Monday, 30 November 2020

Coronavirus Question for Intelligent [sic] Design Creationists

SARS-CoV-2 virus particles
SARS-CoV-2 mutations do not appear to increase transmissibility | UCL News - UCL – University College London

Findings published, open access, a few days ago in Nature Communications, raises a worrying question for intelligent [sic] design Creationists.

Creationist dogma states that there are no such thing as random, purposeless mutations because all changes to a genome are made by their putative sentient designer for a purpose. The question then is why do the mutations in the SARS-CoV-2 virus not appear to do anything in terms of the virus' ability to infect people or to replicate more quickly or successfully? All of them appear to be neutral and apparently random and purposeless - exactly what Creationist dogma states never happens.

This was the conclusion of a team of researchers, led by Professor Francois Balloux, of University College of London (UCL) Genetics Institute, from their analysis of the genome of viruses recovered from more than 46,000 patients who had been infected with the virus during 2020. The team includes scientists from the Université de la Réunion and the University of Oxford.

As the UCL press release explains:
Coronaviruses like SARS-CoV-2 are a type of RNA virus, which can all develop mutations in three different ways: by mistake from copying errors during viral replication, through interactions with other viruses infecting the same cell (recombination or reassortment), or they can be induced by host RNA modification systems which are part of host immunity (e.g. a person’s own immune system).

Most mutations are neutral, while others can be advantageous or detrimental to the virus. Both neutral and advantageous mutations can become more common as they get passed down to descendant viruses.

[...]

The researchers have so far identified 12,706 mutations in SARS-CoV-2, the virus causing COVID-19. For 398 of the mutations, there is strong evidence that they have occurred repeatedly and independently. Of those, the researchers honed in on 185 mutations which have occurred at least three times independently during the course of the pandemic.

To test if the mutations increase transmission of the virus, the researchers modelled the virus’s evolutionary tree, and analysed whether a particular mutation was becoming increasingly common within a given branch of the evolutionary tree – that is, testing whether, after a mutation first develops in a virus, descendants of that virus outperform closely-related SARS-CoV-2 viruses without that particular mutation.

The researchers found no evidence that any of the common mutations are increasing the virus’s transmissibility. Instead, they found most common mutations are neutral for the virus. This includes one mutation in the virus spike protein called D614G, which has been widely reported as being a common mutation that may make the virus more transmissible. The new evidence finds that this mutation is in fact not associated with significantly increasing transmission.

The researchers found that most of the common mutations appear to have been induced by the human immune system, rather than being the result of the virus adapting to its novel human host. This situation is in contrast with another analysis by the same team of what happened when SARS-CoV-2 later jumped from humans into farmed minks.

Dr van Dorp said: “When we analysed virus genomes sourced from mink, we were amazed to see the same mutation appearing over and again in different mink farms, despite those same mutations having rarely been observed in humans before.”

Lead author Professor Francois Balloux (UCL Genetics Institute) added: “We may well have missed this period of early adaptation of the virus in humans. We previously estimated SARS-CoV-2 jumped into humans in October or November 2019, but the first genomes we have date to the very end of December. By that time, viral mutations crucial for the transmissibility in humans may have emerged and become fixed, precluding us from studying them.”

It is only to be expected that a virus will mutate and eventually diverge into different lineages as it becomes more common in human populations, but this does not necessarily imply that any lineages will emerge that are more transmissible or harmful.

Dr van Dorp said: “The virus seems well adapted to transmission among humans, and it may have already reached its fitness optimum in the human host by the time it was identified as a novel virus.”
In summary, the evidence of the recent jump from humans into mink appears to have been followed by a rapid increase in adaptive mutations in mink as the virus evolved a fitness optimum in this new species. However, this period of evolving fitness in humans happened quickly, before we had become fully aware of the threat and all mutations since then appear to be random and have no adaptive function.

ID Creationists might like to ponder on why their putative designer needed to tweak its 'perfect' designs to make them fitter at doing what they were 'designed' to do.

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.

van Dorp, Lucy; Richard, Damien; Tan, Cedric C. S.; Shaw, Liam P.; Acman, Mislav; Balloux, François
No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Nature Communications 11, 5986 (2020). doi: 10.1038/s41467-020-19818-2

Copyright: © 2020 The authors. Published by Springer Nature Ltd.
Open access.
Reprinted under a Creative Commons Attribution 4.0 International License (CC BY 4.0)
So, the big questions for Creationists is why are these apparently pointless modifications being made so frequently and prolifically by their putative designer, and if this is not the result of deliberate design, what process is driving it if not random mutations and genetic drift - in other words, by one of the mechanisms by which biologists say evolution occurs? And why can these mutations be arranged in family trees that look exactly as they would be expected to look if this was an evolutionary process?

And I note that I have still to receive a sane response from any Creationist to my question, why is 'evolution' the only explanation for the SARS-CoV-2 virus pandemic that doesn't leave their putative intelligent designer looking like a misanthropic, genocidal, sadistic monster?







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