Spatiotemporal invasion dynamics of SARS-CoV-2 lineage B.1.1.7 emergence
The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant has greater transmissibility than its predecessors, but this capacity has been amplified in some circumstances to tragic effect by a combinati...
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| Published in | Science (American Association for the Advancement of Science) Vol. 373; no. 6557; pp. 889 - 895 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
The American Association for the Advancement of Science
20.08.2021
American Association for the Advancement of Science (AAAS) American Association for the Advancement of Science |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant has greater transmissibility than its predecessors, but this capacity has been amplified in some circumstances to tragic effect by a combination of human behavior and local immunity. What are the extrinsic factors that help or hinder the rapid dissemination of variants? Kraemer
et al
. explored the invasion dynamics of B.1.1.7. in fine detail, from its location of origin in Kent, UK, to its heterogenous spread around the country. A combination of mobile phone and virus data including more than 17,000 genomes shows how distinct phases of dispersal were related to intensity of mobility and the timing of lockdowns. As the local outbreaks grew, importation from the London source area became less important. Had B.1.1.7. emerged at a slightly different time of year, its impact might have been different. —CA
Disentangling the factors that contribute to the rapid spread of virus variants is essential for understanding their epidemiological consequences.
Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7’s increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates. |
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| AbstractList | Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7's increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates. The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant has greater transmissibility than its predecessors, but this capacity has been amplified in some circumstances to tragic effect by a combination of human behavior and local immunity. What are the extrinsic factors that help or hinder the rapid dissemination of variants? Kraemer et al . explored the invasion dynamics of B.1.1.7. in fine detail, from its location of origin in Kent, UK, to its heterogenous spread around the country. A combination of mobile phone and virus data including more than 17,000 genomes shows how distinct phases of dispersal were related to intensity of mobility and the timing of lockdowns. As the local outbreaks grew, importation from the London source area became less important. Had B.1.1.7. emerged at a slightly different time of year, its impact might have been different. —CA Disentangling the factors that contribute to the rapid spread of virus variants is essential for understanding their epidemiological consequences. Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7’s increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates. Fueling outbreaks The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant has greater transmissibility than its predecessors, but this capacity has been amplified in some circumstances to tragic effect by a combination of human behavior and local immunity. What are the extrinsic factors that help or hinder the rapid dissemination of variants? Kraemer et al . explored the invasion dynamics of B.1.1.7. in fine detail, from its location of origin in Kent, UK, to its heterogenous spread around the country. A combination of mobile phone and virus data including more than 17,000 genomes shows how distinct phases of dispersal were related to intensity of mobility and the timing of lockdowns. As the local outbreaks grew, importation from the London source area became less important. Had B.1.1.7. emerged at a slightly different time of year, its impact might have been different. —CA Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7's increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates.Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7's increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates. Fueling outbreaksThe B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant has greater transmissibility than its predecessors, but this capacity has been amplified in some circumstances to tragic effect by a combination of human behavior and local immunity. What are the extrinsic factors that help or hinder the rapid dissemination of variants? Kraemer et al. explored the invasion dynamics of B.1.1.7. in fine detail, from its location of origin in Kent, UK, to its heterogenous spread around the country. A combination of mobile phone and virus data including more than 17,000 genomes shows how distinct phases of dispersal were related to intensity of mobility and the timing of lockdowns. As the local outbreaks grew, importation from the London source area became less important. Had B.1.1.7. emerged at a slightly different time of year, its impact might have been different.Science, abj0113, this issue p. 889Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to pandemic control yet difficult to achieve because they arise in the context of variable human behavior and immunity. We investigated the spatial invasion dynamics of lineage B.1.1.7 by jointly analyzing UK human mobility, virus genomes, and community-based polymerase chain reaction data. We identified a multistage spatial invasion process in which early B.1.1.7 growth rates were associated with mobility and asymmetric lineage export from a dominant source location, enhancing the effects of B.1.1.7’s increased intrinsic transmissibility. We further explored how B.1.1.7 spread was shaped by nonpharmaceutical interventions and spatial variation in previous attack rates. Our findings show that careful accounting of the behavioral and epidemiological context within which variants of concern emerge is necessary to interpret correctly their observed relative growth rates. |
| Author | Kraemer, Moritz U. G. Volz, Erik du Plessis, Louis Klein, Brennan Rambaut, Andrew Parag, Kris V. Gutierrez, Bernardo Jackson, Ben Cauchemez, Simon Battle, Anya Lindström Pybus, Oliver G. Bajaj, Sumali Faria, Nuno R. Loman, Nicholas J. Baele, Guy Aanensen, David M. Ruis, Christopher McCrone, John T. Dellicour, Simon Colquhoun, Rachel Vespignani, Alessandro Scarpino, Samuel V. Hill, Verity O’Toole, Áine |
| Author_xml | – sequence: 1 givenname: Moritz U. G. orcidid: 0000-0001-8838-7147 surname: Kraemer fullname: Kraemer, Moritz U. G. organization: Department of Zoology, University of Oxford, Oxford, UK – sequence: 2 givenname: Verity orcidid: 0000-0002-3509-8146 surname: Hill fullname: Hill, Verity organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 3 givenname: Christopher orcidid: 0000-0003-0977-5534 surname: Ruis fullname: Ruis, Christopher organization: Molecular Immunity Unit, Department of Medicine, Cambridge University, Cambridge, UK – sequence: 4 givenname: Simon orcidid: 0000-0001-9558-1052 surname: Dellicour fullname: Dellicour, Simon organization: Spatial Epidemiology Lab (SpELL), Université Libre de Bruxelles, Bruxelles, Belgium., Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, 3000 Leuven, Belgium., Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, University of Oxford, Oxford, UK – sequence: 5 givenname: Sumali orcidid: 0000-0002-8313-819X surname: Bajaj fullname: Bajaj, Sumali organization: Department of Zoology, University of Oxford, Oxford, UK – sequence: 6 givenname: John T. orcidid: 0000-0002-9846-8917 surname: McCrone fullname: McCrone, John T. organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 7 givenname: Guy orcidid: 0000-0002-1915-7732 surname: Baele fullname: Baele, Guy organization: Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, 3000 Leuven, Belgium – sequence: 8 givenname: Kris V. orcidid: 0000-0002-7806-3605 surname: Parag fullname: Parag, Kris V. organization: MRC Centre for Global Infectious Disease Analysis, Jameel Institute for Disease and Emergency Analytics, Imperial College London, London, UK – sequence: 9 givenname: Anya Lindström orcidid: 0000-0001-6356-4688 surname: Battle fullname: Battle, Anya Lindström organization: Department of Plant Sciences, University of Oxford, Oxford, UK – sequence: 10 givenname: Bernardo orcidid: 0000-0002-9220-2739 surname: Gutierrez fullname: Gutierrez, Bernardo organization: Department of Zoology, University of Oxford, Oxford, UK – sequence: 11 givenname: Ben orcidid: 0000-0002-9981-0649 surname: Jackson fullname: Jackson, Ben organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 12 givenname: Rachel orcidid: 0000-0002-5577-9897 surname: Colquhoun fullname: Colquhoun, Rachel organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 13 givenname: Áine orcidid: 0000-0001-8083-474X surname: O’Toole fullname: O’Toole, Áine organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 14 givenname: Brennan orcidid: 0000-0001-8326-5044 surname: Klein fullname: Klein, Brennan organization: Network Science Institute, Northeastern University, Boston, USA – sequence: 15 givenname: Alessandro orcidid: 0000-0003-3419-4205 surname: Vespignani fullname: Vespignani, Alessandro organization: Network Science Institute, Northeastern University, Boston, USA – sequence: 16 givenname: Erik orcidid: 0000-0001-6268-8937 surname: Volz fullname: Volz, Erik organization: MRC Centre for Global Infectious Disease Analysis, Jameel Institute for Disease and Emergency Analytics, Imperial College London, London, UK – sequence: 17 givenname: Nuno R. orcidid: 0000-0002-9747-8822 surname: Faria fullname: Faria, Nuno R. organization: Department of Zoology, University of Oxford, Oxford, UK., MRC Centre for Global Infectious Disease Analysis, Jameel Institute for Disease and Emergency Analytics, Imperial College London, London, UK., Instituto de Medicina Tropical, Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil – sequence: 18 givenname: David M. orcidid: 0000-0001-6688-0854 surname: Aanensen fullname: Aanensen, David M. organization: Centre for Genomic Pathogen Surveillance, Wellcome Genome Campus, Hinxton, UK., Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, University of Oxford, Oxford, UK – sequence: 19 givenname: Nicholas J. orcidid: 0000-0002-9843-8988 surname: Loman fullname: Loman, Nicholas J. organization: Institute of Microbiology and Infection, University of Birmingham, Birmingham, UK – sequence: 20 givenname: Louis orcidid: 0000-0003-0352-6289 surname: du Plessis fullname: du Plessis, Louis organization: Department of Zoology, University of Oxford, Oxford, UK – sequence: 21 givenname: Simon orcidid: 0000-0001-9186-4549 surname: Cauchemez fullname: Cauchemez, Simon organization: Mathematical Modelling of Infectious Diseases Unit, Institut Pasteur, UMR2000, CNRS, Paris, France – sequence: 22 givenname: Andrew orcidid: 0000-0003-4337-3707 surname: Rambaut fullname: Rambaut, Andrew organization: Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK – sequence: 23 givenname: Samuel V. orcidid: 0000-0001-5716-2770 surname: Scarpino fullname: Scarpino, Samuel V. organization: Network Science Institute, Northeastern University, Boston, USA., Vermont Complex Systems Center, University of Vermont, Burlington, USA., Santa Fe Institute, Santa Fe, USA – sequence: 24 givenname: Oliver G. orcidid: 0000-0002-8797-2667 surname: Pybus fullname: Pybus, Oliver G. organization: Department of Zoology, University of Oxford, Oxford, UK., Department of Pathobiology and Population Sciences, Royal Veterinary College London, London, UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34301854$$D View this record in MEDLINE/PubMed https://hal.science/hal-04095294$$DView record in HAL |
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| ContentType | Journal Article |
| Copyright | Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works Distributed under a Creative Commons Attribution 4.0 International License Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY). 2021 The Authors |
| Copyright_xml | – notice: Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. – notice: Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works – notice: Distributed under a Creative Commons Attribution 4.0 International License – notice: Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY). 2021 The Authors |
| CorporateAuthor | COVID-19 Genomics UK (COG-UK) Consortium |
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| Snippet | The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally. Intrinsically, this variant... Understanding the causes and consequences of the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern is crucial to... Fueling outbreaksThe B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally.... Fueling outbreaks The B.1.1.7 lineage of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fast-spreading outbreaks globally.... |
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| SubjectTerms | Communicable Disease Control Context Coronavirus Coronaviruses COVID-19 COVID-19 - epidemiology COVID-19 - prevention & control COVID-19 - transmission COVID-19 - virology COVID-19 Nucleic Acid Testing Disease transmission Dispersal Ecology Emerging diseases Epidemiology Genome, Viral Genomes Growth rate Human behavior Human health and pathology Humans Immunity Importation Incidence Infectious diseases Life Sciences Microbiology and Parasitology Mobility Outbreaks Pandemics Phylogeography Polymerase chain reaction Respiratory diseases Santé publique et épidémiologie SARS-CoV-2 - genetics SARS-CoV-2 - pathogenicity Severe acute respiratory syndrome coronavirus 2 Spatial variations Spatio-Temporal Analysis Travel United Kingdom - epidemiology Viral diseases Virology Viruses |
| Title | Spatiotemporal invasion dynamics of SARS-CoV-2 lineage B.1.1.7 emergence |
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