Genomics and epidemiology of the P.1 SARS-CoV-2 lineage in Manaus, Brazil

Nuno R Faria, Thomas A Mellan, Charles Whittaker, Ingra M Claro, Darlan da S Candido, Swapnil Mishra, Myuki A E Crispim, Flavia C S Sales, Iwona Hawryluk, John T McCrone, Ruben J G Hulswit, Lucas A M Franco, Mariana S Ramundo, Jaqueline G de Jesus, Pamela S Andrade, Thais M Coletti, Giulia M Ferreira, Camila A M Silva, Erika R Manuli, Rafael H M PereiraPedro S Peixoto, Moritz U G Kraemer, Nelson Gaburo, Cecilia da C Camilo, Henrique Hoeltgebaum, William M Souza, Esmenia C Rocha, Leandro M de Souza, Mariana C de Pinho, Leonardo J T Araujo, Frederico S V Malta, Aline B de Lima, Joice do P Silva, Danielle A G Zauli, Alessandro C de S Ferreira, Ricardo P Schnekenberg, Daniel J Laydon, Patrick G T Walker, Hannah M Schlüter, Ana L P Dos Santos, Maria S Vidal, Valentina S Del Caro, Rosinaldo M F Filho, Helem M Dos Santos, Renato S Aguiar, José L Proença-Modena, Bruce Nelson, James A Hay, Mélodie Monod, Xenia Miscouridou, Helen Coupland, Raphael Sonabend, Michaela Vollmer, Axel Gandy, Carlos A Prete, Vitor H Nascimento, Marc A Suchard, Thomas A Bowden, Sergei L K Pond, Chieh-Hsi Wu, Oliver Ratmann, Neil M Ferguson, Christopher Dye, Nick J Loman, Philippe Lemey, Andrew Rambaut, Nelson A Fraiji, Maria do P S S Carvalho, Oliver G Pybus, Seth Flaxman, Samir Bhatt, Ester C Sabino

Research output: Contribution to journalArticlepeer-review

Abstract

Cases of SARS-CoV-2 infection in Manaus, Brazil, resurged in late 2020, despite previously high levels of infection. Genome sequencing of viruses sampled in Manaus between November 2020 and January 2021 revealed the emergence and circulation of a novel SARS-CoV-2 variant of concern. Lineage P.1, acquired 17 mutations, including a trio in the spike protein (K417T, E484K and N501Y) associated with increased binding to the human ACE2 receptor. Molecular clock analysis shows that P.1 emergence occurred around mid-November 2020 and was preceded by a period of faster molecular evolution. Using a two-category dynamical model that integrates genomic and mortality data, we estimate that P.1 may be 1.7-2.4-fold more transmissible, and that previous (non-P.1) infection provides 54-79% of the protection against infection with P.1 that it provides against non-P.1 lineages. Enhanced global genomic surveillance of variants of concern, which may exhibit increased transmissibility and/or immune evasion, is critical to accelerate pandemic responsiveness.

Original languageEnglish
Article numbereabh2644
Number of pages14
JournalScience
Early online date14 Apr 2021
DOIs
Publication statusPublished - 14 Apr 2021

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