A vaccine-induced public antibody protects against SARS-CoV-2 and emerging variants

Aaron J. Schmitz, Jackson S. Turner, Zhuoming Liu, Julian Q. Zhou, Ishmael D. Aziati, Rita E. Chen, Astha Joshi, Traci L. Bricker, Tamarand L. Darling, Daniel C. Adelsberg, Clara G. Altomare, Wafaa B. Alsoussi, James Brett Case, Laura A. VanBlargan, Tingting Lei, Mahima Thapa, Fatima Amanat, Trushar Jeevan, Thomas Fabrizio, Jane A. O'HalloranPei Yong Shi, Rachel M. Presti, Richard J. Webby, Florian Krammer, Sean P.J. Whelan, Goran Bajic, Michael S. Diamond, Adrianus C.M. Boon, Ali H. Ellebedy

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

The emergence of SARS-CoV-2 antigenic variants with increased transmissibility is a public health threat. Some variants show substantial resistance to neutralization by SARS-CoV-2 infection- or vaccination-induced antibodies. Here, we analyzed receptor binding domain-binding monoclonal antibodies derived from SARS-CoV-2 mRNA vaccine-elicited germinal center B cells for neutralizing activity against the WA1/2020 D614G SARS-CoV-2 strain and variants of concern. Of five monoclonal antibodies that potently neutralized the WA1/2020 D614G strain, all retained neutralizing capacity against the B.1.617.2 variant, four also neutralized the B.1.1.7 variant, and only one, 2C08, also neutralized the B.1.351 and B.1.1.28 variants. 2C08 reduced lung viral load and morbidity in hamsters challenged with the WA1/2020 D614G, B.1.351, or B.1.617.2 strains. Clonal analysis identified 2C08-like public clonotypes among B cells responding to SARS-CoV-2 infection or vaccination in 41 out of 181 individuals. Thus, 2C08-like antibodies can be induced by SARS-CoV-2 vaccines and mitigate resistance by circulating variants of concern.

Original languageEnglish
Pages (from-to)2159-2166.e6
JournalImmunity
Volume54
Issue number9
DOIs
StatePublished - Sep 14 2021

Keywords

  • B cell
  • SARS-CoV-2
  • germinal center
  • hamster
  • lymph node
  • mRNA vaccine
  • neutralizing antibodies
  • public clone
  • receptor binding domain
  • spike protein

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