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SARS-CoV-2变异株B.1.351可从天然和疫苗诱导的血清中逃逸
2021-02-25 16:16

英国牛津大学Gavin R. Screaton等研究人员合作发现,SARS-CoV-2变异株B.1.351可从天然和疫苗诱导的血清中逃逸。该研究于2021年2月23日在线发表于国际一流学术期刊《细胞》。

研究人员报道了使用大量恢复期和疫苗后血清样品对B.1.351结构功能分析。受体结合结构域突变提供了更紧密的ACE2结合,并从很大程度上由E484K驱动的单克隆抗体中和作用中逃逸,尽管K417N和N501Y共同作用于一些重要的抗体类型。在许多情况下,恢复期和某些疫苗血清似乎对这种变异仅提供了有限的保护。 

据介绍,SARS-CoV-2疫苗的生产竞赛始于第一个序列的发布,这构成了目前全球部署的疫苗的基础。最近报告了SARS-CoV-2的独立谱系:英国–B.1.1.7,南非–B.1.351和巴西–P.1。这些变体在免疫显性刺突蛋白中具有多种变化,从而促进病毒细胞通过ACE2受体进入细胞。刺突上受体识别位点的突变使得人们非常担心它们的免疫逃逸能力。

附:英文原文

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

Author: 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, Cesar Lopez-Camacho, Jose Slon-Campos, Bassam Hallis, Naomi Coombes, Kevin Bewley, Sue Charlton, Thomas S. Walter, Donal Skelly, Sheila F. Lumley, Christina Dold, Robert Levin, Tao Dong, Andrew J. Pollard, Julian C. Knight, Derrick Crook, Teresa Lambe, Elizabeth Clutterbuck, Sagida Bibi, Amy Flaxman, Mustapha Bittaye, Sandra Belij-Rammerstorfer, Sarah Gilbert, William James, Miles W. Carroll, Paul Klenerman, Eleanor Barnes, Susanna J. Dunachie, Elizabeth E. Fry, Juthathip Mongkolspaya, Jingshan Ren, David I. Stuart, Gavin R. Screaton

Issue&Volume: 2021-02-23

Abstract: The race to produce vaccines against 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 which 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.

DOI: 10.1016/j.cell.2021.02.037

Source: https://www.cell.com/cell/fulltext/S0092-8674(21)00226-9

Cell:《细胞》,创刊于1974年。隶属于细胞出版社,最新IF:66.85
官方网址:https://www.cell.com/
投稿链接:https://www.editorialmanager.com/cell/default.aspx

本期文章:《细胞》:Online/在线发表

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