RT Journal Article
SR Electronic
T1 SARS-CoV-2 spike P681R mutation, a hallmark of the Delta variant, enhances viral fusogenicity and pathogenicity
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.06.17.448820
DO 10.1101/2021.06.17.448820
A1 Akatsuki Saito
A1 Takashi Irie
A1 Rigel Suzuki
A1 Tadashi Maemura
A1 Hesham Nasser
A1 Keiya Uriu
A1 Yusuke Kosugi
A1 Kotaro Shirakawa
A1 Kenji Sadamasu
A1 Izumi Kimura
A1 Jumpei Ito
A1 Jiaqi Wu
A1 Kiyoko Iwatsuki-Horimoto
A1 Mutsumi Ito
A1 Seiya Yamayoshi
A1 Seiya Ozono
A1 Erika P Butlertanaka
A1 Yuri L Tanaka
A1 Ryo Shimizu
A1 Kenta Shimizu
A1 Kumiko Yoshimatsu
A1 Ryoko Kawabata
A1 Takemasa Sakaguchi
A1 Kenzo Tokunaga
A1 Isao Yoshida
A1 Hiroyuki Asakura
A1 Mami Nagashima
A1 Yasuhiro Kazuma
A1 Ryosuke Nomura
A1 Yoshihito Horisawa
A1 Kazuhisa Yoshimura
A1 Akifumi Takaori-Kondo
A1 Masaki Imai
A1 The Genotype to Phenotype Japan (G2P-Japan) Consortium
A1 So Nakagawa
A1 Terumasa Ikeda
A1 Takasuke Fukuhara
A1 Yoshihiro Kawaoka
A1 Kei Sato
YR 2021
UL http://biorxiv.org/content/early/2021/07/19/2021.06.17.448820.abstract
AB During the current SARS-CoV-2 pandemic, a variety of mutations have been accumulated in the viral genome, and currently, four variants of concerns (VOCs) are considered as the hazardous SARS-CoV-2 variants to the human society1. The newly emerging VOC, the B.1.617.2/Delta variant, closely associates with a huge COVID-19 surge in India in Spring 20212. However, its virological property remains 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 the spike protein cleavage and enhances viral fusogenicity. Moreover, we demonstrate that the P681R-bearing virus exhibits higher pathogenicity than the parental virus. Our data suggest that the P681R mutation is a hallmark that characterizes the virological phenotype of the B.1.617.2/Delta variant and is closely associated with enhanced pathogenicity.Competing Interest StatementThe authors have declared no competing interest.