No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Lucy Dorp (),
Damien Richard,
Cedric C. S. Tan,
Liam P. Shaw,
Mislav Acman and
François Balloux ()
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Lucy Dorp: University College London
Damien Richard: Cirad, UMR PVBMT
Cedric C. S. Tan: University College London
Liam P. Shaw: University of Oxford
Mislav Acman: University College London
François Balloux: University College London
Nature Communications, 2020, vol. 11, issue 1, 1-8
Abstract:
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.
Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19818-2
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DOI: 10.1038/s41467-020-19818-2
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