Reduced antibody cross-reactivity following infection with B.1.1.7 than with parental SARS-CoV-2 strains
Nikhil Faulkner, Kevin W. Ng, Mary Wu, Ruth Harvey, Marios Margaritis, Stavroula Paraskevopoulou, Catherine Houlihan, Saira Hussain, Maria Greco, William Bolland, Scott Warchal, Judith Heaney, Hannah M. Rickman, Moria Spyer, Daniel Frampton, Matthew Byott, Túlio de Oliveira, Alex Sigal, Svend Kjær, Charles Swanton, Sonia Gandhi, Rupert Beale, Steve Gamblin, John W. McCauley, Rodney S. Daniels, Michael Howell, David L.V. Bauer, Eleni Nastouli, George Kassiotis
Abstract
Background: The degree of heterotypic immunity induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains is a major determinant of the spread of emerging variants and the success of vaccination campaigns, but remains incompletely understood. Methods: We examined the immunogenicity of SARS-CoV-2 variant B.1.1.7 (Alpha) that arose in the United Kingdom and spread globally. We determined titres of spike glycoprotein-binding antibodies and authentic virus neutralising antibodies induced by B.1.1.7 infection to infer homotypic and heterotypic immunity. Results: Antibodies elicited by B.1.1.7 infection exhibited significantly reduced recognition and neutralisation of parental strains or of the South Africa variant B.1.351 (Beta) than of the infecting variant. The drop in cross-reactivity was significantly more pronounced following B.1.1.7 than parental strain infection. Conclusions: The results indicate that heterotypic immunity induced by SARS-CoV-2 variants is asymmetric. Funding: This work was supported by the Francis Crick Institute and the Max Planck Institute for Dynamics of Complex Technical Systems, Magdeburg.