You have insulted the scientists at the global virus network. A study by scientists at the NIH says the same thing essentially. The affinity to bind to ace2 will vary between the variants of SARS_Co_V2 based on structure of variant or sub variant. Consider this study the on the omnicron sub variants and their affinity to bind to ACE2.I'm not saying the sequencing has no effect , just a minimal one compared with the cleavage site.
From tthe link:
The currently circulating Omicron sub-variants are the SARS-CoV-2 strains with the highest number of known mutations. Herein, we found that human angiotensin-converting enzyme 2 (hACE2) binding affinity to the receptor-binding domains (RBDs) of the four early Omicron sub-variants (BA.1, BA.1.1, BA.2, and BA.3) follows the order BA.1.1 > BA.2 > BA.3 ≈ BA.1. The complex structures of hACE2 with RBDs of BA.1.1, BA.2, and BA.3 reveal that the higher hACE2 binding affinity of BA.2 than BA.1 is related to the absence of the G496S mutation in BA.2.
The symbol "G" is the amino acid Glycine. It's absence results in BA.2 having a higher affinity to bind to ACE2 than sub-variant BA.1.
https://pubmed.ncbi.nlm.nih.gov/35809570/
As for the behavior of man made virus compared to a naturally occurring virus, I am not aware of any studies comparing the two. Originally Posted by adav8s28
The title of the paper is: "Furin Cleavage Site Is Key to SARS-CoV-2 Pathogenesis"
From the abstract.
"Together, these results demonstrate a critical role for the furin cleavage site insertion in SARS-CoV-2 replication and pathogenesis. "
https://pubmed.ncbi.nlm.nih.gov/32869021/
The paper basically says that without the cleavage site pathogenesis is attenuated.
As for the behavior of man made viruses compared to naturally occuring ones, you just made some stuff up. Got it.