501Y.V2 and 501Y.V3 variants of SARS-CoV-2 lose binding to bamlanivimab in vitro

The newly emerging variants of SARS-CoV-2 from South Africa (B.1.351/501Y.V2) and Brazil (P.1/501Y.V3) have led to a higher infection rate and reinfection of COVID-19 patients. We found that the mutations K417N, E484K, and N501Y within the receptor-binding domains (RBDs) of the virus could confer ~2...

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Main Authors: Haolin Liu (Author), Pengcheng Wei (Author), Qianqian Zhang (Author), Zhongzhou Chen (Author), Katja Aviszus (Author), Walter Downing (Author), Shelley Peterson (Author), Lyndon Reynoso (Author), Gregory P. Downey (Author), Stephen K. Frankel (Author), John Kappler (Author), Philippa Marrack (Author), Gongyi Zhang (Author)
Format: Book
Published: Taylor & Francis Group, 2021-01-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Haolin Liu  |e author 
700 1 0 |a Pengcheng Wei  |e author 
700 1 0 |a Qianqian Zhang  |e author 
700 1 0 |a Zhongzhou Chen  |e author 
700 1 0 |a Katja Aviszus  |e author 
700 1 0 |a Walter Downing  |e author 
700 1 0 |a Shelley Peterson  |e author 
700 1 0 |a Lyndon Reynoso  |e author 
700 1 0 |a Gregory P. Downey  |e author 
700 1 0 |a Stephen K. Frankel  |e author 
700 1 0 |a John Kappler  |e author 
700 1 0 |a Philippa Marrack  |e author 
700 1 0 |a Gongyi Zhang  |e author 
245 0 0 |a 501Y.V2 and 501Y.V3 variants of SARS-CoV-2 lose binding to bamlanivimab in vitro 
260 |b Taylor & Francis Group,   |c 2021-01-01T00:00:00Z. 
500 |a 10.1080/19420862.2021.1919285 
500 |a 1942-0870 
500 |a 1942-0862 
520 |a The newly emerging variants of SARS-CoV-2 from South Africa (B.1.351/501Y.V2) and Brazil (P.1/501Y.V3) have led to a higher infection rate and reinfection of COVID-19 patients. We found that the mutations K417N, E484K, and N501Y within the receptor-binding domains (RBDs) of the virus could confer ~2-fold higher binding affinity to the human receptor, angiotensin converting enzyme 2 (ACE2), compared to the wildtype RBD. The mutated version of RBD also completely abolishes the binding of bamlanivimab, a therapeutic antibody, in vitro. Detailed analysis shows that the ~10-fold gain of binding affinity between ACE2 and Y501-RBD, which also exits in the high contagious variant B.1.1.7/501Y.V1 from the United Kingdom, is compromised by additional introduction of the K417/N/T mutation. Mutation of E484K leads to the loss of bamlanivimab binding to RBD, although this mutation does not affect the binding between RBD and ACE2. 
546 |a EN 
690 |a SARS-COV-2 
690 |a COVID-19 
690 |a B.1.1.7/501Y.V1 
690 |a B.1.351/501Y.V2 
690 |a P.1/501Y.V3 
690 |a ACE2 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
690 |a Immunologic diseases. Allergy 
690 |a RC581-607 
655 7 |a article  |2 local 
786 0 |n mAbs, Vol 13, Iss 1 (2021) 
787 0 |n https://www.tandfonline.com/doi/10.1080/19420862.2021.1919285 
787 0 |n https://doaj.org/toc/1942-0862 
787 0 |n https://doaj.org/toc/1942-0870 
856 4 1 |u https://doaj.org/article/8fedadc2ee61424d849e04c78d26f524  |z Connect to this object online.