2009-09-25

How Long Will the Pandemic Last?

The Road to Post-Omega PF11

How long will the Pandemic last?

Process: Predictions involving the outcomes of unprecedented or entirely new events must utilise theory.  Very few outside the scientific community revel in the joys of Theory, but today you may come to appreciate the practical value of theoretical reasoning.  Theory, the primary tool to explore anything unknown, generally begins with new tags or agreed definitions so that the discussion may embark.  The present framework of discussion, of theory, around PF11 appears to be lacking several important terms, specificity, control variables, causality determination and scientific rigour. 

So let's make an attempt to plant some markers and comport a discussion on one simple and important area of measurement, PF11 Timing.  Let's call today's virus, PF11β, and a future tipping point, PF11Ω, for ease of discussion.  Let's agree that we must progress beyond that future event of PF11Ω before the Pandemic will dissipate.  (Glossary)

The distance between PF11β and PF11Ω is unknown.

And that delta, that difference, will remain unknown until some point in the distant future when we can retrospectively measure the closing event. Today, we'll talk about the road that everyone will travel from this moment until that closing event.

The journey between the two points will be progressively inundated with higher levels of impediment to the traveler. The traveler may not declare an optional routing. Due to decisions made by others, the traveler’s only available option is to agree and undertake the journey as given.

We all are driving the only highway (ΣPF11) between this small town of Bad (PF11β) and the metropolis of Worst (PF11Ω).  We know that no one knows the rate of speed we are traveling because no speedometer may be calibrated for a non-uniform progression.  Measurement is incomplete for all practical purposes. Fits and starts will be the norm.  We also know that each family will be affected by various types of collisions along the way.  In the veritable infinity of infectious vectors, few will emerge without themselves, their family or some important person in their lives being impacted.  Density, proximity and movement guarantee collision in any bounded system and this system is distinctly bounded.

As the traveler succeeds in passing each mile with the almost certain collisions and if they are able to survive the increasing number of attack vehicles (recombinants from the Influenza Flux), the lost segments of road (poorly chosen mediation measures) and the dwindling availability of fueling stations, eventually they will arrive at a better place. Though PF11, this first city on the other side of Worst, is not the ultimate destination, any relief after that pandemic journey will be appreciated and any glimmer of light will be a sight for sore eyes.

Eventual arrival is the key concept. How long will this journey last and what must you do to eventually arrive are the important questions.

Someday long hence, you may rate this trip as “Somewhat Unpleasant” or “Utterly Devastating” depending on how well you’ve equipped your individual journey with actionable Knowledge and viable provisions. Though a fully intact arrival might be your goal, the most capable and well-Led travelers will realise that completion of this journey with only minor impact is a deep blessing because you’re going to need to see around corners to get there at all. While others planned your route straight through renegade territory, the responsibility now falls on you to cross this expanse of impediments and the ostensible rest areas are unprotected.

Renegades abide no law and a virus abides no social messaging campaign. A virus does not care and a virus does not feel. A virus just makes copies and reacts to the environment by acquiring new genetics. A virus escapes and evades. You are now being forced to drive your family directly into a hundred-mile wide, bone-dry forest in a three-year drought that has been primed by summer heat. From the moment you enter the expanse, you can feel the dryness of the stick wood and you know the logical outcome, but your route planners have given you no exit from this road. You can’t race this virus. One stray spark and everything changes.

On what type of journey do you wish to lead your family? Where on the scale between “Somewhat Unpleasant” and “Utterly Devastating” do you wish for your future rating to stand? Your actions today select your rating for tomorrow. This article provides you the initiative you need to act.

The route has been decided by our lack of determination, by our abdication of responsibility to untrustworthy people. Continue to Follow or Start to Lead, but be certain to load your vehicle well because your journey is beginning.

Glossary

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.


Please visit GeneWurx.com for insight into the latest published studies.

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2009-09-24

TamiFlu Shortage in Prime Risk Group Occurs Only 4 Weeks After School Starts

Children congregating in schools and universities appear to be the highest risk group for PF11 infection.  School has been in session for approximately 4 weeks.  Very little cold weather has occurred in the United States at this time.

Roche announced today that a shortage exists in their production of TamiFlu for children (liquid form).  The company advised pharmacists to grind the adult pill-based drug and adjust the dosage for children. 

Health officials say that priority will be given to those hospitalised.  If TamiFlu is effective only if used within 48 hours of symptoms and more than half of some populations do not present with the official case definition of fever, then few who are hospitalised will be within that 48 hour window.  Hospitalisation will primarily occur after significant viral replication time has passed (>48 hours) and the patient presents with incapacitating signals.  This prioritisation appears to be misguided given the Facts.

  • TamiFlu resistance is geographically widespread in PF11 as demonstrated in the sequence databases.
  • PF11 has not yet begun to peak. 
  • Public health officials expect cold weather combined with the school gatherings to spur the case count substantially.
These three material impacts on the pandemic combined with the early shortage of the primary mediation measure espoused by public health officials leaves the public with very few, publicly-messaged, viable options.

Please review our research section discussing proposed mediation measures for further information.

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.


Please visit GeneWurx.com for insight into the latest published studies.

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2009-09-15

TamiFlu Resistance Database Expands, But Remains Incomplete. Two Year Pandemic Predicted.

Many TamiFlu Resistant cases have been reported that have not been sequenced and deposited in the United States and worldwide. 

Dr. Jonathan McCullers of St. Jude Children's Research Hospital in Tennessee reported a TamiFlu Resistant case yesterday, along with 12 child ICU cases and one child death.  Dr. McCullers indicates "a tremendous rise in cases" which began approximately one week after school resumed, well within the 3-10 day incubation period that we predicted post-congregation.  Dr. McCullers maintains that we are in the beginning of a two year pandemic that will have multiple peaks.  We agree that a period of 13 to 24 months from March 2009 is well within the expected duration.  Considering PF11's current position in the inter-species Influenza Flux and the high genetic variance demonstrated by the Hydra Effect, the lower boundary of our estimate (13 months) is unlikely unless the Case Fatality Rate increases significantly because PF11 rapidly depletes the population of potential hosts.

23 clinical observations have been publically discussed as TamiFlu Resistant in recent weeks around the world and most are not yet sequenced and deposited.  These cases concur with many of the geographic regions having sequences on file that match current TamiFlu Resistant sequences but for the H275Y.  In other words, the genetic acquisitions were predictable and expected to occur upon a proximal donor with 275Y co-infecting a host in that region.  An opportunity to review the full diversity of the anti-viral resistant strains would allow determination if, in fact, a silent spread of human-fit and reasonably transmissible TamiFlu Resistant strains is underway at this time or if we are seeing the improbability of an extensive and accurate selection due to treatment that is currently being purported as an explanation.  Evidence exists tending toward a silent spread, including that a substantial list is described with very early sampling and detection of H275Y, prior to any acceptable period for de novo / selective revision.  A minor sub-population of 275Y may be incorporated widely into the PF11 reservoir at this time.

The two youth in early July attending the North Carolina summer camp either spread their PF11 version one to the other or were each infected from a common carrier with a parental PF11 275Y Neuraminidase as is evidenced by the co-factor SNP on the NA of their sequences coding for 223V, known to amplify the 275Y TamiFlu resistance in H3N2.

We would like to thank those teams who have placed their sequences on deposit at GenBank and GISAID for the scientific community to evaluate.  The NA and HA for TamiFlu Resistant A/Singapore/57 from 2009-05-30 are again downloadable from the European EpiFlu database as GISAID has thankfully been able to re-establish access to their data.

TamiFlu Resistance is indicated in typical PF11 fashion via a Single Nucleotide Polymorphism on Singapore57 coding for 275Y on the Neuraminidase. The sequence displays the following NA Quadruple Combination:

106I, 248D, 275Y, 286S

The following permutations are now represented on the nine PF11 anti-viral resistant sequences:

106V, 248N, 275Y, 286S = WA28, WA29, TX47
106I, 248N, 275Y, 286S = Osaka180
106I, 248D, 275Y, 286S = HK2369, Yamaguchi22, Denmark528, Hunan SWL3, Singapore57

Until the 2009-08-21 deposit of the two Washington sequences at GenBank, all 275Y TamiFlu-Resistant specimens on PF11 backgrounds were paired with 106I. Today we see 3 of 9 with 106V.

The addition of Singapore57 re-leverages position 248 to Aspartate (D) with 5 specimens versus 4 with Asparagine (N).  No TamiFlu Resistant specimen on file displays 286G as yet.

A more robust database of sequences would be useful to invigorate the scientific community and the public in navigating this distant journey.

An n higher than 9 may assist us to align.


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.



Please visit GeneWurx.com for insight into the latest published studies.

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2009-08-29

"Back to School" Early News Reports, including 25% Absenteeism

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.


Please visit GeneWurx.com for insight into the latest published studies.

GeneWurx.com

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.
  1. Why should I care about Pandemic Influenza H1N1?
  2. What features does PF11 engage inside a human body?
  3. What human outcomes has PF11 demonstrated in this FirstWave?
  4. What part of our population is affected by PF11?
  5. What is the Nation Level Response to PF11?
  6. Where is PF11 going?
  7. Environmental Factors
  8. Genetic Acquisition Point Studies
  9. Glossary


Please visit GeneWurx.com for insight into the latest published studies.

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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.


Please visit GeneWurx.com for insight into the latest published studies.

GeneWurx.com

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.

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 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.


Please visit GeneWurx.com for insight into the latest published studies.

GeneWurx.com

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.

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.


Please visit GeneWurx.com for insight into the latest published studies.

GeneWurx.com

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.


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.


Please visit GeneWurx.com for insight into the latest published studies.

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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?
  • 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
In the rare cases of death after a normal seasonal influenza infection, a secondary infection is generally the cause of expiration. A bacterium will have opportunistically overtaken the damaged lungs. PF11, on the other hand, has demonstrated the singular ability to kill from direct viral-induced lytic activity and the associated Cytokinic Dysregulation, rapidly destroying masses of cells of its own accord without the involvement of secondary infection. You will understand more about this ability when we cover the Influenza Flux topic, the dangerous period when Influenza is transitioning between species, the Hydra Effect and the gene progression details as you read the Genetic Acquisitions discussion.

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.


Please visit GeneWurx.com for insight into the latest published studies.

GeneWurx.com