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

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Unmitigated spread in Brazil

Despite an extensive network of primary care availability, Brazil has suffered profoundly during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. Using daily data from state health offices, Castro et al. analyzed the pattern of spread of COVID-19 cases and deaths in the country from February to October 2020. Clusters of deaths before cases became apparent indicated unmitigated spread. SARS-CoV-2 circulated undetected in Brazil for more than a month as it spread north from S o Paulo. In Manaus, transmission reached unprecedented levels after a momentary respite in mid-2020. Faria et al. tracked the evolution of a new, more aggressive lineage called P.1, which has 17 mutations, including three (K417T, E484K, and N501Y) in the spike protein. After a period of accelerated evolution, this variant emerged in Brazil during November 2020. Coupled with the emergence of P.1, disease spread was accelerated by stark local inequalities and political upheaval, which compromised a prompt federal response.

Science, abh1558 and abh2644, this issue p. [Related article:]821 and p. 815

Abstract

A variant lineage of SARS-CoV-2 associated with rapid transmission in Manaus, Brazil, evolved in November 2020 with immune escape characteristics.

Abstract

Cases of severe acute respiratory syndrome coronavirus 2 (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 (angiotensin-converting enzyme 2) 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- to 2.4-fold more transmissible and that previous (non-P.1) infection provides 54 to 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.

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Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor

Jun Lan, Jiwan Ge, Jinfang Yu … (2020)

A new and highly pathogenic coronavirus (severe acute respiratory syndrome coronavirus-2, SARS-CoV-2) caused an outbreak in Wuhan city, Hubei province, China, starting from December 2019 that quickly spread nationwide and to other countries around the world1-3. Here, to better understand the initial step of infection at an atomic level, we determined the crystal structure of the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 bound to the cell receptor ACE2. The overall ACE2-binding mode of the SARS-CoV-2 RBD is nearly identical to that of the SARS-CoV RBD, which also uses ACE2 as the cell receptor4. Structural analysis identified residues in the SARS-CoV-2 RBD that are essential for ACE2 binding, the majority of which either are highly conserved or share similar side chain properties with those in the SARS-CoV RBD. Such similarity in structure and sequence strongly indicate convergent evolution between the SARS-CoV-2 and SARS-CoV RBDs for improved binding to ACE2, although SARS-CoV-2 does not cluster within SARS and SARS-related coronaviruses1-3,5. The epitopes of two SARS-CoV antibodies that target the RBD are also analysed for binding to the SARS-CoV-2 RBD, providing insights into the future identification of cross-reactive antibodies.

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Author and article information

Journal

Journal ID (nlm-ta): Science

Journal ID (iso-abbrev): Science

Journal ID (publisher-id): SCIENCE

Journal ID (hwp): science

Title: Science (New York, N.y.)

Publisher: American Association for the Advancement of Science

ISSN (Print): 0036-8075

ISSN (Electronic): 1095-9203

Publication date (Print): 21 May 2021

Publication date (Electronic): 14 April 2021

Volume: 372

Issue: 6544

Pages: 815-821

Affiliations

[1 ]MRC Centre for Global Infectious Disease Analysis, School of Public Health, Imperial College London, London, UK.

[2 ]The Abdul Latif Jameel Institute for Disease and Emergency Analytics (J-IDEA), School of Public Health, Imperial College London, London, UK.

[3 ]Instituto de Medicina Tropical, Faculdade de Medicina da Universidade de So Paulo, So Paulo, Brazil.

[4 ]Department of Zoology, University of Oxford, Oxford, UK.

[5 ]Departamento de Molstias Infecciosas e Parasitrias, Faculdade de Medicina da Universidade de So Paulo, So Paulo, Brazil.

[6 ]Fundao Hospitalar de Hematologia e Hemoterapia, Manaus, Brazil.

[7 ]Diretoria de Ensino e Pesquisa, Fundao Hospitalar de Hematologia e Hemoterapia, Manaus, Brazil.

[8 ]Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK.

[9 ]Division of Structural Biology, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.

[10 ]Departamento de Epidemiologia, Faculdade de Sade Pblica da Universidade de So Paulo, Sao Paulo, Brazil.

[11 ]Laboratrio de Virologia, Instituto de Cincias Biomdicas, Universidade Federal de Uberlndia, Uberlndia, Brazil.

[12 ]Institute for Applied Economic ResearchIpea, Braslia, Brazil.

[13 ]Institute of Mathematics and Statistics, University of So Paulo, So Paulo, Brazil.

[14 ]DB Diagnsticos do Brasil, So Paulo, Brazil.

[15 ]Department of Mathematics, Imperial College London, London, UK.

[16 ]Virology Research Centre, Ribeiro Preto Medical School, University of So Paulo, Ribeiro Preto, SP, Brazil.

[17 ]Laboratory of Quantitative Pathology, Center of Pathology, Adolfo Lutz Institute, So Paulo, Brazil.

[18 ]Instituto Hermes Pardini, Belo Horizonte, Brazil.

[19 ]Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.

[20 ]CDL Laboratrio Santos e Vidal, Manaus, Brazil.

[21 ]Departamento de Gentica, Ecologia e Evoluo, Instituto de Cincias Biolgicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

[22 ]Laboratory of Emerging Viruses, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, University of Campinas (UNICAMP), So Paulo, Brazil.

[23 ]Instituto Nacional de Pesquisas da Amaznia, Manaus, Brazil.

[24 ]Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.

[25 ]Center for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, Boston, MA, USA.

[26 ]Departamento de Engenharia de Sistemas Eletrnicos, Escola Politcnica da Universidade de So Paulo, So Paulo, Brazil.

[27 ]Department of Biomathematics, Department of Biostatistics, and Department of Human Genetics, University of California, Los Angeles, CA, USA.

[28 ]Institute for Genomics and Evolutionary Medicine, Temple University, Philadelphia, PA, USA.

[29 ]Mathematical Sciences, University of Southampton, Southampton, UK.

[30 ]Institute for Microbiology and Infection, University of Birmingham, Birmingham, UK.

[31 ]Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.

[32 ]Diretoria Clnica, Fundao Hospitalar de Hematologia e Hemoterapia do Amazonas, Manaus, Brazil.

[33 ]Diretoria da Presidncia, Fundao Hospitalar de Hematologia e Hemoterapia do Amazonas, Manaus, Brazil.

[34 ]Department of Pathobiology and Population Sciences, The Royal Veterinary College, London, UK.

[35 ]Section of Epidemiology, Department of Public Health, University of Copenhagen, Copenhagen, Denmark.

Author notes

[]

These authors contributed equally to this work.

[]

These authors contributed equally to this work.

[* ]Corresponding author. Email: n.faria@ 123456imperial.ac.uk (N.R.F.); samir.bhatt@ 123456sund.ku.dk (S.B.); sabinoec@ 123456usp.br (E.S.C.)

Article

Publisher ID: abh2644

DOI: 10.1126/science.abh2644

PMC ID: 8139423

PubMed ID: 33853970

SO-VID: 30fa922a-4304-4953-a9cc-ddfef24fbf7e

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.