Abstract
The SARS-CoV-2 Delta (Pango lineage B.1.617.2) variant of concern spread globally, causing resurgences of COVID-19 worldwide1,2. The emergence of the Delta variant in the UK occurred on the background of a heterogeneous landscape of immunity and relaxation of non-pharmaceutical interventions. Here we analyse 52,992 SARS-CoV-2 genomes from England together with 93,649 genomes from the rest of the world to reconstruct the emergence of Delta and quantify its introduction to and regional dissemination across England in the context of changing travel and social restrictions. Using analysis of human movement, contact tracing and virus genomic data, we find that the geographic focus of the expansion of Delta shifted from India to a more global pattern in early May 2021. In England, Delta lineages were introduced more than 1,000 times and spread nationally as non-pharmaceutical interventions were relaxed. We find that hotel quarantine for travellers reduced onward transmission from importations; however, the transmission chains that later dominated the Delta wave in England were seeded before travel restrictions were introduced. Increasing inter-regional travel within England drove the nationwide dissemination of Delta, with some cities receiving more than 2,000 observable lineage introductions from elsewhere. Subsequently, increased levels of local population mixing—and not the number of importations—were associated with the faster relative spread of Delta. The invasion dynamics of Delta depended on spatial heterogeneity in contact patterns, and our findings will inform optimal spatial interventions to reduce the transmission of current and future variants of concern, such as Omicron (Pango lineage B.1.1.529).
| Original language | English |
|---|---|
| Pages (from-to) | 154-160 |
| Number of pages | 7 |
| Journal | Nature |
| Volume | 610 |
| Issue number | 7930 |
| Early online date | 11 Aug 2022 |
| DOIs | |
| Publication status | Published - 6 Oct 2022 |
Bibliographical note
Funding Information: COG-UK is supported by funding from the Medical Research Council (MRC) part of UK Research and Innovation (UKRI), the National Institute of Health Research (NIHR) (grant code: MC_PC_19027), and Genome Research Limited, operating as the Wellcome Sanger Institute. M.U.G.K. acknowledges support from a Branco Weiss Fellowship, Reuben College Oxford, Google.org, the Foreign, Commonwealth and Development Office and Wellcome (225288/Z/22/Z), and The Rockefeller Foundation. S.D. and M.U.G.K. acknowledge support from the European Union Horizon 2020 project MOOD (grant agreement number 874850). O.G.P., M.U.G.K., L.d.P. and A.E.Z. acknowledge support from the Oxford Martin School. V.H. was supported by the Biotechnology and Biological Sciences Research Council (BBSRC) (grant number BB/M010996/1). S.D. is supported by the Fonds National de la Recherche Scientifique (FNRS) (Belgium). J.T.M., R.C. and A.R. acknowledge support from the Wellcome Trust (Collaborators Award 206298/Z/17/Z—ARTIC network). A.R. is also supported by the European Research Council (grant agreement number 725422—ReservoirDOCS) and Bill and Melinda Gates Foundation (OPP1175094—HIV-PANGEA II). C.R. was supported by a Fondation Botnar Research Award (programme grant 6063). G.B. acknowledges support from the Research Foundation—Flanders (Fonds voor Wetenschappelijk Onderzoek—Vlaanderen) (G0E1420N and G098321N) and from the Interne Fondsen KU Leuven (Internal Funds KU Leuven) under grant agreement C14/18/094. A.O. is supported by the Wellcome Trust Hosts, Pathogens and Global Health Programme (grant number 203783/Z16/Z) and Fast Grants (award number 2236). S. Bajaj is supported by the Clarendon Scholarship, University of Oxford and NERC DTP (grant number NE/S007474/1). M.A.S. acknowledges support from US National Institutes of Health grant R01 AI153044. X.J. acknowledges support from US National Institutes of Health grant U19 AI135995. T.P.P. and W.S.B. acknowledge support from the G2P–UK National Virology Consortium funded by the MRC (MR/W005611/1). I.I.B. is supported by the Canadian Institutes of Health Research (grant 02179-000). N.R.F. acknowledges support from the Wellcome Trust and Royal Society Sir Henry Dale Fellowship (204311/Z/16/Z), Bill and Melinda Gates Foundation (INV-034540), the Medical Research Council-Sao Paulo Research Foundation (FAPESP) CADDE partnership award (MR/S0195/1 and FAPESP 18/14389-0) and the MRC Centre for Global Infectious Disease Analysis (reference MR/R015600/1). E.V. acknowledges support from the Wellcome Trust (220885/Z/20/Z). The contents of this publication are the sole responsibility of the authors and do not necessarily reflect the views of the European Commission or any of the other funders.Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Publisher Copyright: © 2022, The Author(s).
Citation: McCrone, J.T., Hill, V., Bajaj, S. et al. Context-specific emergence and growth of the SARS-CoV-2 Delta variant. Nature 610, 154–160 (2022). https://doi.org/10.1038/s41586-022-05200-3
DOI: https://doi.org/10.1038/s41586-022-05200-3