The emergence and ongoing convergent evolution of the SARS-CoV-2 N501Y lineages.
Martin, Darren P
San, James Emmanuel
Shank, Stephen D
Lucaci, Alexander G
Lessells, Richard J
COVID-19 Genomics UK (COG-UK),
Wertheim, Joel O
Harkins, Gordon W
MacLean, Oscar A
Robertson, David L
de Oliveira, Tulio
Kosakovsky Pond, Sergei L
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Martin, D. P., Weaver, S., Tegally, H., San, J. E., Shank, S. D., Wilkinson, E., Lucaci, A. G., et al. (2021). The emergence and ongoing convergent evolution of the SARS-CoV-2 N501Y lineages.. Cell, 184 (20), 5189-5200.e7. https://doi.org/10.1016/j.cell.2021.09.003
In the first 11 months of the SARS-CoV-2 pandemic (December 2019 – October 2020), the evolution of the virus worldwide was in the context of a highly susceptible new host population (Dearlove et al., 2020; MacLean et al., 2021). Other than the early identification of the D614G substitution in the viral Spike protein (Korber et al., 2020; Plante et al., 2021; Zhang et al., 2020) and P323L in the viral RNA-dependent RNA polymerase protein (Garvin et al., 2020), both of which may have increased viral transmissibility without impacting pathogenesis (Peacock et al., 2021), few mutations were epidemiologically significant and the evolutionary dynamics of the virus were predominantly characterized by a mutational pattern of slow and selectively neutral random genetic drift (Dearlove et al., 2020; MacLean et al., 2021). This behavior is consistent with exponential growth in a population of naive susceptible hosts that do not exert significant selective pressures on the pathogen prior to transmission events (MacLean et al., 2021). Past pandemics and long-term evolutionary dynamics of RNA viruses attest to the fact that such an evolutionary “lull” rarely lasts. Indeed, in late 2020, three relatively divergent SARS-CoV-2 lineages emerged in rapid succession: (1) alpha, B.1.1.7 or 501Y.V1 which will hereafter be referred to as V1 (Rambaut et al., 2020a), (2) beta, B.1.351 or 501Y.V2 which will hereafter be referred to as V2 (Tegally et al., 2021), and (3) gamma, P.1 or 501Y.V3, which will hereafter be referred to as V3 (Faria et al., 2021).
NGS-SA, COVID-19 Genomics UK (COG-UK), Humans, Codon, Public Health, Evolution, Molecular, Phylogeny, Amino Acid Sequence, Genetic Drift, Mutation, Genes, Viral, Immune Evasion, Pandemics, COVID-19, SARS-CoV-2, Host Adaptation
We gratefully acknowledge all of the authors from the originating laboratories responsible for obtaining the specimens and the submitting laboratories where genetic sequence data were generated and shared via the GISAID Initiative, on which this research is based (Table S5). We thank Carolyn Williamson, Robert Wilkinson, Valarie Mizrahe, Jonathan Blackburn, and Nicola Mulder for reading and commenting on the manuscript. The Wellcome Trust funded D.P.M. (222574/Z/21/Z), D.L.R. (220977/Z/20/Z), P.L. (2206298/Z/17/Z), and O.A.M. (206369/Z/17/Z). The US National Institutes of Health funded S.L.K.P. (R01 AI134384 and AI140970), J.O.W. (R01 AI13599), G.W.H. (1U01Al152151-01), and J.E.S. and H.T. (via H3ABioNet U24HG006941). The US National Science Foundation funded S.L.K.P. (RAPID 2027196 NSF/DBI,BIO), The UK Medical Research Council funded D.L.R. (MC_UU_1201412) and COG-UK (via UK Research & Innovation, the National Institute of Health Research, and Genome Research Limited operating as the Wellcome Sanger Institute). The European Research Council funded P.L. (725422-ReservoirDOCS and 874850-MOOD). The South African Medical Research Council funded NGS-SA via the Strategic Health Innovation Partnerships Unit of the South African Medical Research Council and Department of Science and Innovation.
Wellcome Trust (108082/A/15/Z)
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External DOI: https://doi.org/10.1016/j.cell.2021.09.003
This record's URL: https://www.repository.cam.ac.uk/handle/1810/329765
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