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mutations occur roughly at the same rate, irrespective of host immune competence. Until the virus clears (a few weeks in healthy patients, many months in immune compromised patients) viral replication continues with resultant mutations.

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Which builds more mutations in the immunocompromised, over more time. You just debunked your own theory, well done.

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For review, selective pressures are unable to drive development of variants without mutations, some of which may have increased fitness.

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Selective pressures are mutation agnostic, they don't "need" anything

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All three characteristics, immune evasion, binding affinity / viral entry and transmission can drive viral fitness.

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So what? We're taking about a novel virus. immune evasion is already baked in if the host has never encountered it before. It already has a leg up in that department.. where it's weak is entry into an alien cell and potentially transmission. Being airborne, covid doesnt have that problem. All the variants of concern have increased binding affinity for ACE2.

Selective pressures don't have a threshold over or under which they cease to exist. A weak selection pressure is still selective pressure, and in this instance, does more to allow the virus to
Sequentially
Accumulate
Beneficial
Mutations
than the immune system of a healthy host, which would shut down the virus in days, not weeks or months.

The rest of your post is pure trash.. these aren't goats. Thankfully the people that understand all this are on the case.