SARS-CoV-2 Omicron-B.1.1.529 leads to widespread escape from neutralizing antibody responses
Dejnirattisai W., Huo J., Zhou D., Zahradník J., Supasa P., Liu C., Duyvesteyn HME., Ginn HM., Mentzer AJ., Tuekprakhon A., Nutalai R., Wang B., Dijokaite A., Khan S., Avinoam O., Bahar M., Skelly D., Adele S., Johnson SA., Amini A., Ritter TG., Mason C., Dold C., Pan D., Assadi S., Bellass A., Omo-Dare N., Koeckerling D., Flaxman A., Jenkin D., Aley PK., Voysey M., Costa Clemens SA., Naveca FG., Nascimento V., Nascimento F., Fernandes da Costa C., Resende PC., Pauvolid-Correa A., Siqueira MM., Baillie V., Serafin N., Kwatra G., Da Silva K., Madhi SA., Nunes MC., Malik T., Openshaw PJM., Baillie JK., Semple MG., Townsend AR., Huang KYA., Tan TK., Carroll MW., Klenerman P., Barnes E., Dunachie SJ., Constantinides B., Webster H., Crook D., Pollard AJ., Lambe T., Conlon C., Deeks AS., Frater J., Frending L., Gardiner S., Jämsén A., Jeffery K., Malone T., Phillips E., Rothwell L., Stafford L., Openshaw PJ., Carson G., Alex B., Andrikopoulos P., Bach B., Barclay WS., Bogaert D., Chand M., Chechi K., Cooke GS., da Silva Filipe A., de Silva T., Docherty AB., dos Santos Correia G., Dumas ME., Dunning J., Fletcher T., Green CA., Greenhalf W., Griffin JL., Gupta RK., Harrison EM., Hiscox JA., Wai Ho AY., Horby PW., Ijaz S.
On 24th November 2021, the sequence of a new SARS-CoV-2 viral isolate Omicron-B.1.1.529 was announced, containing far more mutations in Spike (S) than previously reported variants. Neutralization titers of Omicron by sera from vaccinees and convalescent subjects infected with early pandemic Alpha, Beta, Gamma, or Delta are substantially reduced, or the sera failed to neutralize. Titers against Omicron are boosted by third vaccine doses and are high in both vaccinated individuals and those infected by Delta. Mutations in Omicron knock out or substantially reduce neutralization by most of the large panel of potent monoclonal antibodies and antibodies under commercial development. Omicron S has structural changes from earlier viruses and uses mutations that confer tight binding to ACE2 to unleash evolution driven by immune escape. This leads to a large number of mutations in the ACE2 binding site and rebalances receptor affinity to that of earlier pandemic viruses.