Molecular basis of immune evasion by the Delta and Kappa SARS-CoV-2 variants
Author(s) -
Matthew McCallum,
Alexandra C. Walls,
Kaitlin R. Sprouse,
John E. Bowen,
Laura E. Rosen,
Ha V. Dang,
Anna De Marco,
Nicholas Franko,
Sasha W. Tilles,
Jennifer K. Logue,
Marcos C. Miranda,
Maggie Ahlrichs,
Lauren Carter,
Gyorgy Snell,
Matteo Samuele Pizzuto,
Helen Y. Chu,
Wesley C. Van Voorhis,
Davide Corti,
David Veesler
Publication year - 2021
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.abl8506
Subject(s) - immune escape , antibody , covid-19 , biology , immune system , monoclonal antibody , virology , neutralizing antibody , kappa , coronavirus , immunity , computational biology , immunology , medicine , disease , infectious disease (medical specialty) , outbreak , linguistics , philosophy , pathology
How the Delta variant evades defenses In the course of the COVID-19 epidemic, variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continue to emerge, some of which evade immunity or increase transmission. In late 2020, the Delta and Kappa variants were detected, and the Delta variant became globally dominant by June 2021. McCallumet al . show that vaccine-elicited serum-neutralizing activity is reduced against these variants. Based on biochemistry and structural studies, the authors show that mutations in the domain that binds the ACE2 receptor abrogate binding to some monoclonal antibodies but do not improve ACE2 binding, suggesting that they emerged to escape immune recognition. Remodeling of the N-terminal domain allows the variants to escape recognition by most neutralizing antibodies that target it. The work could guide the development of next-generation vaccines and antibody therapies. —VV
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