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| The binding affinity for the ACE2 receptors with the spike protein of SARS-CoV-2 across eight different species compared to humans (the blue baseline). Species above the threshold are vulnerable to letting the coronavirus enter the cell while those below have significantly lower or no risk for infection. |
As human medical science releases the first of several vaccines intended to regain control of our lives and bring the coronavirus under control, we have news of the pre-emptive plans Creationism's putative designer has already made to enable it to launch another attack on humans.
This, of course, assumes anyone has been fooled into believing in this magic designer in the first place, as so many Creationist dupes have been.
What scientists working at the Barcelona-based Centre For Genomic Regulation (CGR) have discovered is which other species, the intelligent [sic] designer has designed the SARS-CoV-2 virus to infect, so they can act as repositories for the virus pending the day when human herd immunity falls below the level required for a new pandemic to occur. This repository can also act as a test-bed for new mutations until one which can overcome the artificially-acquired immunity in uhmans is chanced upon.
They have discovered that the virus is able to infect ferrets, cats, civets and to a lesser extent, dogs. We already know about its ability to infect mink and bats, of course. This ability is because of the similarity between the ACE2 proteins on their cell surfaces to those on our cells. It is by binding to these proteins using the 'spike' proteins on their surface that the virus gains access to the cells and begins to replicate itself, destroying the cells and tissues in the process.
Since this is what the virus does, Creationists are obliged by dogma to believe that this is exactly what it was designed by their putative, omniscient, inerrant and omnipotent designer to do, since nothing can happen without their putative designer's deliberate intervention, in full and certain knowledge of the consequences of its actions.
From the CGR press release:
Humans, followed by ferrets and to a lesser extent cats, civets and dogs are the most susceptible animals to SARS-CoV-2 infection, according to an analysis of ten different species carried out by researchers at the Centre for Genomic Regulation (CRG), based in Barcelona.
The findings, published in PLOS Computational Biology, found that ducks, rats, mice, pigs and chickens had lower or no susceptibility to infection compared to humans.
“Knowing which animals are susceptible to SARS-CoV-2 helps us prevent building up animal reservoirs from which the coronavirus can re-emerge at a later date,” says Luis Serrano, ICREA Research Professor, Director of the CRG and senior author of the study. “Our findings offer a clue for why minks – which are closely related to the ferret – are being infected by the disease, which is probably made worse by their packed living conditions and close contact with human workers.”
“Though we also find a potential susceptibility to infection by cats, they don’t co-exist with humans in the same conditions as other animals, which may explain why so far there are no known cases of people being infected by their pets,” adds Dr. Serrano.
Ten species were studied in this paper. Five species – humans, cats, ferrets, civets, and dogs – have had documented cases of infection by SARS-CoV-2. There are no reports of infection in the other five species – mice, rats, pigs, chickens and ducks.
The researchers used computer modelling to test how the coronavirus uses its spike proteins, which protrude from the surface of the virus, to infiltrate the cells of different animals. The main point of entry on a cell’s surface is the ACE2 receptor, which binds with the spike protein through a lock-and-key mechanism. There are many different variants of ACE2 within human populations and across different species.
Variants of the ACE2 receptor in humans followed by ferrets, cats, dogs and civets have the highest binding affinities to the viral spike protein, while mice, rats, chicken and ducks have poor binding energy.
As the press release says, the groups findings were published recently in PLOS Computational Biology.
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| Binding affinities on animal species. (A) ACE2 full sequence alignment of the selected species for the binding region to the S protein (B) Global ΔΔG interaction for different species by adding single residue contributions with respect to hACE2. Green bars for species susceptible to be infected, red bars for species not infected. (C) Per-residue interaction ΔΔG values in kcal/mol with respect to the hACE2 residues. We dont show the results for K353 in this table since it is not on the helical interface and it is only mutated to His in mice. |
What fully signed-up members of the intelligent [sic] design cult are forbidden by dogma from accepting or even acknowledging, is that these different binding affinities between the SARS-C0V-2 'spike' proteins and cell ACE2 proteins is related to an evolutionary relationship between the different species, with the ACE2 proteins representing a molecular evolutionary tree with increasing distance representing greater divergence and so reduced binding affinity. They therefore have no option but to present this phenomenon as the intentional, and so mendacious work of their putative intelligent [sic] designer.Abstract
The coronavirus disease COVID-19 constitutes the most severe pandemic of the last decades having caused more than 1 million deaths worldwide. The SARS-CoV-2 virus recognizes the angiotensin converting enzyme 2 (ACE2) on the surface of human cells through its spike protein. It has been reported that the coronavirus can mildly infect cats, and ferrets, and perhaps dogs while not pigs, mice, chicken and ducks. Differences in viral infectivity among different species or individuals could be due to amino acid differences at key positions of the host proteins that interact with the virus, the immune response, expression levels of host proteins and translation efficiency of the viral proteins among other factors. Here, first we have addressed the importance that sequence variants of different animal species, human individuals and virus isolates have on the interaction between the RBD domain of the SARS-CoV-2 spike S protein and human angiotensin converting enzyme 2 (ACE2). Second, we have looked at viral translation efficiency by using the tRNA adaptation index. We find that integration of both interaction energy with ACE2 and translational efficiency explains animal infectivity. Humans are the top species in which SARS-CoV-2 is both efficiently translated as well as optimally interacting with ACE2. We have found some viral mutations that increase affinity for hACE and some hACE2 variants affecting ACE2 stability and virus binding. These variants suggest that different sensitivities to coronavirus infection in humans could arise in some cases from allelic variability affecting ACE2 stability and virus binding.
Author summary
In these early stages of the COVID-19 pandemic it is urgent to understand all features determining the new virus expansion. Two significant factors conditioning infection are ACE2-mediated SARS-CoV-2 cellular entry and viral proteome translation efficiency. Genomic variability across species, including humans, results in ACE2 variants that destabilize its fold, modify ACE2/SARS-CoV-2 recognition, or both. We also point out the importance of considering waters at the interface of protein-protein interactions when performing in silico mutagenesis.
Delgado Blanco J, Hernandez-Alias X, Cianferoni D, Serrano L (2020)
In silico mutagenesis of human ACE2 with S protein and translational efficiency explain SARS-CoV-2 infectivity in different species.
PLoS Comput Biol 16(12): e1008450. doi: 10.1371/journal.pcbi.1008450
Copyright: © 2020 The authors. Published by PLOS
Open access
Reprinted under a Creative Commons Attribution 4.0 International License (CC BY 4.0)
Making their reputedly loving and omnibenevolent god look like a mendacious, misanthropic, genocidal monster seems preferable to these unfortunate dupes than to accept that the better explanation is that provided by their hated evolution by natural selection. If their intelligent [sic] designer were real, I wonder how it would feel about this characterisation of it as somethign no sane person could ever worhip let alone have any respect for, in preference to admitting they could be wrong.
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