@article{Willett_B-2022_83247,
title = {The hyper-transmissible SARS-CoV-2 Omicron variant exhibits significant antigenic change, vaccine escape and a switch in cell entry mechanism},
author = {Willett, B. and Grove, J. and MacLean, O. and Wilkie, C. and Logan, N. and De Lorenzo, G. and Furnon, W. and Scott, S. and Manali, M. and Szemiel, A. and Ashraf, S. and Vink, E. and Harvey, W. and Davis, C. and Orton, R. and Hughes, J. and Holland, P. and Silva, V. and Pascall, D. and Puxty, K. and da Silva Filipe, A. and Yebra, G. and Shabaan, S. and Holden, M. and Pinto, R. and Gunson, R. and Templeton, K. and Murcia, P. and Patel, A. and The COVID-19 Genomics UK (COG-UK) Consortium and Haughney, J. and Robertson, D. and Palmarini, M. and Ray, S. and Thomson, E.},
month = {jan},
year = {2022},
abstract = {Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron, the fifth VOC to be described, harbours 30 amino acid mutations in spike including 15 in the receptor-binding domain. Here, we demonstrate substantial evasion of neutralisation by Omicronin vitrousing sera from vaccinated individuals. Importantly, these data are mirrored by a substantial reduction in real-world vaccine effectiveness that is partially restored by booster vaccination. We also demonstrate that Omicron does not induce cell syncytia and favours a TMPRSS2-independent endosomal entry pathway. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant.},
journal = {MedRxiv},
publisher = {medRxiv},
url = {https://doi.org/10.1101/2022.01.03.21268111},
}
