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

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Evidence of escape of SARS-CoV-2 variant B.1.351 from natural and vaccine-induced sera
Cell ( IF 45.5 ) Pub Date : 2021-02-23 , DOI: 10.1016/j.cell.2021.02.037
Daming Zhou ₁ , Wanwisa Dejnirattisai ₂ , Piyada Supasa ₂ , Chang Liu ₃ , Alexander J Mentzer ₄ , Helen M Ginn ₅ , Yuguang Zhao ₁ , Helen M E Duyvesteyn ₁ , Aekkachai Tuekprakhon ₂ , Rungtiwa Nutalai ₂ , Beibei Wang ₂ , Guido C Paesen ₁ , Cesar Lopez-Camacho ₂ , Jose Slon-Campos ₂ , Bassam Hallis ₆ , Naomi Coombes ₆ , Kevin Bewley ₆ , Sue Charlton ₆ , Thomas S Walter ₂ , Donal Skelly ₇ , Sheila F Lumley ₈ , Christina Dold ₉ , Robert Levin ₁₀ , Tao Dong ₁₁ , Andrew J Pollard ₉ , Julian C Knight ₁₂ , Derrick Crook ₁₃ , Teresa Lambe ₁₄ , Elizabeth Clutterbuck ₉ , Sagida Bibi ₉ , Amy Flaxman ₁₄ , Mustapha Bittaye ₁₄ , Sandra Belij-Rammerstorfer ₁₄ , Sarah Gilbert ₁₄ , William James ₁₅ , Miles W Carroll ₁₆ , Paul Klenerman ₁₇ , Eleanor Barnes ₁₇ , Susanna J Dunachie ₁₈ , Elizabeth E Fry ₁ , Juthathip Mongkolsapaya ₁₉ , Jingshan Ren ₁ , David I Stuart ₂₀ , Gavin R Screaton ₃

Affiliation

Division of Structural Biology, Nuffield Department of Medicine, University of Oxford, The Wellcome Centre for Human Genetics, Oxford, UK.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK; Chinese Academy of Medical Science (CAMS), Oxford Institute (COI), University of Oxford, Oxford, UK.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK; Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Instruct-ERIC, Oxford House, Parkway Court, John Smith Drive, Oxford, UK.
National Infection Service, Public Health England (PHE), Porton Down, Salisbury, UK.
Oxford University Hospitals NHS Foundation Trust, Oxford, UK; Peter Medawar Building for Pathogen Research, Oxford, UK; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Oxford University Hospitals NHS Foundation Trust, Oxford, UK; Nuffield Department of Medicine, University of Oxford, Oxford, UK.
NIHR Oxford Biomedical Research Centre, Oxford, UK; Oxford Vaccine Group, Department of Paediatrics, University of Oxford, Oxford, UK.
Worthing Hospital, Worthing, UK.
Chinese Academy of Medical Science (CAMS), Oxford Institute (COI), University of Oxford, Oxford, UK; Nuffield Department of Medicine, University of Oxford, Oxford, UK; MRC Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK; Chinese Academy of Medical Science (CAMS), Oxford Institute (COI), University of Oxford, Oxford, UK; Oxford University Hospitals NHS Foundation Trust, Oxford, UK; NIHR Oxford Biomedical Research Centre, Oxford, UK.
Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Sir William Dunn School of Pathology University of Oxford, Oxford, UK.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK; National Infection Service, Public Health England (PHE), Porton Down, Salisbury, UK.
Oxford University Hospitals NHS Foundation Trust, Oxford, UK; Peter Medawar Building for Pathogen Research, Oxford, UK; NIHR Oxford Biomedical Research Centre, Oxford, UK; Translational Gastroenterology Unit, University of Oxford, Oxford, UK.
Oxford University Hospitals NHS Foundation Trust, Oxford, UK; Peter Medawar Building for Pathogen Research, Oxford, UK; Nuffield Department of Medicine, University of Oxford, Oxford, UK; Centre For Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK; Mahidol-Oxford Tropical Medicine Research Unit, Bangkok, Thailand.
Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK; Chinese Academy of Medical Science (CAMS), Oxford Institute (COI), University of Oxford, Oxford, UK; Siriraj Center of Research Excellence in Dengue & Emerging Pathogens, Dean Office for Research, Faculty of Medicine Siriraj Hospital, Mahidol University, Thailand.
Division of Structural Biology, Nuffield Department of Medicine, University of Oxford, The Wellcome Centre for Human Genetics, Oxford, UK; Chinese Academy of Medical Science (CAMS), Oxford Institute (COI), University of Oxford, Oxford, UK; Diamond Light Source Ltd, Harwell Science & Innovation Campus, Didcot, UK; Instruct-ERIC, Oxford House, Parkway Court, John Smith Drive, Oxford, UK.

The 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.

中文翻译：

SARS-CoV-2 变种 B.1.351 从天然和疫苗诱导血清中逃逸的证据

当第一个序列公布时，针对严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的疫苗生产竞赛就开始了，这构成了目前全球部署的疫苗的基础。最近报道了 SARS-CoV-2 的独立谱系：UK，B.1.1.7；南非，B.1.351；和巴西，P.1。这些变体的免疫显性刺突蛋白有多种变化，可促进病毒通过血管紧张素转换酶 2 (ACE2) 受体进入细胞。刺突上受体识别位点的突变因其免疫逃逸的潜力而受到高度关注。在这里，我们描述了使用大量恢复期和疫苗接种者血清样本对 B.1.351 进行的结构功能分析。尽管 K417N 和 N501Y 共同作用于一些重要的抗体类别，但受体结合域突变提供了更紧密的 ACE2 结合，并广泛逃避主要由 E484K 驱动的单克隆抗体中和作用。在许多情况下，恢复期血清和某些疫苗血清对这种变体的保护作用似乎有限。

更新日期：2021-04-29

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