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| s41586-021-04266-9.pdf | 10.66 MB | Adobe PDF | View/Open |
| Title: | Enhanced fusogenicity and pathogenicity of SARS-CoV-2 Delta P681R mutation |
| Authors: | Saito, Akatsuki Irie, Takashi Suzuki, Rigel Maemura, Tadashi Nasser, Hesham Uriu, Keiya Kosugi, Yusuke Shirakawa, Kotaro    https://orcid.org/0000-0002-7469-1276 (unconfirmed)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 Chiba, Mika Furihata, Hirotake Hasebe, Haruyo Kitazato, Kazuko Kubo, Haruko Misawa, Naoko Morizako, Nanami Noda, Kohei Oide, Akiko Suganami, Mai Takahashi, Miyoko Tsushima, Kana Yokoyama, Miyabishara Yuan, Yue Tanaka, Shinya Nakagawa, So Ikeda, Terumasa Fukuhara, Takasuke Kawaoka, Yoshihiro Sato, Kei |
| Author's alias: | 齊藤, 暁 入江, 崇 鈴木, 理滋 前村, 忠 瓜生, 慧也 小杉, 優介 白川, 康太郎 貞升, 健志 木村, 出海 伊東, 潤平 呉, 佳齊 岩附, 研子 伊藤, 睦美 山吉, 誠也 津田, 真寿美 大園, 誠也 バトラー田中, 英里佳 田中, 友理 清水, 凌 清水, 健太 吉松, 組子, 川端, 涼子 坂口, 剛正 徳永, 研三 吉田, 勲 浅倉, 弘幸 長島, 真美 数馬, 安浩 野村, 亮介 堀澤, 欣史 吉村, 和久 高折, 晃史 今井, 正樹 田中, 伸哉 中川, 草 池田, 輝政 福原, 崇介 河岡, 義裕 佐藤, 佳 |
| Keywords: | SARS-CoV-2 Viral pathogenesis |
| Issue Date: | 10-Feb-2022 |
| Publisher: | Springer Nature |
| Journal title: | Nature |
| Volume: | 602 |
| Issue: | 7896 |
| Start page: | 300 |
| End page: | 306 |
| Abstract: | During the current SARS-CoV-2 pandemic, a variety of mutations have accumulated in the viral genome, and currently, four variants of concern (VOCs) are considered potentially hazardous to human society1. The recently emerged B.1.617.2/Delta VOC is closely associated with the COVID-19 surge that occurred in India in the spring of 20212. However, its virological properties 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 spike protein cleavage and enhances viral fusogenicity. Moreover, we demonstrate that the P681R-bearing virus exhibits higher pathogenicity than 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. |
| Description: | SARS-CoV-2デルタ株に特徴的なP681R変異は ウイルスの病原性を増大させる. 京都大学プレスリリース. 2021-11-26. |
| Rights: | © The Author(s) 2021 This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. |
| URI: | http://hdl.handle.net/2433/275414 |
| DOI(Published Version): | 10.1038/s41586-021-04266-9 |
| PubMed ID: | 34823256 |
| Related Link: | https://www.kyoto-u.ac.jp/ja/research-news/2021-11-26 |
| Appears in Collections: | Journal Articles |
This item is licensed under a Creative Commons License
