By contrast SARS-CoV-2 only has a single chromosome, and so it primarily evolves via "genetic drift". While it's _possible_ for a cell infected by multiple SARS-CoV-2 variants to generate "chimeric" offspring via a process called "crossover" AKA "homologous recombination", that mechanism is much less effective than the simple segment-reassortment that drives flu evolution.
Like the 1918 H1N1 second wave mutation that caused ARDS in 20 year olds?
We still have no idea how that happened, but with this coronavirus evolving to be more transmissible/virulent that is still on the table. If it can evolve to become more transmissible but at the cost of triggering ARDS like that, then it will face evolutionary pressure to do so.
And hospitalization rates of 20-29 year olds aren't anywhere near as good as the fatality rates. While the death rate drops by a factor of 2 every 8 years, the hospitalization rate drops by a factor of 2 every ~15 years. And delta has 2x the hospitalization rate of alpha across age/sex/deprevation/comorbidity matched controls. It should still be about a 1-in-50 chance of hospitalization for 20-29 year olds. There's no proof that number can't continue to get worse.
We could look at the flu for clues, in that case every year will have one or more variants that are the most prominent.
I'd argue that in the age category with the most infected (10-29 years old) in the UK, that these people are not killing themselves due to their young age.
And the elderly have already gotten the vaccine and are thus up to eight times more likely to not get infected.