This is untrue. I'd point to this quote:
“It’s pretty apparent that there’s this evolutionary arms race between the receptor binding domain and ACE2 that’s happening within the bats themselves,” says Tyler Starr, a postdoc in the lab of genome scientist Jesse Bloom at Fred Hutchinson Cancer Research Center. “Whatever it’s doing is ratcheting up this evolution and sometimes spitting out things that can bind potentially to many different ACE2s, including ours.”[1]
The unique thing about COVID is the transmission and the long incubation time.
There are plenty of naturally occurring mutations that have occurred that are more contagious than COVID (AIDS R0=~4.5, Ebola=~2.5 are two major ones that spring to mind). And SARS1 had a very similar binding behaviour, and the jumping behavior via civets is very similar to COVID.
[1] https://cen.acs.org/biological-chemistry/infectious-disease/...
This is a good summary of the current consensus:
It is clear from our analysis that viruses closely related to SARS-CoV-2 have been circulating in horseshoe bats for many decades. The unsampled diversity descended from the SARS-CoV-2/RaTG13 common ancestor forms a clade of bat sarbecoviruses with generalist properties—with respect to their ability to infect a range of mammalian cells—that facilitated its jump to humans and may do so again. Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses. Furthermore, the other key feature thought to be instrumental in the ability of SARS-CoV-2 to infect humans—a polybasic cleavage site insertion in the S protein—has not yet been seen in another close bat relative of the SARS-CoV-2 virus.
b) Genetic analysis indicates that it most likely came from bats directly to humans, but picked up the ACE2 receptors from a Pangolin virus that was passed back to bats, evolved there and then infected humans. To quote the same nature article I lined above:
However, on closer inspection, the relative divergences in the phylogenetic tree (Fig. 2, bottom) show that SARS-CoV-2 is unlikely to have acquired the variable loop from an ancestor of Pangolin-2019 because these two sequences are approximately 10–15% divergent throughout the entire S protein (excluding the N-terminal domain). It is RaTG13 that is more divergent in the variable-loop region (Extended Data Fig. 1) and thus likely to be the product of recombination, acquiring a divergent variable loop from a hitherto unsampled bat sarbecovirus28. This is notable because the variable-loop region contains the six key contact residues in the RBD that give SARS-CoV-2 its ACE2-binding specificity27,37. These residues are also in the Pangolin Guangdong 2019 sequence. The most parsimonious explanation for these shared ACE2-specific residues is that they were present in the common ancestors of SARS-CoV-2, RaTG13 and Pangolin Guangdong 2019, and were lost through recombination in the lineage leading to RaTG13. This provides compelling support for the SARS-CoV-2 lineage being the consequence of a direct or nearly-direct zoonotic jump from bats, because the key ACE2-binding residues were present in viruses circulating in bats.
and:
Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses.