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Generation and transmission of interlineage recombinants in the SARS-CoV-2 pandemic
Author(s) -
Ben Jackson,
Maciej F. Boni,
Matthew Bull,
Amy Colleran,
Rachel Colquhoun,
Alistair C. Darby,
Sam Haldenby,
Verity Hill,
Anita O. Lucaci,
John T. McCrone,
Samuel M. Nicholls,
Áine O’Toole,
Nicole Pacchiarini,
Radoslaw Poplawski,
Emily Scher,
Flora Todd,
Hermione J. Webster,
Mark Whitehead,
Claudia Wierzbicki,
Nicholas J. Loman,
Thomas R. Connor,
David L. Robertson,
Oliver G. Pybus,
Andrew Rambaut
Publication year - 2021
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2021.08.014
Subject(s) - biology , genome , transmission (telecommunications) , genetics , lineage (genetic) , virology , recombinant dna , virus , pandemic , gene , covid-19 , disease , medicine , pathology , infectious disease (medical specialty) , electrical engineering , engineering
We present evidence for multiple independent origins of recombinant SARS-CoV-2 viruses sampled from late 2020 and early 2021 in the United Kingdom. Their genomes carry single-nucleotide polymorphisms and deletions that are characteristic of the B.1.1.7 variant of concern but lack the full complement of lineage-defining mutations. Instead, the remainder of their genomes share contiguous genetic variation with non-B.1.1.7 viruses circulating in the same geographic area at the same time as the recombinants. In four instances, there was evidence for onward transmission of a recombinant-origin virus, including one transmission cluster of 45 sequenced cases over the course of 2 months. The inferred genomic locations of recombination breakpoints suggest that every community-transmitted recombinant virus inherited its spike region from a B.1.1.7 parental virus, consistent with a transmission advantage for B.1.1.7's set of mutations.

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