The Bloom lab thread about how elderly may not improve in terms of mortality while the younger population does could be at least partially confounded.
It uses graphs from the 1918 H1N1 flu, and the 1968 pandemic invasion of H3N2 into the human population.
The work of Michael Worobey and company strongly suggests that the first flu you are exposed to, and to a lesser extend the whole ensemble of immune memory you have built up, strongly affects your response to other novel flus for the rest of your life. Specifically, they have evidence that the odd age distribution of deaths in the 1918 pandemic was because people in their 40s onwards had pre-existing immune memory to H1 flu viruses from their childhood while younger adults did not, and so to those young adults it was a high severity novel virus while to the elderly cohort it was much more like an ordinary seasonal flu.
They have weaker evidence from serum samples rather than viral genomes that between 1890 and 1900 H3 flu viruses circulated in the human population. People older than 68 thus would have at least some immune memory against the new virus, which could skew their initial mortality downwards compared to something completely novel. Note that the split used is for those under/over 65.
In short, in both of these circumstances the young population was definitely seeing a novel virus they had never seen before, but in probably one and quite possibly both of them the elderly population was already prepared by immune memory from childhood and you would expect it to be much more like ordinary seasonal flu.
The 2009 swine flu was another relevant circumstance—it was a new H1N1 flu invading the human population from pigs, with a common ancestor with the H1N1 already in humans a century in the past so the drift was more than enough to make sure that we were all very easily infected. This lead to bizarre disease dynamics for more than a year, people getting sick all out of season in multiple waves. But deaths were barely above a normal flu season, because even though the similarity was not enough for immune memory to reliably prevent infection, it held off severe disease.
Unlike all of these circumstances, no one of any age who didn’t already have SARS had any relevant immune memory to SARS-2.
The 1951 Liverpool virus described is fascinating.
The Bloom lab thread about how elderly may not improve in terms of mortality while the younger population does could be at least partially confounded.
It uses graphs from the 1918 H1N1 flu, and the 1968 pandemic invasion of H3N2 into the human population.
The work of Michael Worobey and company strongly suggests that the first flu you are exposed to, and to a lesser extend the whole ensemble of immune memory you have built up, strongly affects your response to other novel flus for the rest of your life. Specifically, they have evidence that the odd age distribution of deaths in the 1918 pandemic was because people in their 40s onwards had pre-existing immune memory to H1 flu viruses from their childhood while younger adults did not, and so to those young adults it was a high severity novel virus while to the elderly cohort it was much more like an ordinary seasonal flu.
They have weaker evidence from serum samples rather than viral genomes that between 1890 and 1900 H3 flu viruses circulated in the human population. People older than 68 thus would have at least some immune memory against the new virus, which could skew their initial mortality downwards compared to something completely novel. Note that the split used is for those under/over 65.
In short, in both of these circumstances the young population was definitely seeing a novel virus they had never seen before, but in probably one and quite possibly both of them the elderly population was already prepared by immune memory from childhood and you would expect it to be much more like ordinary seasonal flu.
The 2009 swine flu was another relevant circumstance—it was a new H1N1 flu invading the human population from pigs, with a common ancestor with the H1N1 already in humans a century in the past so the drift was more than enough to make sure that we were all very easily infected. This lead to bizarre disease dynamics for more than a year, people getting sick all out of season in multiple waves. But deaths were barely above a normal flu season, because even though the similarity was not enough for immune memory to reliably prevent infection, it held off severe disease.
Unlike all of these circumstances, no one of any age who didn’t already have SARS had any relevant immune memory to SARS-2.
The 1951 Liverpool virus described is fascinating.