While we fritter away our last week at the beach, here's another installment of past posts on flu science. There are three subjects, but one of them took three installments to relate. That's because these involve cutting edge science papers in influenza science and we wanted to take enough time to explain them in ways that were understandable to non scientists. It's likely we weren't completely successful in every case, but even if you don't understand every detail, you can get a flavor for the struggle taking place in laboratories all over the world to understand this virus:
- "The complexity of the spread of flu virus"
- "Antibodies from survivors of 1918 era pandemic"
- "Important new flu paper in Cell":
Part I, Part II, Part III
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Two questions related to the "1918-papers":
1. How does the new H1N1 (swinw flu) compare to the 1918 H1N1 with respect to the mentioned "virulence markers" (PB1,PB2,PA) then ?
2. As even the 1918 flu was not more severe than "normal" flu in the vast majority of cases (given a 3% CFR, the disease must have been harmless & self-limiting in 97% of all cases given the absence of ventilators, antibiotics, antivirals) So shouldn't we look for the main factor responsible for the severity of the 3% severe cases to be in the host rather than in the virus ?
And It's the same disturbing pattern we are seeing with the novel H1N1 in 2009 ...
Where are the papers addressing the question what differences make some hosts so much more suspectible than others ?
Why does the same virus send 99% of its hosts to bed with a cold for a few days while at the same time sending the remaining 1% to the ICU struggling for their lives ?
I forgot to add to Question2: I know the standard "explanation" of "underlying health factors" like Obesity or Smoking ... But most of those alleged "factors" explanatory power disappear if we account for their prevalence in the general population ...
Unrelated to thread: it might be cost-effective to federally permit an added week of paid sick-leave over the potential 2009-10 Swine Flu season. The logic being people would be less likely to infect co-workers. Depends on whether R0 (the component of it that is physiological transmission) is low enough for this strategy to reduce # of infected or more likely reduce peak load; thin out the peak of flu infection graph.
IDK if honour principle or later antibody test or whatever, would be enough. If workers can be educated about early flu symptoms, is another issue.
Inspired to have an out-of-season public health idea today for some reason...
There is a Canadian province that intends to 5x doctor pay if fall/winter Swine Flu pandemic. To me this is a bad strategy as it encourages doctors to come in sick and communicable; I would for $500/hr (one shift would exceed the most $$ I've ever saved). In Canada healthcare providers are permitted to refuse flu vaccinations and employers are allowed to send them home without pay. But in practise this wouldn't occur because of lawsuit fears.
IDK how things are in rest of world, but it should probably be institutionalized if a certain mortality rate is breached in a pandemic, that it be socially acceptable all non vaccine recipient go home no pay, and even criminal to work without the vaccine (assuming no vaccine safety issues). The extra pay would work if you could ensure not working sick, IDK how this would be possible...