Published Aug 8, 2010
indigo girl
5,173 Posts
Genetic Acquisition Analysis
Pandemic Influenza H1N1 Genetic Acquisitions: Introduction to PF11
PF11 refers to the pandemic flu virus, H1N1 otherwise known to us as the swine flu. This first intro piece was written a year ago.
PF11 in the human-form has now been sequence-confirmed in birds and in swine, allowing hundreds of species as additional "mixing vessels" or recombination reservoirs. This predicted species jump, more importantly, provides flight-based transportation vectors that will easily number in the millions of infected birds with a potential pool of billions in various seasons.Recall the CDC reports that 70% of all emerging diseases are zoonotic (originate in animals). The asymptomatic flight-based animals transport the disease from their land-based counterparts, the swine, who are playing their normal role as ideal mixing reservoirs for recombination due to their robust tolerance to many strains of Influenza. Pig=>Duck=>Human=>Chicken=>Pig and dozens of additional paired vectors of transmission have been confirmed between human, swine and avian species. The genetic transition state between species, the Influenza Flux, is dangerous for humans due to continual creation of novel antigen and species-specific phenotypical traits that strain the human immune system, elevate the potential for vaccine escape and may produce a negative interplay with that nemesis of vaccine scientists, Original Antigenic Sin (OAS). OAS, in a few words, describes the physiological phenomenon observed since 1960 that antibody production to a novel virus is mediated and frequently downgraded by the priming epitope or first infection in an individual host from that species of virus (original childhood infection). Frequent exposure to novel antigens within a virus species (notably Influenza), via vaccine and/or natural infection, tends to create fewer and fewer new antibodies that bind properly to the slightly dissimilar recent virus / antigen. The documented process counter-intuitively invokes high-specificity memory B cells from the priming epitope (original childhood infection) which then feeds back signals to reduce the activation of naive B cells toward the new antigen. Studies observe situations where Antibody Secreting Cells (ASC) produce antibodies to earlier infections in a ratio higher than antibodies to the new infection.In short, PF11 at this time continues to create a Hydra Effect, attacking the human with many different heads or genetic variations. The Hydra Effect coupled with the observed Interferon-Deranging, Rapid Replicating Viral (IDRRV) property creates a unique and daunting foe.
PF11 in the human-form has now been sequence-confirmed in birds and in swine, allowing hundreds of species as additional "mixing vessels" or recombination reservoirs. This predicted species jump, more importantly, provides flight-based transportation vectors that will easily number in the millions of infected birds with a potential pool of billions in various seasons.
Recall the CDC reports that 70% of all emerging diseases are zoonotic (originate in animals). The asymptomatic flight-based animals transport the disease from their land-based counterparts, the swine, who are playing their normal role as ideal mixing reservoirs for recombination due to their robust tolerance to many strains of Influenza. Pig=>Duck=>Human=>Chicken=>Pig and dozens of additional paired vectors of transmission have been confirmed between human, swine and avian species. The genetic transition state between species, the Influenza Flux, is dangerous for humans due to continual creation of novel antigen and species-specific phenotypical traits that strain the human immune system, elevate the potential for vaccine escape and may produce a negative interplay with that nemesis of vaccine scientists, Original Antigenic Sin (OAS).
OAS, in a few words, describes the physiological phenomenon observed since 1960 that antibody production to a novel virus is mediated and frequently downgraded by the priming epitope or first infection in an individual host from that species of virus (original childhood infection). Frequent exposure to novel antigens within a virus species (notably Influenza), via vaccine and/or natural infection, tends to create fewer and fewer new antibodies that bind properly to the slightly dissimilar recent virus / antigen. The documented process counter-intuitively invokes high-specificity memory B cells from the priming epitope (original childhood infection) which then feeds back signals to reduce the activation of naive B cells toward the new antigen. Studies observe situations where Antibody Secreting Cells (ASC) produce antibodies to earlier infections in a ratio higher than antibodies to the new infection.
In short, PF11 at this time continues to create a Hydra Effect, attacking the human with many different heads or genetic variations. The Hydra Effect coupled with the observed Interferon-Deranging, Rapid Replicating Viral (IDRRV) property creates a unique and daunting foe.
Pandemic Influenza Trends and Issues
Looking at where we are now, and what could still happen in this commentary. WHO has not yet stepped us down the pandemic ladder from Phase 6. We are still in a holding pattern waiting to see what will transpire. In other words, it ain't over till it's over.
Kids are starting back to school in California next week, and in the southern states they should be going back around the same time period. No flu yet here, but it is still ongoing in other countries as noted in the quote below.
Of special interest is the fact that by August of 1918, the disease had caused substantial fatality in areas less affected in the first wave including a severe epidemic in India. Does that season parallel 2010? Today, we stand at 2010-07-26 with reports from India indicating a profound upswing in case count and fatality level. In a recent count of two days (July 21st and 22nd) within Pune, India, officials went to the expense of testing 7,800 people and placing 1,286 on Tami-Flu.One city, two days. Late July 2010. India demonstrates current genetic sequences that suggest accumulation of pathogenic traits. Those same genetic markers appear across the United States and other parts of the world today....we have documented the persistent hyper-morphic behaviour of the pandemic reservoir since April 2009 and the recent concentration of Avian Influenza genetic changes onto the human influenza strains. The present series of accumulated changes demonstrate that this virus is far from stable and is positioned for additional waves with genetics predictive of higher mortality and long-term sequelae.
Of special interest is the fact that by August of 1918, the disease had caused substantial fatality in areas less affected in the first wave including a severe epidemic in India. Does that season parallel 2010? Today, we stand at 2010-07-26 with reports from India indicating a profound upswing in case count and fatality level. In a recent count of two days (July 21st and 22nd) within Pune, India, officials went to the expense of testing 7,800 people and placing 1,286 on Tami-Flu.
One city, two days. Late July 2010. India demonstrates current genetic sequences that suggest accumulation of pathogenic traits. Those same genetic markers appear across the United States and other parts of the world today.
...we have documented the persistent hyper-morphic behaviour of the pandemic reservoir since April 2009 and the recent concentration of Avian Influenza genetic changes onto the human influenza strains. The present series of accumulated changes demonstrate that this virus is far from stable and is positioned for additional waves with genetics predictive of higher mortality and long-term sequelae.