Journal
NATURE
Volume 607, Issue 7917, Pages 119-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41586-022-04856-1
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Funding
- Research Program on Emerging and Re-emerging Infectious Diseases from the Japan Agency for Medical Research and Development (AMED) [JP20fk0108412, JP20fk0108502, JP21fk0108615, JP20fk0108472, JP21fk0108104, JP20nk0101632, JP22wm0125002]
- Project Promoting Support for Drug Discovery from the Japan Agency for Medical Research and Development (AMED) [JP20nk0101632]
- Japan Program for Infectious Diseases Research and Infrastructure from the Japan Agency for Medical Research and Development (AMED) [JP22wm0125002]
- National Institutes of Allergy and Infectious Diseases Center for Research on Influenza Pathogenesis [HHSN272201400008C]
- NIAID [R01 AI157155]
- Center for Research on Influenza Pathogenesis and Transmission (CRIPT) [75N93021C00014]
- Collaborative Influenza Vaccine Innovation Center [75N93019C00051]
- Ministry of Health, Labour and Welfare, Japan [JPMH20HA1006, JPMH 20HA2007]
- Intramural Research Program of National Center for Global Health and Medicine
- Intramural Research Program of the Center for Cancer Research, National Cancer Institute, National Institutes of Health
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The replicative ability and pathogenicity of Omicron BA.2 variant is similar to that of BA.1 in rodents, but it shows less pathogenicity compared to early SARS-CoV-2 strains. There is a marked reduction in the neutralizing activity of plasma from individuals who had recovered from COVID-19 and vaccine recipients against BA.2 variant.
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 variants(1,2). The original Omicron lineage, BA.1, prevailed in many countries, but more recently, BA.2 has become dominant in at least 68 countries(3). 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 backbone(4), 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.
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