作者
Piyada Supasa, Daming Zhou, Wanwisa Dejnirattisai, Chang Liu, Alexander J Mentzer, Helen M Ginn, Yuguang Zhao, Helen ME Duyvesteyn, Rungtiwa Nutalai, Aekkachai Tuekprakhon, Beibei Wang, Guido C Paesen, Jose Slon-Campos, César López-Camacho, Bassam Hallis, Naomi Coombes, Kevin R Bewley, Sue Charlton, Thomas S Walter, Eleanor Barnes, Susanna J Dunachie, Donal Skelly, Sheila F Lumley, Natalie Baker, Imam Shaik, Holly E Humphries, Kerry Godwin, Nick Gent, Alex Sienkiewicz, Christina Dold, Robert Levin, Tao Dong, Andrew J Pollard, Julian C Knight, Paul Klenerman, Derrick Crook, Teresa Lambe, Elizabeth Clutterbuck, Sagida Bibi, Amy Flaxman, Mustapha Bittaye, Sandra Belij-Rammerstorfer, Sarah Gilbert, David R Hall, Mark A Williams, Neil G Paterson, William James, Miles W Carroll, Elizabeth E Fry, Juthathip Mongkolsapaya, Jingshan Ren, David I Stuart, Gavin R Screaton
发表日期
2021/4/15
期刊
Cell
卷号
184
期号
8
页码范围
2201-2211. e7
出版商
Cell Press
简介
SARS-CoV-2 has caused over 2 million deaths in little over a year. Vaccines are being deployed at scale, aiming to generate responses against the virus spike. The scale of the pandemic and error-prone virus replication is leading to the appearance of mutant viruses and potentially escape from antibody responses. Variant B.1.1.7, now dominant in the UK, with increased transmission, harbors 9 amino acid changes in the spike, including N501Y in the ACE2 interacting surface. We examine the ability of B.1.1.7 to evade antibody responses elicited by natural SARS-CoV-2 infection or vaccination. We map the impact of N501Y by structure/function analysis of a large panel of well-characterized monoclonal antibodies. B.1.1.7 is harder to neutralize than parental virus, compromising neutralization by some members of a major class of public antibodies through light-chain contacts with residue 501. However, widespread …
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