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Message: [QUOTE="pj, post: 3479490, member: 2524"] "The overall sequence 120 similarities between 2019 -nCoV spike and SARS -CoV spike (isolated from human, civet 121 or bat) are around 76% -78% for the whole protein, around 73% -76% for the RBD, and 50%-53% for the RBM (Fig. 3A, 3 B )" Source: [URL]https://jvi.asm.org/content/jvi/early/2020/01/23/JVI.00127-20.full.pdf[/URL]. There is enough similarity to show that SARS-CoV-2 uses ACE2 as its receptor, but not much similarity. At this point, it is just a hypothesis that the bats could be a pool for such a large variety of viruses that one of them might evolve to be a perfect infectious agent in humans. This is very much like the idea of monkeys typing randomly on typewriters and hoping they'll produce Shakespeare: it takes more monkeys than the numbers of atoms in the universe billions of years to have a chance. The chance of SARS-CoV-2 evolving in such a bat pool is hardly "perfectly plausible," it is statistically akin to the monkeys writing Shakespeare. There just aren't enough bats in the world to make a large enough reservoir for this to work. Meanwhile the classic model, while it does rely on a series of rare events, is known to have happened many times in human history - most pathogens enter humans this way. It will generate pathogens regularly - but not pathogens as super-adapted to humans as SARS-CoV-2. The classic process can and no doubt did generate the 2002 SARS, but it cannot have generated SARS-CoV-2. Debating whether Dr. Baric's hypothesis is plausible based on statistics is not necessary, because we can go to animals and search for viruses. If the hypothesis that SARS-CoV-2 was one of a diverse pool of randomly varying bat viruses is correct, we'll see a huge range of viruses in bats ranging in genomic similarity from 98% to 100%. In fact, we don't see any closer than 96%. The hypothesis is being disproven by ongoing research. The fact that SARS-CoV-2 is related to previous SARS (at a low level) does not tell us its origins, because a bioengineer would also begin working from the SARS-CoV sequence. What is key is that the SARS-CoV-2 has improved human binding compared to all those others, but worse animal binding -- yet it did no evolution in humans. There is no natural process that can bring that about (apart from the gazillion monkeys typing hypothesis). [/QUOTE]

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