Author:
Yamasoba Daichi,Kimura Izumi,Nasser Hesham,Morioka Yuhei,Nao Naganori,Ito Jumpei,Uriu Keiya,Tsuda Masumi,Zahradnik Jiri,Shirakawa Kotaro,Suzuki Rigel,Kishimoto Mai,Kosugi Yusuke,Kobiyama Kouji,Hara Teppei,Toyoda Mako,Tanaka Yuri L,Butlertanaka Erika P,Shimizu Ryo,Ito Hayato,Wang Lei,Oda Yoshitaka,Orba Yasuko,Sasaki Michihito,Nagata Kayoko,Yoshimatsu Kumiko,Asakura Hiroyuki,Nagashima Mami,Sadamasu Kenji,Yoshimura Kazuhisa,Kuramochi Jin,Seki Motoaki,Fujiki Ryoji,Kaneda Atsushi,Shimada Tadanaga,Nakada Taka-aki,Sakao Seiichiro,Suzuki Takuji,Ueno Takamasa,Takaori-Kondo Akifumi,Ishii Ken J,Schreiber Gideon,Sawa Hirofumi,Saito Akatsuki,Irie Takashi,Tanaka Shinya,Matsuno Keita,Fukuhara Takasuke,Ikeda Terumasa,Sato Kei,
Abstract
AbstractSoon after the emergence and global spread of a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron lineage, BA.1 (ref1, 2), another Omicron lineage, BA.2, has initiated outcompeting BA.1. Statistical analysis shows that the effective reproduction number of BA.2 is 1.4-fold higher than that of BA.1. Neutralisation experiments show that the vaccine-induced humoral immunity fails to function against BA.2 like BA.1, and notably, the antigenicity of BA.2 is different from BA.1. Cell culture experiments show that BA.2 is more replicative in human nasal epithelial cells and more fusogenic than BA.1. Furthermore, infection experiments using hamsters show that BA.2 is more pathogenic than BA.1. Our multiscale investigations suggest that the risk of BA.2 for global health is potentially higher than that of BA.1.
Publisher
Cold Spring Harbor Laboratory
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