Emerging variants develop total escape from potent monoclonal antibodies induced by BA.4/5 infection

Chang Liu, Raksha Das, Aiste Dijokaite-Guraliuc, Daming Zhou, Alexander J. Mentzer, Piyada Supasa, Muneeswaran Selvaraj, Helen M. E. Duyvesteyn, Thomas G. Ritter, Nigel Temperton, Paul Klenerman, Susanna J. Dunachie, Neil G. Paterson, Mark A. Williams, David R. Hall, Elizabeth E. Fry (), Juthathip Mongkolsapaya (), Jingshan Ren (), David I. Stuart () and Gavin R. Screaton ()
Additional contact information
Chang Liu: University of Oxford
Raksha Das: University of Oxford
Aiste Dijokaite-Guraliuc: University of Oxford
Daming Zhou: University of Oxford
Alexander J. Mentzer: University of Oxford
Piyada Supasa: University of Oxford
Muneeswaran Selvaraj: University of Oxford
Helen M. E. Duyvesteyn: The Wellcome Centre for Human Genetics
Thomas G. Ritter: Oxford University Hospitals NHS Foundation Trust
Nigel Temperton: University of Kent and Greenwich Chatham Maritime
Paul Klenerman: Oxford University Hospitals NHS Foundation Trust
Susanna J. Dunachie: Oxford University Hospitals NHS Foundation Trust
Neil G. Paterson: Harwell Science & Innovation Campus
Mark A. Williams: Harwell Science & Innovation Campus
David R. Hall: Harwell Science & Innovation Campus
Elizabeth E. Fry: The Wellcome Centre for Human Genetics
Juthathip Mongkolsapaya: University of Oxford
Jingshan Ren: The Wellcome Centre for Human Genetics
David I. Stuart: University of Oxford
Gavin R. Screaton: University of Oxford

Nature Communications, 2024, vol. 15, issue 1, 1-10

Abstract: Abstract The rapid evolution of SARS-CoV-2 is driven in part by a need to evade the antibody response in the face of high levels of immunity. Here, we isolate spike (S) binding monoclonal antibodies (mAbs) from vaccinees who suffered vaccine break-through infections with Omicron sub lineages BA.4 or BA.5. Twenty eight potent antibodies are isolated and characterised functionally, and in some cases structurally. Since the emergence of BA.4/5, SARS-CoV-2 has continued to accrue mutations in the S protein, to understand this we characterize neutralization of a large panel of variants and demonstrate a steady attrition of neutralization by the panel of BA.4/5 mAbs culminating in total loss of function with recent XBB.1.5.70 variants containing the so-called ‘FLip’ mutations at positions 455 and 456. Interestingly, activity of some mAbs is regained on the recently reported variant BA.2.86.

Date: 2024
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DOI: 10.1038/s41467-024-47393-3

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