I'll confess I've only ever passed through CT and have no experience with your states certification process, but if there's requirements for structural biology, immunology, virology, and cell bio these days, kudos.. you still have a drastically less than complete grasp of what you're writing, and this is the last time I'm bothering pointing that out.
Mutation rate isn't moot, it's baseline.. this is about Variants of Concern vs previous variants they're outclassing. For the nth time. They all have roughly the same mutation rate regardless of host.. it's non-relevant with respect to this comparison, not irrelevant in general. You don't comprehend this.
Again, immune evasion is not the only or I'd argue even the primary selective force for a novel virus.. binding affinity and transmission are of higher relative importance. The strength of the host immune system does matter: in that weaker ones allow the pathogen more time to become familiar and increase binding affinity to the pathogens receptors of choice. This is elementary. You don't comprehend this.
A strong, functional host doesn't allow the pathogen the luxury of time to increase binding affinity, as evidenced by the multitude of papers describing weeks-months long, active covid infections in the immunocompromised, with several advantage conferring mutations, with sequential viral samples/references exquisitely building the roadmap of these accumulated mutations... And literally zero of the same detailing a similar process in hosts that have a disease course that lasts for days, max. I've posted several, read them on repeat until it sinks in.
200M cases does provide ample grounds for mutations. Those that are in immunocompromised hosts do even more.
No, it's an incomplete analogy, because fighting isn't the only thing the virus is doing. It's travelling, picking a lock, and fucking as well. If it fails on any of those fronts, it doesn't reproduce. The immunocompromised allow for mutations in the most crucial of those factors.. for a Novel Virus.. binding affinity to a new species receptor.
The non-compromised hosts don't have "healthier locks".. they have roughly the same ACE2 receptors as the immunocompromised. The virus has less time trying to pick at ACE2 in a healthy host. Less mutations.. even you can't argue this. And what you don't understand is, this process is iterative and *greater at driving the increase in binding affinity of the viral spike protein and ACE2 in compromised hosts*. The exact opposite of what you're suggesting.
I'm out of ways to explain this.. these are rudimentary concepts, well illustrated in the literature. Again, your issues are yours to bear from here on out.
Mutation rate isn't moot, it's baseline.. this is about Variants of Concern vs previous variants they're outclassing. For the nth time. They all have roughly the same mutation rate regardless of host.. it's non-relevant with respect to this comparison, not irrelevant in general. You don't comprehend this.
Again, immune evasion is not the only or I'd argue even the primary selective force for a novel virus.. binding affinity and transmission are of higher relative importance. The strength of the host immune system does matter: in that weaker ones allow the pathogen more time to become familiar and increase binding affinity to the pathogens receptors of choice. This is elementary. You don't comprehend this.
A strong, functional host doesn't allow the pathogen the luxury of time to increase binding affinity, as evidenced by the multitude of papers describing weeks-months long, active covid infections in the immunocompromised, with several advantage conferring mutations, with sequential viral samples/references exquisitely building the roadmap of these accumulated mutations... And literally zero of the same detailing a similar process in hosts that have a disease course that lasts for days, max. I've posted several, read them on repeat until it sinks in.
200M cases does provide ample grounds for mutations. Those that are in immunocompromised hosts do even more.
No, it's an incomplete analogy, because fighting isn't the only thing the virus is doing. It's travelling, picking a lock, and fucking as well. If it fails on any of those fronts, it doesn't reproduce. The immunocompromised allow for mutations in the most crucial of those factors.. for a Novel Virus.. binding affinity to a new species receptor.
The non-compromised hosts don't have "healthier locks".. they have roughly the same ACE2 receptors as the immunocompromised. The virus has less time trying to pick at ACE2 in a healthy host. Less mutations.. even you can't argue this. And what you don't understand is, this process is iterative and *greater at driving the increase in binding affinity of the viral spike protein and ACE2 in compromised hosts*. The exact opposite of what you're suggesting.
I'm out of ways to explain this.. these are rudimentary concepts, well illustrated in the literature. Again, your issues are yours to bear from here on out.
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