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Quoting Nick Moffitt (nick at zork.net): > There is another angle on this story, which is the way that the 1918 > flu seemed to be comparatively benign to populations over 40. There's > a lot to be said about the way WW1 concentrated transmission vectors > among soldiers and field hospitals, but even well into 1919 the > primary losses were among the young. I'm commenting off the cuff, raising the chance of getting things wrong and missing important points, but: Also relevant to the worse effects on the young was their stronger immune reactions to any infection, in the sense that their immune systems sent a surge of activated immune cells into the lungs (a "cytokine storm"), causing severe inflammation and fluid buildup, thus respiratory distress and in many cases secondary bacterial pneumonia. Thus, in that way, having a robust immune system was a major risk factor. Tying this matter back to Deirdre's point, in 2011, the central orchestrators of the cytokine storm and immune cell infiltration, in response to H1N1 flu infection (of which the 1918 strain was one) got traced by scientists at The Scripps Research Institute to -- ta-da! -- endothelial cells lining blood vessels in the patient's lungs. That epiphany opened up possible ways to address the immune-freakout problem medically, not just using steroids but also less-harsh drugs that can modulate that response. I don't know about application of that to severe COVID, though. https://www.sciencedaily.com/releases/2014/02/140227142250.htm