This is about Variants of Concern, and evolution of variants more fit to infect human hosts. Background mutation rate is a footnote.

The hosts' immune systems are the selective pressure, and the immunocompromised are well suited selectors for viral fitness because they allow for accumulation of beneficial mutations without destroying the infection outright, before those combinations have a chance to arise.

This is a novel virus, supposedly the first time it's coming in contact with human beings.. it's innately unfit out of the gate. Simulations suggest the spike protein could have a binding affinity with ACE2 several orders of magnitude (hundreds of times higher) than currently. It's not absolutely clear what that means with regards to transmission and disease course, but odds are it's really, really bad. That's generally the viral "goal".. increase affinity and get better at accessing reproductive machinery.

Healthy hosts don't allow the virus as much time to "pick the lock" or increase affinity.. immunocompromised hosts do. Immunocompromised hosts allow the virus several bites at that apple, merely swatting it away instead of smashing it outright.

You're the one who ventured into ad hominem attacks.. I understand these mechanisms absolutely, you do not. Dunning- Kruger. No amount of repetition of these fallacies make you correct. Your petulance regarding this is your own problem.