In the case of infectious disease, clearly your scenario isn't what happens in the real world. Otherwise no disease could be cured.
In the case of aging, everyone ages for the same reasons. A few types of underlying molecular damage that are comparatively straightforward to investigate and address, when compared to the enormous complexity of metabolism. Look at senolytic drugs: remove senescent cells, life span increases, aspects of aging are reversed in old individuals. Aging is like rust in a complex metal structure; the failure modes appear varied and complex because the structure is complex. But rust isn't complicated. Aging is the same story.
Genetic variation is not particularly meaningful for the vast majority of age-related disease. It isn't important for most of the life span. It only becomes even somewhat influential in very late life where there is variation in resistance to damage and consequences of damage. But why care thing one about that when the right strategy is to repair the underlying damage in order to ensure that people either never enter or are removed from the situation in which genetics start to matter a little?
"In the case of infectious disease, clearly your scenario isn't what happens in the real world. Otherwise no disease could be cured."
Note that your statement is only true for a relatively narrow range of infectious diseases, and mostly in special cases where we have "Nuke the site from orbit" class drugs that don't target things eukaryotic cells use.
In the case of aging, everyone ages for the same reasons. A few types of underlying molecular damage that are comparatively straightforward to investigate and address, when compared to the enormous complexity of metabolism. Look at senolytic drugs: remove senescent cells, life span increases, aspects of aging are reversed in old individuals. Aging is like rust in a complex metal structure; the failure modes appear varied and complex because the structure is complex. But rust isn't complicated. Aging is the same story.
Genetic variation is not particularly meaningful for the vast majority of age-related disease. It isn't important for most of the life span. It only becomes even somewhat influential in very late life where there is variation in resistance to damage and consequences of damage. But why care thing one about that when the right strategy is to repair the underlying damage in order to ensure that people either never enter or are removed from the situation in which genetics start to matter a little?