Although most of my work is on photosynthetic protists, a long-term interest has been the role of horizontal gene transfer in evolution. That led a former student, Torstein Tengs, who now works for the Norwegian Institute of Public Health, to contact me for some help regarding evidence of gene transfer in the evolution of SARS-CoV-2, the causative agent of Covid-19. It is an interesting story, because there is striking, clearly non-random, sequence similarity between a noncoding functional element near the 3′ end of the viral genome and sequences found in insect viruses or integrated into some insect genomes. There is still a lot of work to be done understanding exactly what is going on, but it looks like horizontal transfer of a functional element may have played an important role in the evolution of coronaviruses. The transfer occurred before the divergence of SARS-CoV and SARS-CoV-2, so it is unlikely to have been critical in the emergence of this particular pathogen. However, the fact that the motif is almost perfectly conserved when present, but is not in all coronaviruses, suggests that it may be a parasitic genetic element. Even viruses can have parasites!
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.001551
Is there been any forensic evidence that ‘gain of function’ research using horizontal gene transfer techniques (perhaps using ‘highly promiscuous’ Hydra Vulgaris) led to the evolution of the cov2 coronavirus?
If so, do simple lifeforms hosting the pathogen – represent a greater breeding pool (and threat) for the generation of new variants of concern in orders of magnitude greater than populations of than licestock like farmed mink?
Have simbiotic organisms been used within vaccines (in the form of spike protein sub-units) to act as ‘TLR tags’ as targets for the innate immune system?
No, there is no evidence of any genetic manipulation of SARS-CoV-2. There are some scientists who think the virus could have been accidentally released from a lab, but no credible evidence has been found of intentional modification. AAAS sponsored a good discussion of the evidence regarding that possibility, which does also address gain of function.
You are right that the total number of replicating virions is a risk factor for the evolution of new variants. However, those variants will evolve in response to the organism in which they are replicating, and the odds of a host-swap derive strongly from the frequency of interactions between organisms. Once the virus spread into humans we became its primary reservoir, and hence the vast majority of SARS-CoV-2 virions are almost certainly in humans (at least up to the present; with case rates falling in humans and us spreading it to other animals there is some risk of back-and-forth transmission like we see with influenza).