Marco, Anna; Li, Kathy; Bassi, Jessica; O’Toole, Aine; Pinto, Dora; Colquhoun, Rachel M.; Culap, Katja; Jackson, Ben; Zatta, Fabrizia; Rambaut, Andrew; Jaconi, Stefano; Sreenu, Vattipally B.; Nix, Jay; Zhang, Ivy; Jarrett, Ruth F.; Glass, William G.; Beltramello, Martina; Nomikou, Kyriaki; Pizzuto, Matteo; Tong, Lily; Cameroni, Elisabetta; Croll, Tristan I.; Johnson, Natasha; Di Iulio, Julia; Wickenhagen, Arthur; Ceschi, Alessandro; Harbison, Aoife M.; Mair, Daniel; Ferrari, Paolo; Smollett, Katherine; Sallusto, Federica; Carmichael, Stephen; Garzoni, Christian; Nichols, Jenna; Galli, Massimo; Hughes, Joseph; Riva, Agostino; Ho, Antonia; Schiuma, Marco; Semple, Malcolm G.; Openshaw, Peter J.M.; Fadda, Elisa; Baillie, J. Kenneth; Chodera, John D.; Rihn, Suzannah J.; Lycett, Samantha J.; Virgin, Herbert W.; Telenti, Amalio; Corti, Davide; Robertson, David L.; Snell, Gyorgy

doi:10.1016/j.cell.2021.01.037

Circulating SARS-CoV-2 spike N439K variants maintain fitness while evading antibody-mediated immunity

Journal Article · Thu Jan 28 00:00:00 EST 2021 · Cell

DOI:https://doi.org/10.1016/j.cell.2021.01.037· OSTI ID:1807486

^[1]; ^[2]; ^[3]; ^[2]; ^[3]; Wojcechowskyj, Jason A. ^[2]; Davis, Chris ^[3]; ^[4]; ^[3]; Dillen, Josh ^[2]; ^[3]; ^[2]; ^[3]; ^[2]; Jesudason, Natasha ^[3]; De Marco, Anna ^[4]; Li, Kathy ^[3]; Bassi, Jessica ^[4]; O’Toole, Aine ^[5]; Pinto, Dora ^[4] more »

Univ. of Glasgow, Scotland (United Kingdom); London School of Hygiene and Tropical Medicine, London (United Kingdom)
Vir Biotechnology, San Francisco, CA (United States)
Univ. of Glasgow, Scotland (United Kingdom)
Humabs Biomed SA, Bellinzona (Switzerland)
Univ. of Edinburgh, Scotland (United Kingdom)
Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
Memorial Sloan Kettering Cancer Center, New York, NY (United States); Weill Cornell Graduate School of Medical Sciences, New York, NY (United States)
Memorial Sloan Kettering Cancer Center, New York, NY (United States)
Univ. of Cambridge (United Kingdom)
Univ. della Svizzera italiana, Lugano (Switzerland); Inst. of Pharmacological Sciences of Southern Switzerland, Lugano (Switzerland); Univ. Hospital, Zurich (Switzerland)
Maynooth Univ. (Ireland)
Ente Ospedaliero Cantonale, Lugano (Switzerland); Univ. of New South Wales, Sydney, NSW (Australia)
Univ. della Svizzera italiana, Bellinzona (Switzerland); Eidgenoessische Technische Hochschule (ETH), Zurich (Switzerland)
Clinica Luganese Moncucco, Lugano (Switzerland)
Luigi Sacco Hospital, Milan (Italy)
Univ. of Liverpool (United Kingdom); Alder Hey Children's Hospital, Liverpool (United Kingdom)
Imperial College, London (United Kingdom)
Univ. of Edinburgh, Scotland (United Kingdom); Royal Infirmary, Edinburgh, Scotland (United Kingdom)
Vir Biotechnology, San Francisco, CA (United States); Washington Univ., St. Louis, MO (United States)

SARS-CoV-2 can mutate and evade immunity, with consequences for efficacy of emerging vaccines and antibody therapeutics. Here, we demonstrate that the immunodominant SARS-CoV-2 spike (S) receptor binding motif (RBM) is a highly variable region of S and provide epidemiological, clinical, and molecular characterization of a prevalent, sentinel RBM mutation, N439K. We demonstrate N439K S protein has enhanced binding affinity to the hACE2 receptor, and N439K viruses have similar in vitro replication fitness and cause infections with similar clinical outcomes as compared to wild type. We show the N439K mutation confers resistance against several neutralizing monoclonal antibodies, including one authorized for emergency use by the US Food and Drug Administration (FDA), and reduces the activity of some polyclonal sera from persons recovered from infection. Immune evasion mutations that maintain virulence and fitness such as N439K can emerge within SARS-CoV-2 S, highlighting the need for ongoing molecular surveillance to guide development and usage of vaccines and therapeutics.

View Accepted Manuscript (DOE)

Research Organization:: Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)

Sponsoring Organization:: Bill and Melinda Gates Foundation; Liverpool Experimental Cancer Medicine Centre; Medical Research Council (MRC); National Institutes of Health (NIH); USDOE Office of Science (SC); University of Oxford; Wellcome Trust

Grant/Contract Number:: AC02-05CH11231

OSTI ID:: 1807486

Journal Information:: Cell, Journal Name: Cell Journal Issue: 5 Vol. 184; ISSN 0092-8674

Publisher:: ElsevierCopyright Statement

Country of Publication:: United States

Language:: English

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Additional file 2 of Comprehensive mapping of binding hot spots of SARS-CoV-2 RBD-specific neutralizing antibodies for tracking immune escape variants Yi, Chunyan; Sun, Xiaoyu; Lin, Yixiao figshare https://doi.org/10.6084/m9.figshare.16815702	dataset	January 2021
Additional file 3 of Comprehensive mapping of binding hot spots of SARS-CoV-2 RBD-specific neutralizing antibodies for tracking immune escape variants Yi, Chunyan; Sun, Xiaoyu; Lin, Yixiao figshare https://doi.org/10.6084/m9.figshare.16815705	dataset	January 2021
Additional file 4 of Comprehensive mapping of binding hot spots of SARS-CoV-2 RBD-specific neutralizing antibodies for tracking immune escape variants Yi, Chunyan; Sun, Xiaoyu; Lin, Yixiao figshare https://doi.org/10.6084/m9.figshare.16815708	dataset	January 2021

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60 APPLIED LIFE SCIENCES
COVID-19
N439K
SARS-CoV-2
monoclonal antibody escape
mutation
protein structure
receptor binding motif
spike
variant

Circulating SARS-CoV-2 spike N439K variants maintain fitness while evading antibody-mediated immunity

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Cited By (3)

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