International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2026
Cross-neutralization of SARS-CoV-2 BA.3.2.2 lineage by JN.1 mRNA vaccine-induced immunity.
СтатьяНазвание и аннотация: Перевод в очереди
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Miyakawa Kei, Sano Kaori, Seki Yohei, Sato Ryoichi, Yoshihara Yasuo, Mizukami Takuo, Hasegawa Hideki
Аннотация
OBJECTIVES: The SARS-CoV-2 BA.3.2.2 sublineage has emerged globally as the dominant branch of BA.3.2 by late 2025, yet its antigenic relationship with JN.1 vaccine-induced immunity remains unclear.
METHODS: We evaluated neutralizing antibody responses in 25 JN.1 mRNA vaccinees against eight variants, stratified by anti-nucleocapsid antibody serostatus.
RESULTS: Postvaccination titers increased significantly against all variants in both N antibody-negative and -positive groups. Cross-neutralization against BA.3.2.2 was detected in both groups despite lower titers compared to JN.1. Antigenic cartography revealed that BA.3.2.2 was antigenically isolated from all JN.1-descendant variants. AZD3152/sipavibart retained potent neutralization against BA.3.2.2 but completely lost activity against all F456L-harboring JN.1-descendant variants, while VYD222/pemivibart and SA55 maintained broad activity.
CONCLUSIONS: Retention of wild-type F456 in BA.3.2.2 preserves class 1/2 antibody epitopes, providing a mechanistic basis for cross-neutralization and suggesting a potential therapeutic window for sipavibart should BA.3.2.2 expand globally, pending clinical confirmation.
METHODS: We evaluated neutralizing antibody responses in 25 JN.1 mRNA vaccinees against eight variants, stratified by anti-nucleocapsid antibody serostatus.
RESULTS: Postvaccination titers increased significantly against all variants in both N antibody-negative and -positive groups. Cross-neutralization against BA.3.2.2 was detected in both groups despite lower titers compared to JN.1. Antigenic cartography revealed that BA.3.2.2 was antigenically isolated from all JN.1-descendant variants. AZD3152/sipavibart retained potent neutralization against BA.3.2.2 but completely lost activity against all F456L-harboring JN.1-descendant variants, while VYD222/pemivibart and SA55 maintained broad activity.
CONCLUSIONS: Retention of wild-type F456 in BA.3.2.2 preserves class 1/2 antibody epitopes, providing a mechanistic basis for cross-neutralization and suggesting a potential therapeutic window for sipavibart should BA.3.2.2 expand globally, pending clinical confirmation.