Examine: Covid-19 Mutations are NOT Serving to the Virus Unfold

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China Accuses Italy of Being the Source of Covid-19

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Guest essay by Eric Worrall

According to study author Professor Francois Balloux, a plausible explanation for why mutant Covid-19 strains are no more infectious than the original is "we missed the early window when it was adapting to humans".

Coronavirus mutations don't seem to be contributing to any faster spread, according to a study

PUBLISHED THU, NOVEMBER 26, 20208: 43 EST
Sam Meredith

LONDON – A global study of 12,000+ coronavirus mutations found none of them spread the virus that causes Covid-19 faster.

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

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

“This begs the question of why # SARSCoV2 is so well suited for transmission in humans. One plausible answer is that we missed the early window when it was adapting to humans, ”Balloux said on Wednesday via Twitter.

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 of increased transferability due to recurring mutations in SARS-CoV-2

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

COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped from a currently uncharacterized animal reservoir into the human population at the end of 2019. Because of this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculation that SARS-CoV-2 may develop into higher transmittability. The most plausible mutations under presumed natural selection are those that have occurred repeatedly and independently of one another (homoplasias). Here we are formally testing whether homoplasias that have previously been observed in SARS-CoV-2 are significantly associated with increased virus transmission. To do this, we are developing a phylogenetic index to quantify the relative number of offspring in sister cages with and without a specific allele. We apply this index to a curated set of recurrent mutations identified in a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this sentence that is convincingly associated with increased virus transmission. Instead, recurring mutations currently floating around appear to be evolutionarily neutral and mainly induced by the human immune system via RNA editing, rather than being signatures of adaptation. At the present time we cannot find any evidence of significantly more transferable lines of SARS-CoV-2 due to recurring mutations.

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

In a way, Professor Balloux's hypothesis seems reassuring. Although it cannot be ruled out that a more dangerous strain will emerge in the future, the virus has so far shown no concrete signs of progression into a more dangerous form despite numerous possibilities.

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