@Godstud The good general doesn’t say what his evidence is, so I can’t do much about that. However, I can start showing the unsupported assertions in the articles by scientists (who should of know better) and then I show how easily falsified those assertions are.
Let’s take this guy...
https://www.bioworld.com/articles/433087-article-headline“From everything I’ve looked at, there is zero evidence for genetic engineering; it looks like normal evolution,” said Trevor Bedford, a computational biologist at Fred Hutchinson Cancer Research Center, who has been using genomes sequences taken from patient samples to track the spread of the virus since Jan. 11.
“Thousands of mutations are distributed across the genome. If you’re engineering something, you wouldn’t do that. There are no signals for biological engineering. It looks like natural evolution,” Bedford told attendees of the AAAS meeting on Feb. 14.
A Spanish team used a bacterial method to clone a virus. So obviously they couldn’t do it without leaving obvious traces. Whereas Baric can do it without leaving traces.
True, they didn’t do it as elegantly as Baric, as their final assembly of the synthetic virus included their added restriction enzyme sites, while Baric learned to combine fragments “seamlessly”. But this is a minor point, the Spanish approach is just as robust — in 2013, with its help, the same authors had created a synthetic clone of MERS, and in 2015 their technique was included in a coronavirus textbook (chapter 13).
https://medium.com/@yurideigin/lab-made-cov2-genealogy-through-the-lens-of-gain-of-function-research-f96dd7413748So that guy’s assertion that it is natural due to lacking the markers he expected is unsupported and easily shown to be false.
Another claim, this one being the commonly cited article for claiming the virus is natural, bases this claim in the assertion that the RDB site was not effectively predicted by computer models, therefore none could have created it. Must be natural.
https://www.nature.com/articles/s41591-020-0820-9While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal7 and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding7,11. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.
OK, so what about taking a binding site from a know virus with high infectivity and just splice it in, without bathing with a computer Model? In fact that is way it has been done for 50 years.
But, I decided to check their references.
https://jvi.asm.org/content/94/7/e00127-20This paper (by Ralph himself) shows the models used by the authors didn’t completely explain the confirmation of the new virus. But it was very close.
Reading the last few paragraphs of these articles can be very informative. They put their assertions at the beginning, but include their doubts in the discussion.
What is the source of 2019-nCoV, and did a key intermediate host play an important role in the current 2019-nCoV outbreak? Similarly to SARS-CoV, 2019-nCoV most likely has originated from bats, given its close phylogenetic relationship with other β-genus lineage b bat SARS-CoV (Fig. 2). Moreover, 2019-nCoV likely recognizes ACE2 from a diversity of animal species, including palm civets, as its receptor. In the case of SARS-CoV, some of its critical RBM residues were adapted to human ACE2, while some others were adapted to civet ACE2 (26); this type of partial viral adaptation to two host species promoted virus replication and cross-species transmission between the two host species. In the case of 2019-nCoV, however, there is no strong evidence for adaptive mutations in its critical RBM residues that specifically promote viral binding to civet ACE2. Hence, either palm civets were not intermediate hosts for 2019-nCoV, or they passed 2019-nCoV to humans quickly before 2019-nCoV had any chance to adapt to civet ACE2. Like SARS-CoV, 2019-nCoV will likely replicate inefficiently in mice and rats, ruling them out as intermediate hosts for 2019-nCoV. Moreover, we predict that either 2019-nCoV or laboratory mice and rats would need to be genetically engineered before a robust mouse or rat model for 2019-nCoV would become available. Pigs, ferrets, cats, and nonhuman primates contain largely favorable 2019-nCoV-contacting residues in their ACE2 and hence may serve as animal models or intermediate hosts for 2019-nCoV. It is worth noting that SARS-CoV was isolated in wild palm civets near Wuhan in 2005 (9), and its RBD had already been well adapted to civet ACE2 (except for residue 487). Thus, bats and other wild animals in and near Wuhan should be screened for both SARS-CoV and 2019-nCoV.
The problem is the virus is thought to have needed 20 - 50 years in an intermediate host species to evolve the binding site sequence from a bat virus origin. That host species must have very similar ACE2 proteins as human proteins. And the virus still needs that cleavage site (a matter a avoided in the earlier article by Anderson).
This is why I say the lab origin hypothesis is more parsimonious than the natural origin hypothesis.
It is still possible that it had a natural origin, but the lab origin seems more plausible, all things considered.
Of course this would be an enormous scandal. Think of the headlines: “Genetically Engineered Virus escapes lab and kills over 200,000 people”.
Having said all of this, you can still accuse anyone of claiming the virus is a bio weapon to be a conspiracy theorist. There is nothing I have seen yet that suggests anything other than this is due to scientists being twats. The research field, as @late might be able to attest, is very competitive.
So we need to ban two things. One is banning live exotic animals in wet markets (they create an ideal environment for introducing zoonotic disease) and the second is banning gain of function research on such diseases.