Reduced antibody cross-reactivity following infection with B.1.1.7 than with parental SARS-CoV-2 strains.
Elife
; 102021 07 29.
Article
in English
| MEDLINE | ID: covidwho-1332333
Preprint
This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
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This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
See preprint
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.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
SARS-CoV-2
/
COVID-19
/
Antibodies, Viral
Type of study:
Observational study
/
Randomized controlled trials
Topics:
Vaccines
/
Variants
Limits:
Humans
Country/Region as subject:
Africa
/
Europa
Language:
English
Year:
2021
Document Type:
Article
Affiliation country:
ELife.69317
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