RT Journal Article
SR Electronic
T1 No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.05.21.108506
DO 10.1101/2020.05.21.108506
A1 Lucy van Dorp
A1 Damien Richard
A1 Cedric CS. Tan
A1 Liam P. Shaw
A1 Mislav Acman
A1 François Balloux
YR 2020
UL http://biorxiv.org/content/early/2020/05/21/2020.05.21.108506.abstract
AB The COVID-19 pandemic is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised reservoir. Due to this extremely recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that some lineages of SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible candidate mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any of the recurrent mutations that have been observed in SARS-CoV-2 to date significantly alter viral transmission. To do so, we developed 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 carefully curated set of recurrent mutations identified within a dataset of over 15,000 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation convincingly associated with increased viral transmission. Instead, recurrent SARS-CoV-2 mutations currently in circulation appear to be either neutral or weakly deleterious. These mutations seem primarily induced by the human immune system via host RNA editing, rather than being signatures of adaption to the novel human host. There is no evidence at this stage for the emergence of more transmissible lineages of SARS-CoV-2 due to recurrent mutations.Competing Interest StatementThe authors have declared no competing interest.