3 ms·

Setting up two likely scenarios is a very reasonable way of approaching future development, both scenarios sound likely to me. We could look at the flu for clu

Setting up two likely scenarios is a very reasonable way of approaching future development, both scenarios sound likely to me. 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.

lamontcg 5y ago
> We could look at the flu for clues 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.
gdp137 5y ago
Flu is a bad example --- it has 8 "segments" (basically "chromosomes") that get reassorted among the offspring when a cell is infected by multiple strains, leading to a crude form of "sexual recombination". (The numbers after the "H" and "N" indicate the variant-numbers of the Hemagglutinin and Neuraminidase "segments" that the flu-variant got; a cell infected by H1N1 and H2N5 will also produce some H2N1 and H1N5 offspring in addition to H1N1 and H2N5, leading to very rapid genepool evolution) 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.

lamontcg 5y ago

> We could look at the flu for clues 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.

gdp137 5y ago

Flu is a bad example --- it has 8 "segments" (basically "chromosomes") that get reassorted among the offspring when a cell is infected by multiple strains, leading to a crude form of "sexual recombination". (The numbers after the "H" and "N" indicate the variant-numbers of the Hemagglutinin and Neuraminidase "segments" that the flu-variant got; a cell infected by H1N1 and H2N5 will also produce some H2N1 and H1N5 offspring in addition to H1N1 and H2N5, leading to very rapid genepool evolution) 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.