See, they use general human coronaviruses as a model, instead of SARS-1, which is incredibly functionally and structurally similar to SARS-2.
Why would you willfully ignore the enormous research literature showing enduring immunity developing from SARS-1? Oh, right, because either you haven't read it or you don't like that it doesn't support your conclusions.
It's like, imagine we're discussing H1N1 reinfection, and we have a highly similar H1N0 which varies very slightly, and we know that doesn't lead to reinfection. But instead you look at a number of Influenza viruses in the same family but not nearly as similar.
Don't you see how ridiculous that is?
We obviously should use SARS-1 as a model for SARS-2.
Why would you willfully ignore the enormous research literature showing enduring immunity developing from SARS-1? Oh, right, because either you haven't read it or you don't like that it doesn't support your conclusions.
It's like, imagine we're discussing H1N1 reinfection, and we have a highly similar H1N0 which varies very slightly, and we know that doesn't lead to reinfection. But instead you look at a number of Influenza viruses in the same family but not nearly as similar.
Don't you see how ridiculous that is?
We obviously should use SARS-1 as a model for SARS-2.