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The closest thing I can think of is https://en.wikipedia.org/wiki/Antibody-dependent_enhancement#Potential_linkage_between_pathophysiology_of_COVID-19_and_ADE h
by __blockcipher__ 6y ago
The closest thing I can think of is https://en.wikipedia.org/wiki/Antibody-dependent_enhancement#Potential_linkage_between_pathophysiology_of_COVID-19_and_ADE https://en.wikipedia.org/wiki/Antibody-dependent_enhancement....
There's no way in which having real antibodies, but a reduced amount of them, would be worse than not having antibodies, but the following is very possible:
> It is likely that in older people the production of antibodies is slower and by the time the antibodies are developed in the titer that is sufficient to neutralize the virus, the virus changes its antigenic determinants. In this case, immuno-dominant neutralizing antibodies might start forming unstable complexes with the new form of the virus and start to infect monocytes/macrophages causing ADE. This process can trigger generalized infection of immune cells in multiple organs and cytokine storm
- solinent 6y agoIt's possibly by type and not mass, ie, one of each type of antibody versus various strains of COVID. I think that would make the most sense to me given the conclusion--if you don't have the right antibodies but have some you may be more susceptible to some strains and less susceptible to other strains. I will see if I get the time to find the original source.
- __blockcipher__ 6y agoYeah that still doesn't make sense haha. It's not really a different strains thing. But if you read about ADE you'll see that, I don't understand it perfectly but more or less you have a partial match which seems to make the immune system turn on itself. (I butchered that but it's been a long day...)
- solinent 6y agoWell it could be based on ADE--certain strains of coronavirus antibodies will help other strains replicate. In any case, I do remember quite clearly "half" but it was towards a very lay audience.