Antibody resistance of SARS-CoV-2 variants B.1.351 and B.1.1.7

Pengfei Wang, Manoj S. Nair, Lihong Liu, Sho Iketani, Yang Luo, Yicheng Guo, Maple Wang, Jian Yu, Baoshan Zhang, Peter D. Kwong, Barney S. Graham, John R. Mascola, Jennifer Y. Chang, Michael T. Yin, Magdalena Sobieszczyk, Christos A. Kyratsous, Lawrence Shapiro, Zizhang Sheng, Yaoxing Huang () and David D. Ho ()
Additional contact information
Pengfei Wang: Columbia University Vagelos College of Physicians and Surgeons
Manoj S. Nair: Columbia University Vagelos College of Physicians and Surgeons
Lihong Liu: Columbia University Vagelos College of Physicians and Surgeons
Sho Iketani: Columbia University Vagelos College of Physicians and Surgeons
Yang Luo: Columbia University Vagelos College of Physicians and Surgeons
Yicheng Guo: Columbia University Vagelos College of Physicians and Surgeons
Maple Wang: Columbia University Vagelos College of Physicians and Surgeons
Jian Yu: Columbia University Vagelos College of Physicians and Surgeons
Baoshan Zhang: National Institutes of Health
Peter D. Kwong: National Institutes of Health
Barney S. Graham: National Institutes of Health
John R. Mascola: National Institutes of Health
Jennifer Y. Chang: Columbia University Vagelos College of Physicians and Surgeons
Michael T. Yin: Columbia University Vagelos College of Physicians and Surgeons
Magdalena Sobieszczyk: Columbia University Vagelos College of Physicians and Surgeons
Christos A. Kyratsous: Regeneron Pharmaceuticals
Lawrence Shapiro: Columbia University Vagelos College of Physicians and Surgeons
Zizhang Sheng: Columbia University Vagelos College of Physicians and Surgeons
Yaoxing Huang: Columbia University Vagelos College of Physicians and Surgeons
David D. Ho: Columbia University Vagelos College of Physicians and Surgeons

Nature, 2021, vol. 593, issue 7857, 130-135

Abstract: Abstract The COVID-19 pandemic has had widespread effects across the globe, and its causative agent, SARS-CoV-2, continues to spread. Effective interventions need to be developed to end this pandemic. Single and combination therapies with monoclonal antibodies have received emergency use authorization1–3, and more treatments are under development4–7. Furthermore, multiple vaccine constructs have shown promise8, including two that have an approximately 95% protective efficacy against COVID-199,10. However, these interventions were directed against the initial SARS-CoV-2 virus that emerged in 2019. The recent detection of SARS-CoV-2 variants B.1.1.7 in the UK11 and B.1.351 in South Africa12 is of concern because of their purported ease of transmission and extensive mutations in the spike protein. Here we show that B.1.1.7 is refractory to neutralization by most monoclonal antibodies against the N-terminal domain of the spike protein and is relatively resistant to a few monoclonal antibodies against the receptor-binding domain. It is not more resistant to plasma from individuals who have recovered from COVID-19 or sera from individuals who have been vaccinated against SARS-CoV-2. The B.1.351 variant is not only refractory to neutralization by most monoclonal antibodies against the N-terminal domain but also by multiple individual monoclonal antibodies against the receptor-binding motif of the receptor-binding domain, which is mostly due to a mutation causing an E484K substitution. Moreover, compared to wild-type SARS-CoV-2, B.1.351 is markedly more resistant to neutralization by convalescent plasma (9.4-fold) and sera from individuals who have been vaccinated (10.3–12.4-fold). B.1.351 and emergent variants13,14 with similar mutations in the spike protein present new challenges for monoclonal antibody therapies and threaten the protective efficacy of current vaccines.

Date: 2021
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DOI: 10.1038/s41586-021-03398-2

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