Characterization and antiviral susceptibility of SARS-CoV-2 Omicron BA.2
Ryuta Uraki,
Maki Kiso,
Shun Iida,
Masaki Imai,
Emi Takashita,
Makoto Kuroda,
Peter J. Halfmann,
Samantha Loeber,
Tadashi Maemura,
Seiya Yamayoshi,
Seiichiro Fujisaki,
Zhongde Wang,
Mutsumi Ito,
Michiko Ujie,
Kiyoko Iwatsuki-Horimoto,
Yuri Furusawa,
Ryan Wright,
Zhenlu Chong,
Seiya Ozono,
Atsuhiro Yasuhara,
Hiroshi Ueki,
Yuko Sakai-Tagawa,
Rong Li,
Yanan Liu,
Deanna Larson,
Michiko Koga,
Takeya Tsutsumi,
Eisuke Adachi,
Makoto Saito,
Shinya Yamamoto,
Masao Hagihara,
Keiko Mitamura,
Tetsuro Sato,
Masayuki Hojo,
Shin-ichiro Hattori,
Kenji Maeda,
Riccardo Valdez,
Moe Okuda,
Jurika Murakami,
Calvin Duong,
Sucheta Godbole,
Daniel C. Douek,
Ken Maeda,
Shinji Watanabe,
Aubree Gordon,
Norio Ohmagari,
Hiroshi Yotsuyanagi,
Michael S. Diamond,
Hideki Hasegawa,
Hiroaki Mitsuya,
Tadaki Suzuki and
Yoshihiro Kawaoka ()
Additional contact information
Ryuta Uraki: University of Tokyo
Maki Kiso: University of Tokyo
Shun Iida: National Institute of Infectious Diseases
Masaki Imai: University of Tokyo
Emi Takashita: National Institute of Infectious Diseases
Makoto Kuroda: University of Wisconsin-Madison
Peter J. Halfmann: University of Wisconsin-Madison
Samantha Loeber: University of Wisconsin-Madison
Tadashi Maemura: University of Wisconsin-Madison
Seiya Yamayoshi: University of Tokyo
Seiichiro Fujisaki: National Institute of Infectious Diseases
Zhongde Wang: Utah State University
Mutsumi Ito: University of Tokyo
Michiko Ujie: University of Tokyo
Kiyoko Iwatsuki-Horimoto: University of Tokyo
Yuri Furusawa: University of Tokyo
Ryan Wright: University of Wisconsin-Madison
Zhenlu Chong: Washington University School of Medicine
Seiya Ozono: National Institute of Infectious Diseases
Atsuhiro Yasuhara: University of Tokyo
Hiroshi Ueki: University of Tokyo
Yuko Sakai-Tagawa: University of Tokyo
Rong Li: Utah State University
Yanan Liu: Utah State University
Deanna Larson: Utah State University
Michiko Koga: University of Tokyo
Takeya Tsutsumi: University of Tokyo
Eisuke Adachi: University of Tokyo
Makoto Saito: University of Tokyo
Shinya Yamamoto: University of Tokyo
Masao Hagihara: Eiju General Hospital
Keiko Mitamura: Eiju General Hospital
Tetsuro Sato: National Center for Global Health and Medicine Hospital
Masayuki Hojo: National Center for Global Health and Medicine Hospital
Shin-ichiro Hattori: National Center for Global Health and Medicine Research Institute
Kenji Maeda: National Center for Global Health and Medicine Research Institute
Riccardo Valdez: University of Michigan
Moe Okuda: University of Tokyo
Jurika Murakami: University of Tokyo
Calvin Duong: University of Tokyo
Sucheta Godbole: National Institutes of Health
Daniel C. Douek: National Institutes of Health
Ken Maeda: National Institute of Infectious Diseases
Shinji Watanabe: National Institute of Infectious Diseases
Aubree Gordon: University of Michigan
Norio Ohmagari: National Center for Global Health and Medicine Hospital
Hiroshi Yotsuyanagi: University of Tokyo
Michael S. Diamond: Washington University School of Medicine
Hideki Hasegawa: National Institute of Infectious Diseases
Hiroaki Mitsuya: National Center for Global Health and Medicine Research Institute
Tadaki Suzuki: National Institute of Infectious Diseases
Yoshihiro Kawaoka: University of Tokyo
Nature, 2022, vol. 607, issue 7917, 119-127
Abstract:
Abstract The recent emergence of SARS-CoV-2 Omicron (B.1.1.529 lineage) variants possessing numerous mutations has raised concerns of decreased effectiveness of current vaccines, therapeutic monoclonal antibodies and antiviral drugs for COVID-19 against these variants1,2. The original Omicron lineage, BA.1, prevailed in many countries, but more recently, BA.2 has become dominant in at least 68 countries3. Here we evaluated the replicative ability and pathogenicity of authentic infectious BA.2 isolates in immunocompetent and human ACE2-expressing mice and hamsters. In contrast to recent data with chimeric, recombinant SARS-CoV-2 strains expressing the spike proteins of BA.1 and BA.2 on an ancestral WK-521 backbone4, we observed similar infectivity and pathogenicity in mice and hamsters for BA.2 and BA.1, and less pathogenicity compared with early SARS-CoV-2 strains. We also observed a marked and significant reduction in the neutralizing activity of plasma from individuals who had recovered from COVID-19 and vaccine recipients against BA.2 compared to ancestral and Delta variant strains. In addition, we found that some therapeutic monoclonal antibodies (REGN10987 plus REGN10933, COV2-2196 plus COV2-2130, and S309) and antiviral drugs (molnupiravir, nirmatrelvir and S-217622) can restrict viral infection in the respiratory organs of BA.2-infected hamsters. These findings suggest that the replication and pathogenicity of BA.2 is similar to that of BA.1 in rodents and that several therapeutic monoclonal antibodies and antiviral compounds are effective against Omicron BA.2 variants.
Date: 2022
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:607:y:2022:i:7917:d:10.1038_s41586-022-04856-1
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DOI: 10.1038/s41586-022-04856-1
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