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Evidence of escape of SARS-CoV-2 variant B.1.351 from natural and vaccine-induced sera

2021; Cell Press; Volume: 184; Issue: 9 Linguagem: Inglês

10.1016/j.cell.2021.02.037

1097-4172

Daming Zhou, Wanwisa Dejnirattisai, Piyada Supasa, Chang Liu, Alexander J. Mentzer, Helen M. Ginn, Yuguang Zhao, Helen M. E. Duyvesteyn, Aekkachai Tuekprakhon, Rungtiwa Nutalai, Beibei Wang, Guido C. Paesen, César López‐Camacho, Jose Slon-Campos, Bassam Hallis, Naomi S. Coombes, Kevin R. Bewley, Sue Charlton, Thomas S. Walter, Donal Skelly, Sheila Lumley, Christina Dold, Robert H. Levin, Tao Dong, Andrew J. Pollard, Julian C. Knight, Derrick W. Crook, Teresa Lambe, Elizabeth Clutterbuck, Sagida Bibi, Amy Flaxman, Mustapha Bittaye, Sandra Belij‐Rammerstorfer, Sarah C. Gilbert, William James, Miles W. Carroll, Paul Klenerman, Eleanor Barnes, Susanna Dunachie, Elizabeth E. Fry, Juthathip Mongkolsapaya, Jingshan Ren, David I. Stuart, Gavin Screaton,

Animal Virus Infections Studies

Highlights•Reduced B.1.351 neutralization by mAbs and sera induced by early SARS-CoV-2 isolates•B.1.351 neutralization titer reduced 8- to 9-fold for Pfizer and AstraZeneca vaccinees•E484K, K417N, and N501Y cause widespread escape from mAbs•NTD deletion in B.1.351 abrogates neutralization by a potent neutralizing human mAbSummaryThe race to produce vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) began when the first sequence was published, and this forms the basis for vaccines currently deployed globally. Independent lineages of SARS-CoV-2 have recently been reported: UK, B.1.1.7; South Africa, B.1.351; and Brazil, P.1. These variants have multiple changes in the immunodominant spike protein that facilitates viral cell entry via the angiotensin-converting enzyme-2 (ACE2) receptor. Mutations in the receptor recognition site on the spike are of great concern for their potential for immune escape. Here, we describe a structure-function analysis of B.1.351 using a large cohort of convalescent and vaccinee serum samples. The receptor-binding domain mutations provide tighter ACE2 binding and widespread escape from monoclonal antibody neutralization largely driven by E484K, although K417N and N501Y act together against some important antibody classes. In a number of cases, it would appear that convalescent and some vaccine serum offers limited protection against this variant.Graphical abstract