Structural basis of SARS-CoV-2 Omicron immune evasion and receptor engagement

  • Matthew McCallum
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • Nadine Czudnochowski
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Laura E. Rosen
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Samantha K. Zepeda
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • John E. Bowen
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • Alexandra C. Walls
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • Kevin Hauser
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Anshu Joshi
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • Cameron Stewart
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.
  • Josh R. Dillen
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Abigail E. Powell
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Tristan I. Croll
    Cambridge Institute for Medical Research, Department of Haematology, University of Cambridge, Cambridge, UK.
  • Jay Nix
    Molecular Biology Consortium, Advanced Light Source, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
  • Herbert W. Virgin
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • Davide Corti
    Humabs Biomed SA, a subsidiary of Vir Biotechnology, 6500 Bellinzona, Switzerland.
  • Gyorgy Snell
    Vir Biotechnology, San Francisco, CA 94158, USA.
  • David Veesler
    Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.

抄録

<jats:p>The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant of concern evades antibody-mediated immunity that comes from vaccination or infection with earlier variants due to accumulation of numerous spike mutations. To understand the Omicron antigenic shift, we determined cryo–electron microscopy and x-ray crystal structures of the spike protein and the receptor-binding domain bound to the broadly neutralizing sarbecovirus monoclonal antibody (mAb) S309 (the parent mAb of sotrovimab) and to the human ACE2 receptor. We provide a blueprint for understanding the marked reduction of binding of other therapeutic mAbs that leads to dampened neutralizing activity. Remodeling of interactions between the Omicron receptor-binding domain and human ACE2 likely explains the enhanced affinity for the host receptor relative to the ancestral virus.</jats:p>

収録刊行物

  • Science

    Science 375 (6583), 864-868, 2022-02-25

    American Association for the Advancement of Science (AAAS)

被引用文献 (4)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ