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• W4362677993 endingPage "106582" @default.
• W4362677993 startingPage "106582" @default.
• W4362677993 abstract "The number of mutations in the omicron (B.1.1.529) BA.1 variant of concern led to an unprecedented evasion of vaccine induced immunity. However, despite rise in global infections, severe disease did not increase proportionally and is likely linked to persistent recognition of BA.1 by T cells and non-neutralizing opsonophagocytic antibodies. Yet, the emergence of new sublineage BA.2, which is more transmissible than BA.1 despite relatively preserved neutralizing antibody responses, has raised the possibility that BA.2 may evade other vaccine-induced responses. Here, we comprehensively profiled the BNT162b2 vaccine-induced response to several VOCs, including omicron BA.1 and BA.2. While vaccine-induced immune responses were compromised against both omicron sublineages, vaccine-induced antibody isotype titers, and non-neutralizing Fc effector functions were attenuated to the omicron BA.2 spike compared to BA.1. Conversely, FcγR2a and FcγR2b binding was elevated to BA.2, albeit lower than BA.1 responses, potentially contributing to persistent protection against severity of disease." @default.
• W4362677993 created "2023-04-07" @default.
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• W4362677993 date "2023-05-01" @default.
• W4362677993 modified "2023-10-01" @default.
• W4362677993 title "Selective SARS-CoV2 BA.2 escape of antibody Fc/Fc-receptor interactions" @default.
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• W4362677993 doi "https://doi.org/10.1016/j.isci.2023.106582" @default.
• W4362677993 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37082529" @default.
• W4362677993 hasPublicationYear "2023" @default.
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