Guest essay by Eric Worrall

According to study author Professor Francois Balloux, a plausible explanation for why mutant Covid-19 strains are not more infectious than the original is “we missed the early window when it adapted to humans”.

Coronavirus mutations do not appear to be helping it spread more rapidly, study says

PUBLISHED THU, NOV 26 20208:43 AM EST
Sam Meredith

LONDON — A global study of more than 12,000 coronavirus mutations has found that none of them appear to have made the virus that causes Covid-19 spread more rapidly.

Researchers at University College London assessed coronavirus mutations in over 46,000 samples taken from people in 99 different countries and concluded the mutations all appeared to be neutral when it comes to speeding up the virus’ spread.

The peer-reviewed study, published Wednesday in the Nature Communications journal, identified a total of 12,706 mutations. Of those, 398 strains of the coronavirus were found to have occurred repeatedly and independently.

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“This raises the question why #SARSCoV2 is so well adapted for transmission in humans. A plausible answer is that we missed the early window when it adapted to humans,” Balloux said via Twitter on Wednesday.

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Read more: https://www.cnbc.com/2020/11/26/covid-mutations-do-not-appear-to-be-helping-the-virus-spread-more-rapidly-study-says.html

The abstract of the study;

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

Lucy van Dorp, Damien Richard, Cedric C. S. Tan, Liam P. Shaw, Mislav Acman & François Balloux 

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.

Read more: https://www.nature.com/articles/s41467-020-19818-2

In a way Professor Balloux’s hypothesis seems reassuring. While it cannot be ruled out that a more dangerous strain may emerge in the future, the virus has not shown tangible signs of progression into a more dangerous form to date, despite plenty of opportunities.

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