Re: How many people had no warning they were in danger from the recurrent wave of H1N1 flu?
pH1N1 is a nasty virus. I think that the powers that be expected it to ameliorate in severity after everyone was exposed, and at risk individuals got vaccinated. There is a lot to learn from this:- I suspect that multiple exposures are needed in those who do not have any innate immunity, and that each time there is an antigenic escape it will come back with a sting in its tail. The 1918 virus continued to cause major problems until at least 1933. There is no reason to suppose that this will be any different.
Mankind has been lulled into a false sense of security because our 'traditional' seasonal flu's have not been too severe for many decades.
pH1N1 is a reminder of what flu can do. Lets hope H7N9 does not complete its adaptation, because if it does, I expect it will cause problems for years in much the same way. It wont be a case of a single peak epidemic wave and then revert to a 'harmless' seasonal flu.
Lets hope that at least important lessons are being learned.
Risk Levels
and
Muted Warnings
We've been
discussing the
pH1N1 future risk level since 2009 with
continual updates. The Warning System must have some
mysterious,
unknowable unknown,
deleterious random mutation that prevents all communications from impacting citizens except the
managed perceptions issued from the podiums of public health officials.
An entire framework placing concern
ONLY with newly emergent strains is
short-sighted. We've demonstrated for 5 years the genetic maturation of the
pH1N1 strain from a 2009 virus that was only a "
starter set" of human-infective genetics. The host-switching process was
only beginning and transition markers from earlier human emergences were available as guides to researchers and policy makers.
Ah, but we forget that the
mysterious deletion mutation must be at play also in the communication process
TO the Influenza
corporate research departments
conveniently located at universities in your neighborhood.
Only very
rarely have we found random mutation or a sloppy polymerase at work as
pH1N1 has matured. What the reservoir has demonstrated is a careful march toward this s2013.
That march is based around a
well-constructed Clade2: 188T platform now sound enough to accept
constrained, high diversity crossing with
quasi-species at key amino locations. Those ever-present
quasi-species of
avian polymorphisms continue to inform
severe clinical outcomes and may be detected under proper examination.
An immunologically naive population is not the only factor in human suffering from Influenza. It's time for the medical and research infrastructure to accept that their 40 year old policies require an update. A virus is perfectly able to create
High Intensity events at the start, the middle and the
end of the reservoir's maturation cycle.
pH1N1 was the perfect candidate for
Post-Emergence surge, as we have
predicted, and as the world is seeing today.
The avian-like
pH1N1 virus appeared
partially-formed, was blamed on swine though none were ever demonstrated, marched directly into
wild diversity in humans, killed at
astonishingly variant rates and then proceeded to carefully gather base genetics while today returning to the early
High-CFR Upsilon subclade for "
tried and true" accumulations.
Those facts would lead any thoughtful investigator to the conclusion that
current models cannot explain today's surge of
vaccinated, healthy young adults expiring by the dozens around the United States of America.
And
pH1N1 has any number of
flashfire scenarios
waiting in the wings.
Time for the policy makers to put on a new hat . . . and
start thinking.
