Sky News Australia reports a scientist (May 24) who explains that SARS-COV-2 binds to the human ACE2 receptor better than any animal’s, including intermediaries from bats (such as civets and pangolins).
Peak Prosperity (Chris Martenson) has explained this problem before. The virus actual cracks open the receptor to get to the furin, which makes it able to infect other cells, especially endothelial cells, effectively.
It is hard to explain why we don’t find evidence that this super-effective connection to ACE2 happened in a particular animal.
Then there is the issue of the PRRA sequence, added in a way that is comparable to increasing a record or message length on a computer.
Had this been a lab experiment gone wrong (“gain of function”), there are workplace-related issues to process control (versions in different test or production systems and the independent automation of their management) which I have seen in my own career that could explain what might have happened. I’ll get into this in the future.
Also, Dana G. Smith has an important article on Medium explaining the concept of COVID-19 as a blood vessel disease.