SARS-CoV-2, the coronavirus that causes COVID-19, appears to have evolved silent changes to its RNA code that gave it a biological edge over previous strains. Credit: Felipe Esquivel Reed |
Sadly, this news came just too late to be included in my new book, The Malevolent Designer: Why Nature’s God is Not Good, because it is a brilliant example of what intelligent [sic] design creationists are obliged to assume was deliberately designed by their putative designer god, and which, if such a god existed, would make it a pestilential, genocidal misanthrope of the highest order.
What researchers at Duke University, Durham, N.C., USA have discovered is the 'silent' mutations that turned a harmless coronavirus, infecting bats and other animals, into a deadly, pandemic virus currently causing mayhem with world economies and deaths in the millions as governments all over the world struggle to contain the virus and avoid local health services being overwhelmed.
DAILY CONFIRMED NEW CASES (7-DAY MOVING AVERAGE)
Outbreak evolution for the current 10 most affected countries. |
ID creationists insist that design changes such as this must be the result of deliberate intent on the part of their favourite god, who, they assume, must have created the deadly virus in the first place, knowing inerrantly what it would do and exactly what the consequences would be.
The Durham University press release explains:
...researchers at Duke University have identified a number of “silent” mutations in the roughly 30,000 letters of the virus’s genetic code that helped it thrive once it made the leap -- and possibly helped set the stage for the global pandemic. The subtle changes involved how the virus folded its RNA molecules within human cells.
For the study, published Oct. 16 in the journal PeerJ, the researchers used statistical methods they developed to identify adaptive changes that arose in the SARS-CoV-2 genome in humans, but not in closely related coronaviruses found in bats and pangolins.
[...]
Previous research detected fingerprints of positive selection within a gene that encodes the “spike” proteins studding the coronavirus’s surface, which play a key role in its ability to infect new cells.
The new study likewise flagged mutations that altered the spike proteins, suggesting that viral strains carrying these mutations were more likely to thrive. But with their approach, study authors Berrio, Wray and Duke Ph.D. student Valerie Gartner also identified additional culprits that previous studies failed to detect.
The researchers report that so-called silent mutations in two other regions of the SARS-CoV-2 genome, dubbed Nsp4 and Nsp16, appear to have given the virus a biological edge over previous strains without altering the proteins they encode.
Instead of affecting proteins, Berrio said, the changes likely affected how the virus’s genetic material -- which is made of RNA -- folds up into 3-D shapes and functions inside human cells.
What these changes in RNA structure might have done to set the SARS-CoV-2 virus in humans apart from other coronaviruses is still unknown, Berrio said. But they may have contributed to the virus’s ability to spread before people even know they have it -- a crucial difference that made the current situation so much more difficult to control than the SARS coronavirus outbreak of 2003.
And that, folks, is how to design a sneaky little killer virus - one that its victims pass on before they even know they've got it! The 'designer' obviously learned the lesson of the 2003 SARS outbreak, where spread was limited because people rapidly became too ill to socialise, so the outbreak fizzled out of its own accord.
The authors of the study, however, attribute the changes to evolution by natural selection. This is because they are biomedical scientists writing for other biomedical scientists who understand the subject and deal in truths, not fundamentalist theologians trying to recruit scientifically illiterate fools into their subversive political cult:
Abstract
Background
The emergence of a novel coronavirus (SARS-CoV-2) associated with severe acute respiratory disease (COVID-19) has prompted efforts to understand the genetic basis for its unique characteristics and its jump from non-primate hosts to humans. Tests for positive selection can identify apparently nonrandom patterns of mutation accumulation within genomes, highlighting regions where molecular function may have changed during the origin of a species. Several recent studies of the SARS-CoV-2 genome have identified signals of conservation and positive selection within the gene encoding Spike protein based on the ratio of synonymous to nonsynonymous substitution. Such tests cannot, however, detect changes in the function of RNA molecules.
Methods
Here we apply a test for branch-specific oversubstitution of mutations within narrow windows of the genome without reference to the genetic code.
Results
We recapitulate the finding that the gene encoding Spike protein has been a target of both purifying and positive selection. In addition, we find other likely targets of positive selection within the genome of SARS-CoV-2, specifically within the genes encoding Nsp4 and Nsp16. Homology-directed modeling indicates no change in either Nsp4 or Nsp16 protein structure relative to the most recent common ancestor. These SARS-CoV-2-specific mutations may affect molecular processes mediated by the positive or negative RNA molecules, including transcription, translation, RNA stability, and evasion of the host innate immune system. Our results highlight the importance of considering mutations in viral genomes not only from the perspective of their impact on protein structure, but also how they may impact other molecular processes critical to the viral life cycle.
Although this came too late for inclusion in my latest book, many similar examples of what creationist dogma forces creationists to attribute to their putative creator god and so present it as a malevolent force in the world, are included in my illustrated book, The Malevolent Designer: Why Nature's God is not Good. Available from Amazon in paperback or ebook for Kindle.
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