https://evolutionnews.org/2020/03/did-covid-19-virus-evolve-by-natural-selection/
Does the conclusion of this article fit? It goes like this:
Design and Evolution
Myers, like the Nature Medicine scientists, uses the scientific inference to intelligent design to search for (and discount) human intelligent agency. Design science is at the forefront of research on the emergence of coronavirus. Based on the available evidence and using the inference to design as a scientific hypothesis, intelligent design of the COVID-19 virus seems unlikely.
But there is another lesson about design and evolution to be learned from scientific research on this virus. Natural selection, if understood as undirected variation and differential reproductive success, is a destructive process. Natural selection destroys biological functional complexity — it produces diseases, cancer, and pandemics. It weakens and kills. Natural selection does to living organisms what rust does to a machine. Natural selection corrodes and destroys life, and plays no role in creating it.
My comment:
if the additional sequence that turns COVID 19 so lethal were a product of natural selection, as the PZ Myers claims, and Egnor concurs, the follow-up conclusion does not logically follow.
COVID 19, if it were the product of natural selection, did NOT destroy biological functional complexity. Quite the contrary is the case: scientists have not seen anything like this in previous strains. But, it was not just a single anomaly. It adds: “Before the emergence of the 2019-nCoV, this important feature was not observed in other coronaviruses.
Strikingly, the 2019-nCoV sequence contains 12 additional nucleotides upstream of the single cleavage site.”
The paper suggests that this part of the DNA chain has been tampered with for
“gain-of-function
to the 2019-nCoV for efficient spreading in the human population compared to other coronaviruses".
So the additional nucleotides did NOT deteriorate the genome but provide a GAIN OF FUNCTION, which is helping the Virus to be enormously successful.
While people are dying, the Virus is well and alive and multiplicating.
Natural selection , if it was the cause of the sequence, is in this case, a TREMENDOUS SUCCESS for the viruses...
The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade.
https://www.ncbi.nlm.nih.gov/pubmed/32057769
Strikingly, the 2019-nCoV S-protein sequence contains 12 additional nucleotides upstream of the single Arg↓ cleavage site 1 (Fig. 1, Fig. 2) leading to a predictively solvent-exposed PRRAR↓SV sequence, which corresponds to a canonical furin-like cleavage site (Braun and Sauter, 2019; Izaguirre, 2019; Seidah and Prat, 2012). This furin-like cleavage site, is supposed to be cleaved during virus egress (Mille and Whittaker, 2014) for S-protein “priming” and may provide a gain-of-function to the 2019-nCoV for efficient spreading in the human population compared to other lineage b betacoronaviruses.
A virus, that has 30000 nucleotides, and 1.24 × 10−3 substitutions per site per year: How much time does it take to have an addition of CCT CGG CGG GCA in the genome? if that addition could be demonstrated to be plausibly the result of recombination by natural selection, then it would as well be a great argument for advocates of darwinian evolution.
Evidence of recombination in coronaviruses implicating pangolin origins of nCoV2019
https://www.biorxiv.org/content/10.1101/2020.02.07.939207v1.full.pdf
Amino acid alignment between pangolin coronavirus and nCoV-2019 at the S1-NTD subdomain results in low sequence similarity. However, increased similarity is observed from the RBD through the S2 domain. This suggests a possible recombination event between a bat coronavirus and the pangolin coronavirus at the S1-NTD and RBD junction. While there is high conservation at the amino-acid level between the pangolin coronavirus and nCoV-2019, this is not reflected in the nucleotide identity, suggesting that the proposed recombination event occurred in the more distant past, allowing subsequent time for genetic drift. One such mutation could be the insertion of the amino acid residues PRRA near the S1/S2 junction which induces a furin cleavage motif.
Last edited by Admin on Tue Apr 14, 2020 5:11 pm; edited 3 times in total