tetano
Editor, Senior Moderator
Nat Commun
. 2020 Nov 25;11(1):5986.
doi: 10.1038/s41467-020-19818-2.
No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Lucy van Dorp[SUP] 1 [/SUP], Damien Richard[SUP] 2 3 [/SUP], Cedric C S Tan[SUP] 4 [/SUP], Liam P Shaw[SUP] 5 [/SUP], Mislav Acman[SUP] 4 [/SUP], Fran?ois Balloux[SUP] 6 [/SUP]
Affiliations
Abstract
COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised animal reservoir. Due to this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we develop a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a curated set of recurrent mutations identified within a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation. At this stage we find no evidence for significantly more transmissible lineages of SARS-CoV-2 due to recurrent mutations.
. 2020 Nov 25;11(1):5986.
doi: 10.1038/s41467-020-19818-2.
No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Lucy van Dorp[SUP] 1 [/SUP], Damien Richard[SUP] 2 3 [/SUP], Cedric C S Tan[SUP] 4 [/SUP], Liam P Shaw[SUP] 5 [/SUP], Mislav Acman[SUP] 4 [/SUP], Fran?ois Balloux[SUP] 6 [/SUP]
Affiliations
- PMID: 33239633
- DOI: 10.1038/s41467-020-19818-2
Abstract
COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised animal reservoir. Due to this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we develop a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a curated set of recurrent mutations identified within a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation. At this stage we find no evidence for significantly more transmissible lineages of SARS-CoV-2 due to recurrent mutations.