Generation and transmission of interlineage recombinants in the SARS-CoV-2 pandemic
Jackson B., Boni MF., Bull MJ., Colleran A., Colquhoun RM., Darby AC., Haldenby S., Hill V., Lucaci A., McCrone JT., Nicholls SM., O’Toole Á., Pacchiarini N., Poplawski R., Scher E., Todd F., Webster HJ., Whitehead M., Wierzbicki C., Loman NJ., Connor TR., Robertson DL., Pybus OG., Rambaut A., Robson SC., Golubchi T., Martinez Nunez RT., Ludden C., Corden S., Johnston I., Bonsall D., Smith CP., Awan AR., Bucca G., Estee Torok M., Saeed K., Prieto JA., Jackson DK., Hamilton WL., Snell LB., Moore C., Harrison EM., Goncalves S., Jackson LM., Goodfellow IG., Fairley DJ., Loose MW., Watkins J., Livett R., Moses S., Amato R., Smith DL., Barrett J., Aanensen DM., Curran MD., Parmar S., Aggarwal D., Shepherd JG., Parker MD., Glaysher S., Bashton M., Underwood AP., Loveson KF., Carabelli AM., Templeton KE., Langford CF., Sillitoe J., Silva TID., Wang D., Kwiatkowski D., O’Grady J., Cottrell S., Holden MTG., Thomson EC., Osman H., Andersson M., Chauhan AJ., Hassan-Ibrahim MO., Lawniczak M., Gupta RK., Alderton A., Chand M., Constantinidou C., Unnikrishnan M., Hiscox JA., Paterson S., Martincorena I., Volz EM., Page AJ., Bassett AR., Ariani CV., Spencer Chapman MH., Li KK., Shah RN., Jesudason NG., Taha Y., McHugh MP., Dewar R., Jahun AS., McMurray C.
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.