Enhanced fusogenicity and pathogenicity of SARS-CoV-2 Delta P681R mutation

Saito, Akatsuki; Irie, Takashi; Suzuki, Rigel; Maemura, Tadashi; Nasser, Hesham; Uriu, Keiya; Kosugi, Yusuke; Shirakawa, Kotaro; Sadamasu, Kenji; Kimura, Izumi; Ito, Jumpei; Wu, Jiaqi; Iwatsuki-Horimoto, Kiyoko; Ito, Mutsumi; Yamayoshi, Seiya; Loeber, Samantha; Tsuda, Masumi; Wang, Lei; Ozono, Seiya; Butlertanaka, Erika P.; Tanaka, Yuri L.; Shimizu, Ryo; Shimizu, Kenta; Yoshimatsu, Kumiko; Kawabata, Ryoko; Sakaguchi, Takemasa; Tokunaga, Kenzo; Yoshida, Isao; Asakura, Hiroyuki; Nagashima, Mami; Kazuma, Yasuhiro; Nomura, Ryosuke; Horisawa, Yoshihito; Yoshimura, Kazuhisa; Takaori-Kondo, Akifumi; Imai, Masaki; Tanaka, Shinya; Nakagawa, So; Ikeda, Terumasa; Fukuhara, Takasuke; Kawaoka, Yoshihiro; Sato, Kei

Enhanced fusogenicity and pathogenicity of SARS-CoV-2 Delta P681R mutation

Akatsuki Saito, Takashi Irie, Rigel Suzuki, Tadashi Maemura, Hesham Nasser, Keiya Uriu, Yusuke Kosugi, Kotaro Shirakawa, Kenji Sadamasu, Izumi Kimura, Jumpei Ito, Jiaqi Wu, Kiyoko Iwatsuki-Horimoto, Mutsumi Ito, Seiya Yamayoshi, Samantha Loeber, Masumi Tsuda, Lei Wang, Seiya Ozono, Erika P. Butlertanaka, Yuri L. Tanaka, Ryo Shimizu, Kenta Shimizu, Kumiko Yoshimatsu, Ryoko Kawabata, Takemasa Sakaguchi, Kenzo Tokunaga, Isao Yoshida, Hiroyuki Asakura, Mami Nagashima, Yasuhiro Kazuma, Ryosuke Nomura, Yoshihito Horisawa, Kazuhisa Yoshimura, Akifumi Takaori-Kondo, Masaki Imai, Shinya Tanaka (), So Nakagawa (), Terumasa Ikeda (), Takasuke Fukuhara (), Yoshihiro Kawaoka () and Kei Sato ()
Additional contact information
Akatsuki Saito: University of Miyazaki
Takashi Irie: Hiroshima University
Rigel Suzuki: Hokkaido University
Tadashi Maemura: University of Tokyo
Hesham Nasser: Kumamoto University
Keiya Uriu: The University of Tokyo
Yusuke Kosugi: The University of Tokyo
Kotaro Shirakawa: Kyoto University
Kenji Sadamasu: Tokyo Metropolitan Institute of Public Health
Izumi Kimura: The University of Tokyo
Jumpei Ito: The University of Tokyo
Jiaqi Wu: Tokai University School of Medicine
Kiyoko Iwatsuki-Horimoto: University of Tokyo
Mutsumi Ito: University of Tokyo
Seiya Yamayoshi: University of Tokyo
Samantha Loeber: University of Wisconsin
Masumi Tsuda: Hokkaido University
Lei Wang: Hokkaido University
Seiya Ozono: National Institute of Infectious Diseases
Erika P. Butlertanaka: University of Miyazaki
Yuri L. Tanaka: University of Miyazaki
Ryo Shimizu: Kumamoto University
Kenta Shimizu: Hokkaido University
Kumiko Yoshimatsu: Hokkaido University
Ryoko Kawabata: Hiroshima University
Takemasa Sakaguchi: Hiroshima University
Kenzo Tokunaga: National Institute of Infectious Diseases
Isao Yoshida: Tokyo Metropolitan Institute of Public Health
Hiroyuki Asakura: Tokyo Metropolitan Institute of Public Health
Mami Nagashima: Tokyo Metropolitan Institute of Public Health
Yasuhiro Kazuma: Kyoto University
Ryosuke Nomura: Kyoto University
Yoshihito Horisawa: Kyoto University
Kazuhisa Yoshimura: Tokyo Metropolitan Institute of Public Health
Akifumi Takaori-Kondo: Kyoto University
Masaki Imai: University of Tokyo
Shinya Tanaka: Hokkaido University
So Nakagawa: Tokai University School of Medicine
Terumasa Ikeda: Kumamoto University
Takasuke Fukuhara: Hokkaido University
Yoshihiro Kawaoka: University of Tokyo
Kei Sato: The University of Tokyo

Nature, 2022, vol. 602, issue 7896, 300-306

Abstract: Abstract During the current coronavirus disease 2019 (COVID-19) pandemic, a variety of mutations have accumulated in the viral genome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and, at the time of writing, four variants of concern are considered to be potentially hazardous to human society1. The recently emerged B.1.617.2/Delta variant of concern is closely associated with the COVID-19 surge that occurred in India in the spring of 2021 (ref. 2). However, the virological properties of B.1.617.2/Delta remain unclear. Here we show that the B.1.617.2/Delta variant is highly fusogenic and notably more pathogenic than prototypic SARS-CoV-2 in infected hamsters. The P681R mutation in the spike protein, which is highly conserved in this lineage, facilitates cleavage of the spike protein and enhances viral fusogenicity. Moreover, we demonstrate that the P681R-bearing virus exhibits higher pathogenicity compared with its parental virus. Our data suggest that the P681R mutation is a hallmark of the virological phenotype of the B.1.617.2/Delta variant and is associated with enhanced pathogenicity.

Date: 2022
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DOI: 10.1038/s41586-021-04266-9

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