2. There is no spike protein anyone knows of which would have been used in this research
3. The PRRAR furin cleavage site is not one humans would have tried it is unlike any other known furin cleavage sites in coronaviruses
4. There are now many known related sarbecoviruses which have been found with furin cleavage sites
5. Furin cleavage sites have independently evolved in multiple different branches of coronaviruses, probably a dozen times that we know of now.
6. The furin cleavage site is short and can easily happen through recombination with another virus due to coinfection.
7. This is very likely what happened due to infection with the SARS-CoV-2 ancestor and an HKU9-like virus.
It is not particularly suspicious that the thing which we were worried about happening and causing a zoonotic spillover event is the thing which actually happened.
It does seem unlikely that the SARS-CoV-2 genome, or spike protein, or even just a small segment including the furin cleavage site, was synthesized. Although without knowing what protein folding modeling capabilities and synthesis capabilities the WIV had, who knows for sure?
And the rest of it is that you're arguing in favor of a science fiction explanation for the capabilities of the WIV lab.
Using this figure, we could have some parameters around how much time such a project must have taken and its latest start date (assuming its evolved from known or closely-related-to-known viruses).
Using this figure, and a theoretical timetable, we can also specify how close a cousin virus we would need to have for such a process to develop SAR-CoV-2.
This could give us a more specific understanding of the feasibility of such research.
For example, RaTG13 is closest known virus was discovered in 2013. Does the rate of serial passage enable evolution from RaTG13 over ~7 years? If not, this provides a factual argument allowing us to determine even if gain-of-function research was imposed on RaTG13 the moment of its discovery, it could not have been developed into SARS-CoV-2. (I don't know how to evaluate the actual accuracy of this, but provided as a example of how knowing the serial passage rate would be helpful).
In the lab you'll get a handful of mutations not thousands.
After serial passage through some large fraction of a billion humans, with large evolutionary pressures due to the recent species jump, the delta variant is still well over 99% homologous to the reference Wu-1 strain.
A 96.1% different would require serial passage through billions of organisms, but they measure this difference in terms of years of evolution in nature which is on the order of 30-40 years.
Wouldn’t this count as parallel passage though? Sure there’s more variability and evolutionary pressure on the mutations, but the speed of evolution (the number nucleotide mutations) is the same over the same period of time regardless of how many billions of people it infects in parallel.