Washington State University, a campus of 19,000 students, reports 2,500 cases of Pandemic Influenza just days after the Fall Session started and projects 5,000 cases before this initial wave ends.
The University of Alabama reported 50 suspect cases on the first day of the session. Several elementary schools in the southern United States have wisely closed to halt the spread of PF11 and protect their children. Multiple reports crossing diverse geography exist of 10-15% absenteeism in the first week of elementary and middle school sessions. Oak Mountain Middle School in Alabama (statewide high count of large population clusters), remains open with 25% absent. A group of elementary and middle schools in Pittsburgh remain open with 15% to 44% of the student population ill with Pandemic Influenza.
The chart represents a small sample from the hundreds of news reports available this week concerning the immediate and deep spread of PF11 in August as our children return to school.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
2009-08-25
PF11 Trends & Issues, Mid-Term, Table of Contents
This analytical paper presented in a blog format attempts to synopsise more than one thousand point studies over a five-year period directed at Pandemic Influenza. Revisions and updates will be made on this blog as the pandemic progresses.
Read the sections first that most interest you and then return to read the complete work. Using the ordered links in this Table of Contents will allow the reader a deeper comprehension as categorical terms are detailed sequentially at the point of introduction.
Please contact me with any concerns so that I may evaluate for revisions.
Read the sections first that most interest you and then return to read the complete work. Using the ordered links in this Table of Contents will allow the reader a deeper comprehension as categorical terms are detailed sequentially at the point of introduction.
Please contact me with any concerns so that I may evaluate for revisions.
- Why should I care about Pandemic Influenza H1N1?
- What features does PF11 engage inside a human body?
- What human outcomes has PF11 demonstrated in this FirstWave?
- What part of our population is affected by PF11?
- What is the Nation Level Response to PF11?
- Where is PF11 going?
- Environmental Factors
- Genetic Acquisition Point Studies
- Glossary
Environmental Factors
Our recent research has opened the door to a new segment of correlated history on plagues that may have been incorrectly categorized as the “Black Death” in the Middle Ages. The presentation and progression in the FirstWave and SecondWave of several ancient plagues are precisely equal to Pandemic Influenza clinical outcomes. The predecessor data directly relates 5 plagues throughout the 1300’s to the 1918 pandemic.
Dr. Thomas Francis, Jr., in a seminal immune response work, On the Doctrine of Original Antigenic Sin, returns us to the history of 1485 and the "sweating sickness" of England, then onward to the 1743 pandemic called variously "Blitzkatarrh" and "the Blue Plague" precursing the 1918 speed of rapid destructive spread in the population and the effect of human skin turning cyanotic blue from hypoxia (oxygen starvation).
On a side note, we may have located the geological event, an earthquake, in the early 1300’s that created a very large inland lake in China from which a plague proceeded therewith and where other plagues have begun in the past 700 years, potentially including PF51 (as yet undeclared Pandemic H5N1) and this PF11 currently circumscribing the globe. That area of research continues to be under review though the field may lead to no new information as very little surveillance data is available to collaborate the concept.
Famines have been highly correlated to plagues throughout history. We postulate that malnourishment of metabolic qualifiers, such as Essential Fatty Acids, B vitamins and vitamin C, reduces the body’s ability to properly feedback after an initial virally-induced Cytokinic Dysregulation. The famished body is left with no nutrients / anti-oxidants to re-regulate the feedback cycle of the immune response.
Without question, the United States suffers and leads the world with a population of malnourished and yet overweight individuals due to the reliance on non-food, processed factory materials for sustenance. An overweight human is at high risk for daily leptin imbalance, a form of Cytokinic Dysregulation. The excess adipose tissue is leptin-inducing, creating a ratio error in cell-to-cell signaling. That daily chronic signaling error may exponentiate in the face of this IDRRV Influenza. Consider the combination of malnourishment with high adipose tissue in the overweight and we may see a Cytokinic Dysregulation occur that does not have the nutrients to feedback and re-regulate, leading to rapid declines and fatal outcomes. Perhaps that cycle is the causality of the high mortality and ICU admittance in Michigan among the overweight?
No one knows where this Pandemic strain is going precisely; however, the standing data lead us to draw one certain conclusion. PF11 is consistently drawing acquisitions from the current Influenza genetic reservoir, acquisitions that appear stable in producing disturbing clinical outcomes and potentially escaping the vaccine target. At this point, too few surveillance points are available to make firm predictions, but a framework may be ascertained. Under that framework, the acquisition path of PF11 suggests a movement toward a foundation of human-specific seasonal Influenza SNPs that will then continue to aggregate changes from H5N1 and 1918 descendants.
Those 1918 descendants and the H5N1 strains concern all researchers and will certainly continue to inform our investigations.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Dr. Thomas Francis, Jr., in a seminal immune response work, On the Doctrine of Original Antigenic Sin, returns us to the history of 1485 and the "sweating sickness" of England, then onward to the 1743 pandemic called variously "Blitzkatarrh" and "the Blue Plague" precursing the 1918 speed of rapid destructive spread in the population and the effect of human skin turning cyanotic blue from hypoxia (oxygen starvation).
On a side note, we may have located the geological event, an earthquake, in the early 1300’s that created a very large inland lake in China from which a plague proceeded therewith and where other plagues have begun in the past 700 years, potentially including PF51 (as yet undeclared Pandemic H5N1) and this PF11 currently circumscribing the globe. That area of research continues to be under review though the field may lead to no new information as very little surveillance data is available to collaborate the concept.
Famines have been highly correlated to plagues throughout history. We postulate that malnourishment of metabolic qualifiers, such as Essential Fatty Acids, B vitamins and vitamin C, reduces the body’s ability to properly feedback after an initial virally-induced Cytokinic Dysregulation. The famished body is left with no nutrients / anti-oxidants to re-regulate the feedback cycle of the immune response.
Without question, the United States suffers and leads the world with a population of malnourished and yet overweight individuals due to the reliance on non-food, processed factory materials for sustenance. An overweight human is at high risk for daily leptin imbalance, a form of Cytokinic Dysregulation. The excess adipose tissue is leptin-inducing, creating a ratio error in cell-to-cell signaling. That daily chronic signaling error may exponentiate in the face of this IDRRV Influenza. Consider the combination of malnourishment with high adipose tissue in the overweight and we may see a Cytokinic Dysregulation occur that does not have the nutrients to feedback and re-regulate, leading to rapid declines and fatal outcomes. Perhaps that cycle is the causality of the high mortality and ICU admittance in Michigan among the overweight?
No one knows where this Pandemic strain is going precisely; however, the standing data lead us to draw one certain conclusion. PF11 is consistently drawing acquisitions from the current Influenza genetic reservoir, acquisitions that appear stable in producing disturbing clinical outcomes and potentially escaping the vaccine target. At this point, too few surveillance points are available to make firm predictions, but a framework may be ascertained. Under that framework, the acquisition path of PF11 suggests a movement toward a foundation of human-specific seasonal Influenza SNPs that will then continue to aggregate changes from H5N1 and 1918 descendants.
Those 1918 descendants and the H5N1 strains concern all researchers and will certainly continue to inform our investigations.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Labels:
1918,
Cytokinic Dysregulation,
famine,
H5N1,
leptin,
malnourishment,
obesity,
overweight
Where is PF11 going?
No one knows as a certainty.
The “science” of Influenza genetics is far from well-developed concerning predictions. The literature remains peppered with phrases like "Surprisingly", "Unexpected" and "Data not provided" in areas that other studies claim to have proven; the "science" foundation for genetic prediction is yet small. Most leading Influenza researchers are unwilling and unable to go on public record with vectors or potential paths of viral development. The “science” of Influenza and viral genetics is relatively young and though ground is being gained in the content arena, predictability using the current two pillars dogma is rarely undertaken because the protocols were built in an era that had only a low quantity of low quality data. New models of thinking and new protocols of investigation are required that incorporate the proofs demonstrated within the current reservoir of available data.
The recent high availability of PF11 sequences and clinical reports has given us data to understand where the virus is going, especially the much desired and appreciated sequences from South America shared by the Mailman School of Public Health at Columbia University. The sequences are from Argentina where the highest official death count in the world has caused healthcare rationing in all 77 hospitals in the socialized medicine system of Argentina. Many other countries in Latin America are refusing health services due to supply, personnel and infrastructure failures.
The reservoir of fitness-inducing polymorphisms available to PF11 is vast as we’ve determined 4 or more backgrounds in circulation that may have been slow, but consistent, donors to PF11.
The related reservoir has much more to offer in the coming months as the most important changes have either not yet been introduced or have not become fixed. Several of these candidate donor backgrounds are matches to provide one or more of the polymorphisms that have been demonstrated in the lab and shown clinically to strengthen Influenza against humans.
Remember that, although many are dying horrible deaths from PF11, this virus, as it stands today, is still most definitely hobbled / limited by many genetic shortcomings. The viral development process appears to be correcting those shortcomings by accepting consistent donations from the able reservoir of circulating Influenza strains worldwide.
We expect that PB2:627K (Increased Human Virulence) and NA:275Y (TamiFlu resistance) will be discovered widely in PF11. Relenza resistance is impossible to characterise at this time due to data paucity.
For a more complete and ongoing analysis, please read our PF11 Genetic Acquisitions studies.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
The “science” of Influenza genetics is far from well-developed concerning predictions. The literature remains peppered with phrases like "Surprisingly", "Unexpected" and "Data not provided" in areas that other studies claim to have proven; the "science" foundation for genetic prediction is yet small. Most leading Influenza researchers are unwilling and unable to go on public record with vectors or potential paths of viral development. The “science” of Influenza and viral genetics is relatively young and though ground is being gained in the content arena, predictability using the current two pillars dogma is rarely undertaken because the protocols were built in an era that had only a low quantity of low quality data. New models of thinking and new protocols of investigation are required that incorporate the proofs demonstrated within the current reservoir of available data.
The recent high availability of PF11 sequences and clinical reports has given us data to understand where the virus is going, especially the much desired and appreciated sequences from South America shared by the Mailman School of Public Health at Columbia University. The sequences are from Argentina where the highest official death count in the world has caused healthcare rationing in all 77 hospitals in the socialized medicine system of Argentina. Many other countries in Latin America are refusing health services due to supply, personnel and infrastructure failures.
Genetic Acquisition Analysis
A managed campaign of political and laboratory messages in the media continues to state that no changes are found in Pandemic Influenza H1N1. The underlying genetics database, however, demonstrates many acquisitions and a consistent trend of fitness-inducing polymorphisms. As samples have been added each week around the world, a pattern has emerged.
The pattern indicates a persistent hyper-morphic state on the PF11 background at certain positions within particular species. Of certain note is the directional movement on the Hemagglutinin (variously termed HA and H1) and Neuraminidase (variously termed NA and N1) segments. Though all Influenza consistently recombines with existing genetic material from proximal non-self strains, PF11 has demonstrated a march toward human-fit acquisition that is remarkable in speed and geographic spread.
The purpose of these point by point studies is to indicate and discuss several of those key polymorphisms and examine the potential next steps in humans. As you have seen finally released in the media, 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 Replication Viral (IDRRV) property creates a unique and daunting foe.
We will overview our findings on four gene segments with discussion on inter-segment correlations.
The pattern indicates a persistent hyper-morphic state on the PF11 background at certain positions within particular species. Of certain note is the directional movement on the Hemagglutinin (variously termed HA and H1) and Neuraminidase (variously termed NA and N1) segments. Though all Influenza consistently recombines with existing genetic material from proximal non-self strains, PF11 has demonstrated a march toward human-fit acquisition that is remarkable in speed and geographic spread.
The purpose of these point by point studies is to indicate and discuss several of those key polymorphisms and examine the potential next steps in humans. As you have seen finally released in the media, 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 Replication Viral (IDRRV) property creates a unique and daunting foe.
We will overview our findings on four gene segments with discussion on inter-segment correlations.
The reservoir of fitness-inducing polymorphisms available to PF11 is vast as we’ve determined 4 or more backgrounds in circulation that may have been slow, but consistent, donors to PF11.
The related reservoir has much more to offer in the coming months as the most important changes have either not yet been introduced or have not become fixed. Several of these candidate donor backgrounds are matches to provide one or more of the polymorphisms that have been demonstrated in the lab and shown clinically to strengthen Influenza against humans.
Remember that, although many are dying horrible deaths from PF11, this virus, as it stands today, is still most definitely hobbled / limited by many genetic shortcomings. The viral development process appears to be correcting those shortcomings by accepting consistent donations from the able reservoir of circulating Influenza strains worldwide.
We expect that PB2:627K (Increased Human Virulence) and NA:275Y (TamiFlu resistance) will be discovered widely in PF11. Relenza resistance is impossible to characterise at this time due to data paucity.
For a more complete and ongoing analysis, please read our PF11 Genetic Acquisitions studies.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
What is the Nation Level Response to PF11?
Central and South American countries are closing schools and rationing health care while Australia is evacuating some hospitals of all patients other than Influenza management due to rapid spread across floors and depth of morbidity. Vietnam closed all schools in the capital in mid-August. No nation’s public health leaders are reporting accurate case counts or death counts, but a careful and ongoing counting of reports correlated with the medical data demonstrates documentation for 522 deaths in the US, 450 in Argentina (since mid-May with 400 awaiting confirmation for a potential total of 850 deaths) and 413 in Brasil (>10% pregnant women). The death counts in South America are rising in some countries as much as 40% every 7 days even with the WHO blackout on measuring and reporting to the public. Though strong intervention measures are reportedly being invoked, many South American countries have more than 100 confirmed PF11 casualties. The UK death count increased by 30% this week. On the European coast, Spain estimates 10,000 new cases per week with at least three concurrent PF11 Variant strains.
Keep in mind that between 31% and 60% of the tests commonly used for PF11 have provided a false negative result. Slightly less than half of all cases that have tested negative may have been positive, suffering from Pandemic Influenza and spreading contagion. As you may realise from the CDC admission during the early phases of this pandemic on June 25th of 1 million cases in the United States when less than 40,000 had been chronicled, surveillance is far less than superficial. The American CDC allowed a factor of 25 times the number of confirmed cases to achieve the estimated total. That factor is a very important number.
Using the CDC-supplied ratio of confirmed to estimated actual cases, we may also measure confirmed to actual deaths. Multiply 522 CDC confirmed US deaths by 25 and you arrive at more than 13,000 deaths across the first 90 days, 13,000 deaths from a “mild” Influenza, deaths in age groups that are only highly represented in a High-CFR pandemic? Political issues are at play, obviously and the public will not at any juncture of this pandemic be provided accurate numbers. We will track the deltas, however, to measure the progressions using any data that is available. We are aware of many cases, some personally, that exhibited all signals of Influenza presentation, progression and expiration, but that have been officially recorded otherwise, blatantly in some cases. These political outcroppings of a failed public health policy were also predicted four years ago and are not a surprise to us or to others tracking this issue closely.
At the same time, we are watching the many different viral strains from around the globe continue to upgrade their genetics. Anti-viral (Neuraminidase Inhibitors) drug resistance in both widely available commercial categories is essentially guaranteed as you will see in our trailing analyses. The vaccine antigen being produced today will be late for the Fall and veers markedly in genetic resemblance from the viral specimens presently being sequenced from active circulation. The current Pandemic H1N1 continues to escape the vaccine target by accumulating and conserving changes each week.
The vaccine seed stock strain for this ostensibly “mild” Influenza is so powerful that growth cannot be well-controlled in the lab and little antigen is harvested. Measure the facts on a timeline. The vaccine is announced for mid-October delivery with a 5 week seroconversion period in the host. You can easily see that the earliest possible point of any benefit to anyone, if the vaccine is safe and matches, is very late November, another 90 days after school starts and well into winter. You’ve seen the impact of this virus in the first 90 days, in 3 months of warm weather in America. We haven’t yet seen this virus at work in the Northern Hemisphere with the Fall and Winter versions operating in colder weather.
Fringe ideas for “extending” the antigen have been introduced and are becoming entrenched in the discussions between vaccine purchasers and producers. Adjuvants that are scientifically known to be highly toxic, including MPL and squalene, are offering a politically-expedient solution to our leaders at the cost of public health.
Though most in the scientific community publicly announce that they rely on pure data, on facts, the current set of circumstances clearly demonstrates the scientific community’s reliance on blind faith in rapidly resisted anti-virals and easily evaded vaccines as primary mediation measures. At this time, the facts don’t support their conclusions, nor do the data support their actions. The medical and scientific community have super-imposed faith and hope in a time when we have trusted them to discover truth and use facts to protect us. Faith is an exceptional practice when placed properly; whereas, a misplaced faith will typically result in a negative impact.
The mediation measures being put in place by our leaders are but minor impact measures that will be used due to ease of execution and lack of Knowledge of the citizenry. Those measures also carry mid-term and long-term negative health effects for the human population, including allowing a higher death rate than other, more reliable, mediation measures. The failed surveillance coupled with a “managed message” campaign will have a higher negative impact on the population than any other aspect of our national response failure. We are being actively triaged while being managed with a disinformation flow stating that first rate health care is being provided and that our interests are foremost in the leaders’ minds.
Science, in a pure form, looks at data, examines the facts and makes transparent decisions based on those facts. Science, in a pure form, is not occurring widely in relation to this pandemic.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Keep in mind that between 31% and 60% of the tests commonly used for PF11 have provided a false negative result. Slightly less than half of all cases that have tested negative may have been positive, suffering from Pandemic Influenza and spreading contagion. As you may realise from the CDC admission during the early phases of this pandemic on June 25th of 1 million cases in the United States when less than 40,000 had been chronicled, surveillance is far less than superficial. The American CDC allowed a factor of 25 times the number of confirmed cases to achieve the estimated total. That factor is a very important number.
Using the CDC-supplied ratio of confirmed to estimated actual cases, we may also measure confirmed to actual deaths. Multiply 522 CDC confirmed US deaths by 25 and you arrive at more than 13,000 deaths across the first 90 days, 13,000 deaths from a “mild” Influenza, deaths in age groups that are only highly represented in a High-CFR pandemic? Political issues are at play, obviously and the public will not at any juncture of this pandemic be provided accurate numbers. We will track the deltas, however, to measure the progressions using any data that is available. We are aware of many cases, some personally, that exhibited all signals of Influenza presentation, progression and expiration, but that have been officially recorded otherwise, blatantly in some cases. These political outcroppings of a failed public health policy were also predicted four years ago and are not a surprise to us or to others tracking this issue closely.
At the same time, we are watching the many different viral strains from around the globe continue to upgrade their genetics. Anti-viral (Neuraminidase Inhibitors) drug resistance in both widely available commercial categories is essentially guaranteed as you will see in our trailing analyses. The vaccine antigen being produced today will be late for the Fall and veers markedly in genetic resemblance from the viral specimens presently being sequenced from active circulation. The current Pandemic H1N1 continues to escape the vaccine target by accumulating and conserving changes each week.
The vaccine seed stock strain for this ostensibly “mild” Influenza is so powerful that growth cannot be well-controlled in the lab and little antigen is harvested. Measure the facts on a timeline. The vaccine is announced for mid-October delivery with a 5 week seroconversion period in the host. You can easily see that the earliest possible point of any benefit to anyone, if the vaccine is safe and matches, is very late November, another 90 days after school starts and well into winter. You’ve seen the impact of this virus in the first 90 days, in 3 months of warm weather in America. We haven’t yet seen this virus at work in the Northern Hemisphere with the Fall and Winter versions operating in colder weather.
Fringe ideas for “extending” the antigen have been introduced and are becoming entrenched in the discussions between vaccine purchasers and producers. Adjuvants that are scientifically known to be highly toxic, including MPL and squalene, are offering a politically-expedient solution to our leaders at the cost of public health.
Though most in the scientific community publicly announce that they rely on pure data, on facts, the current set of circumstances clearly demonstrates the scientific community’s reliance on blind faith in rapidly resisted anti-virals and easily evaded vaccines as primary mediation measures. At this time, the facts don’t support their conclusions, nor do the data support their actions. The medical and scientific community have super-imposed faith and hope in a time when we have trusted them to discover truth and use facts to protect us. Faith is an exceptional practice when placed properly; whereas, a misplaced faith will typically result in a negative impact.
No Hallelujah Pill and No Hallelujah Vaccine
will reliably save us from this virus.
The mediation measures being put in place by our leaders are but minor impact measures that will be used due to ease of execution and lack of Knowledge of the citizenry. Those measures also carry mid-term and long-term negative health effects for the human population, including allowing a higher death rate than other, more reliable, mediation measures. The failed surveillance coupled with a “managed message” campaign will have a higher negative impact on the population than any other aspect of our national response failure. We are being actively triaged while being managed with a disinformation flow stating that first rate health care is being provided and that our interests are foremost in the leaders’ minds.
Science, in a pure form, looks at data, examines the facts and makes transparent decisions based on those facts. Science, in a pure form, is not occurring widely in relation to this pandemic.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
What part of our population is affected by PF11?
Most.
A virus that spread to 168 countries with a speed that is unmatched by any disease outside of historical plagues is a virus that must be examined closely.
We expect a 90%+ Clinical Attack Rate (CAR) over two years, if the trend demonstrated with serological data from 1918 survivors holds true. More than 97% carried antibodies to the 1918 Influenza.
Though a 2% Clinical Fatality Rate (CFR) may appear slight and unconcerning, be mindful of the practical mathematics. That 2% equates 1 death of every 55 people in your community, in your company and in your family if the CAR holds at 90%. As the case exponentiation occurs from school openings, colder weather and human-fit Genetic Acquisitions, the general risk factors of today will give way to a “sheer randomness” of attack, as one colleague astutely commented. If life-long debility holds as a statistically significant feature of this type of IDRRV Influenza, many of the survivors will bear neurological artifacts of this avoidable disease for the rest of their lives.
Although most have obviously survived the FirstWave and most will obviously survive the SecondWave, no guarantees are available to any individual human with this Influenza serotype. An expert on Influenza History recalled for me recently the documented "three-time loser" from the 1918 Spanish Influenza. That individual in 1918 was struck during all three waves and recovered in the first two. His antibody product from two illnesses certainly did not protect him from the third wave that killed him. This evidence of the “three-time loser” and many other cases with back-to-back illnesses during the 1918 plague suggests that Adaptive Immunity did not play the most significant role in survival. A robust, but properly regulated Innate Immune response appears to be the proper solution to an IDRRV assault.
As you have seen in media reports, children and young adults represent a statistically large portion of the confirmed cases and the confirmed deaths at a rate not seen since 1918. After four years of focused research on these types of viral strains in these particular hosts, we continue to speculate that an endogenous growth factor, yet unidentified may be involved (termed as GFλ ). Though research abounds on single molecule signalers, little is actually known about the complex systems of cell-to-cell signaling and even less about the interdependence of intra-cellular signals. GFλ could perhaps be an interactive system of hormones, cytokines or chemokines.
Growth Factor Lambda will be found to either be present in higher levels or normally only present within children, young adults and pregnant women. GFλ will be found to affect metabolism at the sub-cellular, organelle level. This factor may even be an anti-factor, a re-tasker, that moves resources away from “base/normal” function and onto high growth activities. That higher or “different” metabolism driven by GFλ may enable an Interferon-Deranging, Rapid Replicating Virus (IDRRV) like PF11 a significant advantage in speed of reproduction, multi-tropism and / or variation in genetic expression and genetic acquisition. We would like to see additional labs moving quickly toward these types of investigations. The implications are astounding. Because the signaling molecules have diverse individual roles and more diverse combination effects with complex feedback cycles, discrete measurement and experiment design allow only for a limited understanding at this stage of research capability. As we have seen in practice these past 90 days, the medical industry cannot safely and successfully regulate these types of complex systems using single-point, synthetic interventions. Most of the confirmed deaths on file occurred during or after advanced medical treatment.
Pregnancy poses a very certain risk for the mother and the child. In South America, one country has reported that 10% of all deaths to date related to pregnancy.
Though most individuals will eventually be infected, certain positions are in a higher risk. Healthcare workers (doctors, nurses, pediatric specialists, respiratory therapists and administrators) and educators (elementary and secondary school teachers, university professors, headmasters and administrators) are dying from this virus as they serve in their respective roles. Most of our military academies, more than one reported USN battle group, soldiers across Iraq and USArmy bases have been affected with quarantines from this virus. We expect that the global trend will be similar with confirmed cases starting in mid-June at Sandhurst, the Royal Military Academy of the UK. Law Enforcement and First Responders have been significantly impacted with reports of deaths from contact in their daily duties and some departments reporting 40% absenteeism. Christian missions and summer camps have been infected widely. Any position, including school and university-based employment, that requires congregation regularly with alternate mixing of individuals creates a higher Influenza virus raw exposure count, thus a higher risk of developing fulminant infection.
We endeavoured to make an “apples to apples” comparison here of Seasonal Influenza death rates to PF11. Obstacles occurred. The primary block is the continued espousal by the CDC of the number “36,000”, a mythical mathematical model output that generalises annual US deaths related to Influenza-Like-Illness (ILI) AND secondary Pneumonia (bacterial, viral or fungal). The figure of “36,000” was created, in a calculation, but nonetheless, created. Facts are not created, nor are they spoken into being by repetition. However, repetition may be used to manage perception toward or away from a fact, even to revise the public perception to a position that is 180 degrees polar from the fact.
Knowledge is discovered, not built by consensus or a popular vote of opinions, not pulled by the wind of political philosophy and certainly not established by the payment of the highest bidder. Data that is surfaced, investigated, repeated and proven may be promoted to the unimpeachable fact category. Although political policy has no effect on creating fact, the reigning political voice does hold a primary strength in creating perception. Much of the recent public health messaging on PF11 appears to be based not on facts, but reliant upon consensus “science” or some other group of non-correlative and causality-free hypotheses. Are we having our perceptions managed?
Seeking the actual Influenza-only data demonstrated no recent year on record with a figure resembling “36,000”. In fact, most years trended very closely to 2,000 deaths, with many nearer to 1,000. When public health officials combine the two similar symptomologies of Influenza and Pneumonia (though the causes are generally diametrically opposed), a portion of the labor involved in testing and surveillance is alleviated from the medical community. Their gain is your loss due to the lowered accuracy, compatibility and actionability of their published data.
The science community has known the risk of a High-CFR Pandemic and yet has failed to surveil the signals. Additional observation of public health reports inspired a validation of reports regarding deaths in the “under 18” category. The historical numbers are markedly lower than we have been led to believe during this “mild” Influenza “social messaging” campaign. When public health officials draw a parallel between Seasonal Influenza and PF11, they mischaracterise their own data. The present number of deaths from PF11 in young people clearly represents a substantial multiplier over previous years, but does not appear in those ratios in the official account.
Table 1 may lead you to perceive that the threat from PF11 is insubstantial, because Table 1 is very misleading for many reasons. The most prominent question that comes to mind is that far more than 29 PF11 deaths have occurred in this group according to state health departments and media reports, but the current surveillance monitoring system may not be up to task for capturing results in response to this summer anomaly. We are left to comparing apples and oranges when lives are at stake. Let’s evaluate other comparisons for a moment.
These data points do not allow us to make an “apples to apples” comparison; however, we may certainly conclude one clear peak using only CDC data. “Deaths per Day” is substantially higher this season than recent previous years and is peaking again during PF11. Again, disclaimers apply. We are working with another’s data.
Consider that rapid testing for PF11 failed to properly classify 31% to 60% of the ill across America, so the derived PF11 average is substantially lower than the actual deaths. Factor the false negative rate of the tests and the actual Deaths per Day quickly distinguishes itself from our earlier .46 to a minimum of .60, maximum of .74 and average of .67 Deaths per Day.
Moving closer to a valid comparison with this moderate data norming, Table 3 with the PF11 average adjustment for false negative testing increases compatibility of the data. Unfortunately, averaging is all that can be accomplished due to the weak surveillance.
A fair evaluation would promote Table 4 for the simple reason that “Seasonal” Influenza is very different than an Influenza that occurs in summer heat; however, the data points are relatively sparse though the situation does directly compare. Few to no deaths in any preceding year and 42 data-normed deaths this summer demonstrate a marked difference.
The average daily death figure in the final column of Tables 2, 3 and 4 is certainly not a product of a statistical model, but a simple division, a measurement of facts across time. When a daily average increases, a careful investigation is always in order because a change that is occurring consistently will accumulate rapidly and may establish variant behaviour and impacts. The data gathered and reported by public health officials fails to parallel, to inform, the “social messaging” emanating from those very same public health officials on PF11? History will examine motivations for this disparity and judge those who have acted dishonorably. We will report the data.
The “managed message” campaign has consistently downplayed the PF11 death count while emphasising that “underlying health conditions” are more of a concern than the actual viral pathogen. We personally are baffled by this direction of messaging. Why are we baffled? The facts speak for themselves.
On a very related note, but not mentioned in the media, Johns Hopkins, in a recent study, found that 60% of Americans suffer from a chronic or degenerative disease and more than 25% suffer from two or more. The Johns Hopkins list of disease factors aligns with the set of complications for PF11. The “underlying health conditions” public messaging that is intended to soften the death count takes on a new light when you realise that 60% of Americans fall into the “pre-existing health conditions” category and, as such, become candidates for the PF11 death roles.
Is weight an “underlying health condition”? Apparently an overweight individual is at higher risk for Acute Respiratory Distress Syndrome (ARDS) and ICU admittance with PF11. The Michigan department of health reported that 90% of the individuals in their Intensive Care Units were overweight.
Is poor immune function a factor? If so, then an additional 23.5 million Americans that are defined as having various levels of Auto Immune Syndrome may face a difficult co-factor situation. Vaccines are known to suppress the maturation of innate immune cells (Th1 response via dendritic cells) at a higher rate within damaged immune systems. Mount Sinai studies have confirmed that a strong innate response is the basis for successful viral clearance. These studies and others suggest that an individual with present immune dysfunction may be at additional risk of derangement by the introduction of vaccine-delivered, Th2-stimulating antigen.
Perhaps we should stop being assuaged by clever interpretations and start reviewing the actual data with our own eyes?
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
A virus that spread to 168 countries with a speed that is unmatched by any disease outside of historical plagues is a virus that must be examined closely.
We expect a 90%+ Clinical Attack Rate (CAR) over two years, if the trend demonstrated with serological data from 1918 survivors holds true. More than 97% carried antibodies to the 1918 Influenza.
Though a 2% Clinical Fatality Rate (CFR) may appear slight and unconcerning, be mindful of the practical mathematics. That 2% equates 1 death of every 55 people in your community, in your company and in your family if the CAR holds at 90%. As the case exponentiation occurs from school openings, colder weather and human-fit Genetic Acquisitions, the general risk factors of today will give way to a “sheer randomness” of attack, as one colleague astutely commented. If life-long debility holds as a statistically significant feature of this type of IDRRV Influenza, many of the survivors will bear neurological artifacts of this avoidable disease for the rest of their lives.
Three-Time Loser in 1918
Although most have obviously survived the FirstWave and most will obviously survive the SecondWave, no guarantees are available to any individual human with this Influenza serotype. An expert on Influenza History recalled for me recently the documented "three-time loser" from the 1918 Spanish Influenza. That individual in 1918 was struck during all three waves and recovered in the first two. His antibody product from two illnesses certainly did not protect him from the third wave that killed him. This evidence of the “three-time loser” and many other cases with back-to-back illnesses during the 1918 plague suggests that Adaptive Immunity did not play the most significant role in survival. A robust, but properly regulated Innate Immune response appears to be the proper solution to an IDRRV assault.
Children and Young Adults
As you have seen in media reports, children and young adults represent a statistically large portion of the confirmed cases and the confirmed deaths at a rate not seen since 1918. After four years of focused research on these types of viral strains in these particular hosts, we continue to speculate that an endogenous growth factor, yet unidentified may be involved (termed as GFλ ). Though research abounds on single molecule signalers, little is actually known about the complex systems of cell-to-cell signaling and even less about the interdependence of intra-cellular signals. GFλ could perhaps be an interactive system of hormones, cytokines or chemokines.
Growth Factor Lambda will be found to either be present in higher levels or normally only present within children, young adults and pregnant women. GFλ will be found to affect metabolism at the sub-cellular, organelle level. This factor may even be an anti-factor, a re-tasker, that moves resources away from “base/normal” function and onto high growth activities. That higher or “different” metabolism driven by GFλ may enable an Interferon-Deranging, Rapid Replicating Virus (IDRRV) like PF11 a significant advantage in speed of reproduction, multi-tropism and / or variation in genetic expression and genetic acquisition. We would like to see additional labs moving quickly toward these types of investigations. The implications are astounding. Because the signaling molecules have diverse individual roles and more diverse combination effects with complex feedback cycles, discrete measurement and experiment design allow only for a limited understanding at this stage of research capability. As we have seen in practice these past 90 days, the medical industry cannot safely and successfully regulate these types of complex systems using single-point, synthetic interventions. Most of the confirmed deaths on file occurred during or after advanced medical treatment.
Pregnancy poses a very certain risk for the mother and the child. In South America, one country has reported that 10% of all deaths to date related to pregnancy.
Though most individuals will eventually be infected, certain positions are in a higher risk. Healthcare workers (doctors, nurses, pediatric specialists, respiratory therapists and administrators) and educators (elementary and secondary school teachers, university professors, headmasters and administrators) are dying from this virus as they serve in their respective roles. Most of our military academies, more than one reported USN battle group, soldiers across Iraq and USArmy bases have been affected with quarantines from this virus. We expect that the global trend will be similar with confirmed cases starting in mid-June at Sandhurst, the Royal Military Academy of the UK. Law Enforcement and First Responders have been significantly impacted with reports of deaths from contact in their daily duties and some departments reporting 40% absenteeism. Christian missions and summer camps have been infected widely. Any position, including school and university-based employment, that requires congregation regularly with alternate mixing of individuals creates a higher Influenza virus raw exposure count, thus a higher risk of developing fulminant infection.
We endeavoured to make an “apples to apples” comparison here of Seasonal Influenza death rates to PF11. Obstacles occurred. The primary block is the continued espousal by the CDC of the number “36,000”, a mythical mathematical model output that generalises annual US deaths related to Influenza-Like-Illness (ILI) AND secondary Pneumonia (bacterial, viral or fungal). The figure of “36,000” was created, in a calculation, but nonetheless, created. Facts are not created, nor are they spoken into being by repetition. However, repetition may be used to manage perception toward or away from a fact, even to revise the public perception to a position that is 180 degrees polar from the fact.
Knowledge is discovered, not built by consensus or a popular vote of opinions, not pulled by the wind of political philosophy and certainly not established by the payment of the highest bidder. Data that is surfaced, investigated, repeated and proven may be promoted to the unimpeachable fact category. Although political policy has no effect on creating fact, the reigning political voice does hold a primary strength in creating perception. Much of the recent public health messaging on PF11 appears to be based not on facts, but reliant upon consensus “science” or some other group of non-correlative and causality-free hypotheses. Are we having our perceptions managed?
Seeking the actual Influenza-only data demonstrated no recent year on record with a figure resembling “36,000”. In fact, most years trended very closely to 2,000 deaths, with many nearer to 1,000. When public health officials combine the two similar symptomologies of Influenza and Pneumonia (though the causes are generally diametrically opposed), a portion of the labor involved in testing and surveillance is alleviated from the medical community. Their gain is your loss due to the lowered accuracy, compatibility and actionability of their published data.
CDC Pediatric Data: Children under Age 18
The science community has known the risk of a High-CFR Pandemic and yet has failed to surveil the signals. Additional observation of public health reports inspired a validation of reports regarding deaths in the “under 18” category. The historical numbers are markedly lower than we have been led to believe during this “mild” Influenza “social messaging” campaign. When public health officials draw a parallel between Seasonal Influenza and PF11, they mischaracterise their own data. The present number of deaths from PF11 in young people clearly represents a substantial multiplier over previous years, but does not appear in those ratios in the official account.
Table 1 may lead you to perceive that the threat from PF11 is insubstantial, because Table 1 is very misleading for many reasons. The most prominent question that comes to mind is that far more than 29 PF11 deaths have occurred in this group according to state health departments and media reports, but the current surveillance monitoring system may not be up to task for capturing results in response to this summer anomaly. We are left to comparing apples and oranges when lives are at stake. Let’s evaluate other comparisons for a moment.
These data points do not allow us to make an “apples to apples” comparison; however, we may certainly conclude one clear peak using only CDC data. “Deaths per Day” is substantially higher this season than recent previous years and is peaking again during PF11. Again, disclaimers apply. We are working with another’s data.
Consider that rapid testing for PF11 failed to properly classify 31% to 60% of the ill across America, so the derived PF11 average is substantially lower than the actual deaths. Factor the false negative rate of the tests and the actual Deaths per Day quickly distinguishes itself from our earlier .46 to a minimum of .60, maximum of .74 and average of .67 Deaths per Day.
Moving closer to a valid comparison with this moderate data norming, Table 3 with the PF11 average adjustment for false negative testing increases compatibility of the data. Unfortunately, averaging is all that can be accomplished due to the weak surveillance.
A fair evaluation would promote Table 4 for the simple reason that “Seasonal” Influenza is very different than an Influenza that occurs in summer heat; however, the data points are relatively sparse though the situation does directly compare. Few to no deaths in any preceding year and 42 data-normed deaths this summer demonstrate a marked difference.
The average daily death figure in the final column of Tables 2, 3 and 4 is certainly not a product of a statistical model, but a simple division, a measurement of facts across time. When a daily average increases, a careful investigation is always in order because a change that is occurring consistently will accumulate rapidly and may establish variant behaviour and impacts. The data gathered and reported by public health officials fails to parallel, to inform, the “social messaging” emanating from those very same public health officials on PF11? History will examine motivations for this disparity and judge those who have acted dishonorably. We will report the data.
Underlying Health Conditions
The “managed message” campaign has consistently downplayed the PF11 death count while emphasising that “underlying health conditions” are more of a concern than the actual viral pathogen. We personally are baffled by this direction of messaging. Why are we baffled? The facts speak for themselves.
On a very related note, but not mentioned in the media, Johns Hopkins, in a recent study, found that 60% of Americans suffer from a chronic or degenerative disease and more than 25% suffer from two or more. The Johns Hopkins list of disease factors aligns with the set of complications for PF11. The “underlying health conditions” public messaging that is intended to soften the death count takes on a new light when you realise that 60% of Americans fall into the “pre-existing health conditions” category and, as such, become candidates for the PF11 death roles.
Is weight an “underlying health condition”? Apparently an overweight individual is at higher risk for Acute Respiratory Distress Syndrome (ARDS) and ICU admittance with PF11. The Michigan department of health reported that 90% of the individuals in their Intensive Care Units were overweight.
Is poor immune function a factor? If so, then an additional 23.5 million Americans that are defined as having various levels of Auto Immune Syndrome may face a difficult co-factor situation. Vaccines are known to suppress the maturation of innate immune cells (Th1 response via dendritic cells) at a higher rate within damaged immune systems. Mount Sinai studies have confirmed that a strong innate response is the basis for successful viral clearance. These studies and others suggest that an individual with present immune dysfunction may be at additional risk of derangement by the introduction of vaccine-delivered, Th2-stimulating antigen.
Perhaps we should stop being assuaged by clever interpretations and start reviewing the actual data with our own eyes?
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Labels:
36000,
asthma,
children,
Christian,
Church,
diabetes,
Growth Factor Lambda,
Healthcare workers,
law enforcement,
military,
Mosque,
Nurse,
obesity,
overweight,
Pregnant,
Synagogue,
Vaccine
What human outcomes has PF11 demonstrated in these Early Waves?
Last Updated 2013-05-30
Does this pandemic H1N1 virus, PF11, display any characteristics that differ from Seasonal Influenza?
Rapid deaths within 12-40 hours of first symptoms generally involving partial viral destruction of major organs including bleeding from the lungs are documented across wide geography (US, Europe, South America, Central America, Africa and Asia) in every age category. Brain infection and kidney damage features robustly across all age categories. Very striking are the sudden heart attacks in 6 year old to 22 year old females and males documented across the globe, with cases occurring after TamiFlu treatment or after being released from a healthcare facility based on achievement of a negative rapid test for a proud announcement of “cured” by the attending physician.
Testing negative is not a firm predictor of recovery. The relapse potential is very high.
Disseminated Intravascular Coagulation (DIC), a Cytokinic Dyregulatory systemic clotting of the blood with a resultant swing in the opposite direction (thinning the blood) has proven fatal in this pandemic and, though the term is recent, past pandemics have displayed very similar clinical outcomes. We have direct clinical reports from one suspect fatal PF11 case (unconfirmed due to no testing) involving necrosis at the skin level, creating a progression of black spots across the body prior to death.
Tracking studies have measured that a well-progressed neurological infection of Influenza leaves long-term loss of function in 25% to 50% of the cases. A retrospective study of California cases admits serious neurological sequelae in 1 of 20 diagnosed cases of pandemic influenza 2009. pH1N1 has demonstrated the pathology of Disseminated Intravascular Coagulation (DIC). We postulate that glucose starvation (brain fuel) and the loss of the detoxifying anti-oxidant effects (O2) from fresh blood may contribute to long-term neurological loss when the blood is clotting in the brain's capillaries. Case studies after the three pandemics of the past century bear evidence of memory loss, cognitive impairment in multiple categories of reasoning and recognition, partial paralysis and accelerated functional degeneration. Many survivors were “never the same again” according to their families and colleagues.
We're concerned that our public health officials appear to have memory loss concerning the documented effects of Pandemic Influenza in this century as they continue to label this present situation as "mild".
Children don't have heart attacks from mild Influenza. Mild Influenza does not harden arteries and then liquefy organs.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Does this pandemic H1N1 virus, PF11, display any characteristics that differ from Seasonal Influenza?
- Large Scale Direct Lytic Activity (Cell Destruction/Pneumonia) without Secondary Infection involvement
- Rapid Deaths
- Sudden Heart Attacks in 9 to 22 year old male and female victims
- Breathing Failure after overnight minor symptoms (22 year old student)
- Diffuse Alveolar Damage (DAD) and necrotising bronchiolitis (bilateral gas-exchange and air passage insult)
- Diffuse Alveolar Hemorrhage (DAH) with hemoptysis (bleeding from lungs)
- Acute Respiratory Distress Syndrome (ARDS)
- Heart Attack, Stroke and Pulmonary Embolism, 34 year old Athletic Male
- Acute Necrotizing Encephalopathy (7F) Comatose 8hr post ER release, Brain Dead Day 2 [PubMed, pdf]
- Acute Necrotizing Encephalopathy (4F) [pdf] with Sequelae
- Loss of Movement Control (Child clusters, Melbourne, Australia 2011-09)
- Bleeding into the Brain with Loss of Eyesight (5M)
- Lung Destruction requiring Double Lung Transplant (24M)
- Liver Destruction requiring Transplant (5M)
- Acute Kidney Injury (AKI)
- Acute Liver Injury (23F)
- Disseminated Intravascular Coagulation (DIC)
- Sepsis (Blood Infection)
- Multiple Blood Clots
- Multiple Amputations (23F)
- False Negative Testing results in more than Half of tested cases.
- Ability to Transmit and Grow in Summer Temperatures within Humans
- High Relapse Potential after Treatment and after Testing Negative, with recorded Death outcomes
- Long-Term Complications from Organ Damage
- Brain
- Heart
- Blood Vessels
- Kidneys
- Lung
Rapid deaths within 12-40 hours of first symptoms generally involving partial viral destruction of major organs including bleeding from the lungs are documented across wide geography (US, Europe, South America, Central America, Africa and Asia) in every age category. Brain infection and kidney damage features robustly across all age categories. Very striking are the sudden heart attacks in 6 year old to 22 year old females and males documented across the globe, with cases occurring after TamiFlu treatment or after being released from a healthcare facility based on achievement of a negative rapid test for a proud announcement of “cured” by the attending physician.
Testing negative is not a firm predictor of recovery. The relapse potential is very high.
Disseminated Intravascular Coagulation (DIC), a Cytokinic Dyregulatory systemic clotting of the blood with a resultant swing in the opposite direction (thinning the blood) has proven fatal in this pandemic and, though the term is recent, past pandemics have displayed very similar clinical outcomes. We have direct clinical reports from one suspect fatal PF11 case (unconfirmed due to no testing) involving necrosis at the skin level, creating a progression of black spots across the body prior to death.
Tracking studies have measured that a well-progressed neurological infection of Influenza leaves long-term loss of function in 25% to 50% of the cases. A retrospective study of California cases admits serious neurological sequelae in 1 of 20 diagnosed cases of pandemic influenza 2009. pH1N1 has demonstrated the pathology of Disseminated Intravascular Coagulation (DIC). We postulate that glucose starvation (brain fuel) and the loss of the detoxifying anti-oxidant effects (O2) from fresh blood may contribute to long-term neurological loss when the blood is clotting in the brain's capillaries. Case studies after the three pandemics of the past century bear evidence of memory loss, cognitive impairment in multiple categories of reasoning and recognition, partial paralysis and accelerated functional degeneration. Many survivors were “never the same again” according to their families and colleagues.
We're concerned that our public health officials appear to have memory loss concerning the documented effects of Pandemic Influenza in this century as they continue to label this present situation as "mild".
Children don't have heart attacks from mild Influenza. Mild Influenza does not harden arteries and then liquefy organs.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
What features does PF11 engage inside a human body?
PF11 moves fast, wears camouflage and is comfortable operating in almost any terrain.
At our institute, we categorise FirstWave PF11 alongside the H5N1 and the 1918 pandemic strains as an Interferon-Deranging, Rapid Replicating Virus strain (IDRRV). The similarities between PF11, today’s Avian Influenza H5N1 and the 1918 strains are quite unappealing, but must be communicated. The SecondWave viral strain cannot be characterised until we see a stable genotype in the coming months because this present virus is persistent in acquiring new genetic material. Although most Influenza-suspect pandemics / plagues that we’ve reviewed in history demonstrate marked clinical differences in the first and second waves, we prefer to measure rather than speculate on this “once in a century” event. Science measures. Measurement may only occur during or after an event.
This virus carries the genetics for extreme illness, sudden death and long-term sequelae (complications) for survivors . . . and PF11 has connections to advance genetically. The circulating strains have clinically demonstrated a destructive multi-tropism (6 major human tissue types at last count), an ability to temporarily deactivate the immune system (interference of a required early cytokine-mediated process) and a swift speed of replication. By having a “head-start” on the body after immediately blunting the immune system and then using the added feature of rapid reproduction, PF11 initially gains a solid grasp in the throat and lungs.
Then the multi-tropism, like H5N1 and 1918, gives the PF11 virus an ability to attack multiple organ systems individually or simultaneously creating a wider battleground inside the host than a typical immune system can manage, culminating at times in a fatal outcome. Many patients demonstrate no fever until after they have deeply progressed (50% - Chile, 33% - Mexico), showing that the first warning signal for Influenza may not occur. The virus has the binding ability to enter many types of organs and has now been documented as using the bloodstream for transport.
What is FirstWave PF11 doing today?
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Why should I care about Pandemic Influenza H1N1?
In the absence of a viable solution to a known future event, logic holds that we will work to Prevent the Event.
Today, we are each facing a potential high impact event. Our team has focused an extensive research project on Pandemic Influenza for 5 years, examining pandemics / plagues, measuring the available facts and associated data on the clinical and epidemiological outcomes and identifying mediation measures that predict success while spotlighting those that allow failure.
Our team, as of this writing, recognises a clear set of signals correlating to our predicted trajectory of a high-impact, pandemic influenza viral march. Investigation of daily genetic and clinical reports, including individual close scrutiny of many rapid deaths among the young, demonstrates a present trend matching numerous historical plagues. You have heard by now about the 1918 Pandemic, but you may not have grasped the weight of a plague so culturally impacting that the Influenza death count among service age young men was a primary factor in ending the World War.
In our estimation, a triple reassortment, multiple recombination-based Pandemic Influenza H1N1 (PF11) was less expected than an H5N1 Avian Influenza spread. However, the PF11 results appear to be very similar in many individual clinical outcomes to H5N1. Moreover, PF11 is much more concerning due to the rapid geographical spread and the suggestion of viral fitness-inducing conservation in the genetics, mimicking the 1918 Pandemic strain that killed 50 to 100 million people globally and destroying 70% of the population in some locations.
Our careful examination of the viral traits and the human biological response strongly suggests that the primary mediation measures (anti-virals and vaccines) being implemented today at the national and international level will be recorded in history as scientific errors when the post-pandemic data is reviewed. Our trusting children, the primary risk group, are known to not respond well to TamiFlu. A review study released last week in the British Medical Journal indicates that the complications from using TamiFlu in children outweigh any minimal benefit. Non-pharmaceutical interventions (NPI) that were proven in our country during 1918 and across the span of history are being downplayed or openly denied today. Those very same NPIs were recorded as essential in many response plans from 2004 until their recent redaction during the early phases of PF11.
Historical data proves that reducing caseload and spread early in a pandemic dramatically decreases future virulence and death peaks for many reasons including denying the virus the wide foothold necessary to recombine and strengthen. Our present national response is guaranteed to increase early peaks, established by mathematical models and observational data to produce a larger future death count. Reliance on faith in a vaccine that will arrive too late, match too little and seroconvert too few is removing focus on more practical actions that can be taken now to reduce the peaks early in the SecondWave.
We appear to have much to learn yet? Would the abundant observational facts assist?
If you care to continue reading, in this blog you will learn facts about PF11 relating to human biology, individual outcomes and population effects. Virulence, pathogenicity and transmissibility will be profiled at those three levels.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Today, we are each facing a potential high impact event. Our team has focused an extensive research project on Pandemic Influenza for 5 years, examining pandemics / plagues, measuring the available facts and associated data on the clinical and epidemiological outcomes and identifying mediation measures that predict success while spotlighting those that allow failure.
Our team, as of this writing, recognises a clear set of signals correlating to our predicted trajectory of a high-impact, pandemic influenza viral march. Investigation of daily genetic and clinical reports, including individual close scrutiny of many rapid deaths among the young, demonstrates a present trend matching numerous historical plagues. You have heard by now about the 1918 Pandemic, but you may not have grasped the weight of a plague so culturally impacting that the Influenza death count among service age young men was a primary factor in ending the World War.
In our estimation, a triple reassortment, multiple recombination-based Pandemic Influenza H1N1 (PF11) was less expected than an H5N1 Avian Influenza spread. However, the PF11 results appear to be very similar in many individual clinical outcomes to H5N1. Moreover, PF11 is much more concerning due to the rapid geographical spread and the suggestion of viral fitness-inducing conservation in the genetics, mimicking the 1918 Pandemic strain that killed 50 to 100 million people globally and destroying 70% of the population in some locations.
Our careful examination of the viral traits and the human biological response strongly suggests that the primary mediation measures (anti-virals and vaccines) being implemented today at the national and international level will be recorded in history as scientific errors when the post-pandemic data is reviewed. Our trusting children, the primary risk group, are known to not respond well to TamiFlu. A review study released last week in the British Medical Journal indicates that the complications from using TamiFlu in children outweigh any minimal benefit. Non-pharmaceutical interventions (NPI) that were proven in our country during 1918 and across the span of history are being downplayed or openly denied today. Those very same NPIs were recorded as essential in many response plans from 2004 until their recent redaction during the early phases of PF11.
Historical data proves that reducing caseload and spread early in a pandemic dramatically decreases future virulence and death peaks for many reasons including denying the virus the wide foothold necessary to recombine and strengthen. Our present national response is guaranteed to increase early peaks, established by mathematical models and observational data to produce a larger future death count. Reliance on faith in a vaccine that will arrive too late, match too little and seroconvert too few is removing focus on more practical actions that can be taken now to reduce the peaks early in the SecondWave.
We appear to have much to learn yet? Would the abundant observational facts assist?
If you care to continue reading, in this blog you will learn facts about PF11 relating to human biology, individual outcomes and population effects. Virulence, pathogenicity and transmissibility will be profiled at those three levels.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Subscribe to:
Posts (Atom)