PT  - JOURNAL ARTICLE
AU  - Lucy van Dorp
AU  - Damien Richard
AU  - Cedric CS. Tan
AU  - Liam P. Shaw
AU  - Mislav Acman
AU  - François Balloux
TI  - No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
AID  - 10.1101/2020.05.21.108506
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.05.21.108506
4099  - http://biorxiv.org/content/early/2020/05/21/2020.05.21.108506.short
4100  - http://biorxiv.org/content/early/2020/05/21/2020.05.21.108506.full
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.