Texas Fatality by County - pH1N1 Season 2013

Publish Date : 2014-02-27
Last Update : 2014-02-27

Texas Fatality by County - pH1N1 Season 2013

For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for pH1N1 Trends & Issues, Mid-Term.

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

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What Can Happen in 30 Days with Pandemic Influenza?

Last Updated 2010-07-27

30 days. One-twelfth of one year. A fraction of time.

What can happen in 30 days? Let’s recount one 30 day fraction in the history of one American city. You are welcome to call this discussion a precautionary tale, but only if you distinguish this precautionary tale as relying strictly on factual data.

Picture a stadium filled with families, over 12,000 souls . . . men, women and children, even a few strapping soldiers. But you don’t hear an orchestra playing or the vociferous clatter of youngsters cheering after their favorite player scores a point. No one is selling food or those great hats emblazoned with the local mascot because no one in any seat has reason to eat or to celebrate. Mothers’ eyes search the rows, praying that none of their children have entered the gates. Suffering children long for the tender mercies of their mother’s care, wondering why no one is helping them.

No one willingly came to this stadium; not a single ticket was purchased for the event. What we find is an entirely different scene. Slumped against each colorful backrest is an expression-less human being with no voice, suffocating under the weight of lungs being destroyed by disease. 12,000 human souls with no uncertain outcome. A stadium packed to capacity.

Let’s begin on September 11th, but not in New York City and not in this century.

In an early review of a text many years ago, we were struck by the speed that a modern pandemic may blindside not only the public, but the leaders and the leading medical “authorities”. Most who follow epidemiology understand that wars and military transport frequently describe the arc of disease movement. This particular matter at hand appears to have been sparked by one such situation.

What can happen in 30 days?

“Shock and Awe” as a military incursion terminology palls in usage to the documented fatal and maiming effects of a rapidly spreading viral outbreak in a populated area. A transmittable, novel influenza virus reservoir is an ongoing, bottomless battery of unguided missiles striking the helpless. The citizens, often relying on the “experts”, are generally guided into their least optimal health position, parked and left there while the public health “authorities” scramble, building press releases touting the success of this campaign or that hygiene program.

We will see the parallels between 1918 and today in this discussion.

Those purported “successes” are typically a paper chase used to advertise the idea of practical progress when little more than “more of the same” has actually occurred. Deftness and agility will not be found as hallmarks of bureaucratic institutions, then or now. But the survivors write the history and the dead speak little. Self-applause is extensive among survivors and is only rarely merited. However, those traces left by our dead may inform us if we measure the events carefully and impartially, if we refuse the cleverly crafted ambassadorial missives and inspect the funding and intentions of the “post”-action situation reports, in short, if we study the factual data, data from 1918 and data from 2009.

Let’s talk about today for a moment. Each of you has at least a hint of the nagging feeling that something is amiss, that the full report is yet to be published. Even in July 2010, activity that does not solve, that cannot work scientifically, has been somehow transformed by diplomatic public health advertisements into progress against the foe. Vaccination campaigns, originally admitted as failed due to low public participation (in a move for sympathy), have recently been widely touted as defeating the virus.

Manipulation of public perception is rife in this arena. Short public attention spans allow for that type of zero to hero transformation by the social messengers, all with the ease of flipping a press release to the mass media or slotting a thinly veiled, corporate position paper under the guise of a “scientific” study into a major academic publication.

As you have seen, a viral reservoir has no eyes for press releases, nor is a novel and rapidly emerging viral reservoir at all interested in “tried and true” solutions. The virus is unaffected by “All Clear” social messaging campaigns, even those geared to alternative media such as blogs, websites and other social networks that have been quietly funded and fueled by the bureaucrats. More of the same is rarely a solution when a novel problem presents.

Not even a monolith of messaging will create gravity, though the campaigns certainly impress a particular perception of gravity upon any but the most particular reader.

A novel viral reservoir like ΣPF11, also known as pH1N1, attacks and waits, then attacks and waits. Smoulder and spark; spark and smoulder until PF11_Ω is achieved. Is this a matter of conjecture or hypothesis? Not at all.

In this matter, the history collected by Gina Kolata allows us to hear the important voices of those lost in 1918, guiding us to reform our systems of thought and action. History affords us the luxury of mistake avoidance, but only if we give way to logic and fact.

Because the clues to today’s mysteries are frequently discovered in a careful reading of the past, historical facts are evaluated as input to our system of discovery. We’d like to thank Gina Kolata for her insightful historical research which she developed into book form in 1999 and published under the title of Flu: The Story of the Great Influenza Pandemic of 1918 and the Search for the Virus That Caused It. The dates reconstructed in this narrative are well documented in Chapter 1, “The Plague Year” and are fact-checked against the Philadelphia Department of Health's review of the 1918 Pandemic in 1976.

What happened prior to the 30 days?

A recap of the 1918 Pandemic is in order. 1917 smouldered, but was not closely tracked. The first wave was officially noted from a tourist area of Spain in February 1918 and spread throughout Europe for the next 4 months. That wave affected the war effort on both sides. The young and healthy were disproportionately ill generally 2 days after exposure with many suffering 3 to 7 days in bed and then a 7-14 malaise thereafter. Deaths occurred, but apparently not in a fashion that obliged officials to carefully count. In the US, a similar pattern occurred throughout late winter and spring.

The notation of a conspicuous prequel to the 30 days may well enlighten those following the course of the current pandemic. Specific attribution may not be made to any particular disease because records were not kept. However, Kolata does cite a detailed retrospective study completed by Gerald Pyle at the University of North Carolina concerning excess fatalities among young adults during 1918 across the globe. The study corroborates the second wave onset with a virus that continued to be contagious and then potentiated to a higher fatality rate. By statistical appearances, the virus genetically self-modified and became more pathogenic. Many died.

Of special interest is the fact that by August of 1918, the disease had caused substantial fatality in areas less affected in the first wave including a severe epidemic in India. Does that season parallel 2010? Today, we stand at 2010-07-26 with reports from India indicating a profound upswing in case count and fatality level. In a recent count of two days (July 21st and 22nd) within Pune, India, officials went to the expense of testing 7,800 people and placing 1,286 on Tami-Flu.

One city, two days. Late July 2010.  India demonstrates current genetic sequences that suggest accumulation of pathogenic traits.  Those same genetic markers appear across the United States and other parts of the world today.

On July 22, 1918, the Department of Public Health and Charities warned US health officials of the upcoming influenza spread into American cities from the strong waves in the Southern Hemisphere.

What happened next in 1918 is the basis of our precautionary tale, a tale of one city that was multiplied nationwide in the ensuing months.

In their official publication just prior to September 1918, JAMA (The Journal of the American Medical Association) got caught in their bed clothes when they proclaimed the Spanish Flu to be of no more concern than ordinary influenza. For lack of a solution, they advertised that no problem existed.

September 11, 1918: Several members of the US Navy reported ill from the Philadelphia, Pennsylvania Naval Yard. Influenza began to spread in the city. On September 18, officials began a public campaign against “coughing, spitting and sneezing”. The Philadelphia Inquirer ran an article on page 4 entitled, “Spanish Influenza Sends 600 Sailors to Hospital Here, No Concern Felt,” on September 19th directly communicating from the officials that the public should not fear, “spread to any great degree among citizens.”

Two days later, September 21, the city made influenza a reportable disease and the local newspaper ran a story undoubtedly inspiring public confidence. Scientists had declared that Pfeiffer’s bacillus was the causative agent of influenza, encouraging the idea that medicine was progressing rapidly to a solution.

Then, as now, printed declarations were not effective against disease spread and disease mortality. In a show of mis-guided patriotism, local and federal officials invited the public to gather for a Liberty Loan Drive. 200,000 people attended that parade on September 28.

October 1, 1918. Three days after the parade and ten days after the proclamation of scientific progress, doctors reported 635 new cases of influenza in Philadelphia, a very serious case count for a disease phrased as “ordinary” by JAMA. Additionally, the count was very likely an understatement due to capacity situations throughout the city. Medical staffs were over-burdened with care at that point and could not accurately report. In a “too little, too late” effort, officials banned all public gatherings on October 3rd.

All the wild horses had exited all the corrals in the city, but the authorities busied themselves with closing the gates and issuing more mollifying proclamations. Those proclamations not only fell on deaf ears, the words toppled into the mortuaries and graveyards onto the dead ears of the citizens that these authorities had been trusted to protect.

In the seven days ending October 5, 1918, Philadelphia reported at least 2,600 deaths. Students were recruited to serve as medical corps. On October 9th, over 4,000 new cases were counted in 24 hours. The city arranged 10 emergency hospitals. For the week ending October 12, 1918, the city reported 9,500 more deaths. The 250 strong nursing staff of Philadelphia General Hospital reported totals of 125 ill with 15 dead. A record 759 deaths of citizens were reported in one day on October 10, 1918.

What did happen in 30 days?

In Philadelphia, Pennsylvania during late 1918, the equivalent count of a packed stadium died of an influenza disease wave in one month. Over 12,000 people on official record suffered and left this world, most in the final two weeks of the period. The Case Fatality Rate for those who received medical care at a hospital was roughly 33%. During that pandemic influenza wave from September 1918 to March 1919, approximately 16,000 people died in Philadelphia.

What have we learned from those deaths in 1918, from the deaths in 2009? Was 2009 the parallel to 1917 and the first wave of 1918?

At GeneWurx, we have documented the persistent hyper-morphic behaviour of the pandemic reservoir since April 2009 and the recent concentration of Avian Influenza genetic changes onto the human influenza strains. The present series of accumulated changes demonstrate that this virus is far from stable and is positioned for additional waves with genetics predictive of higher mortality and long-term sequelae.


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.

The Overblown Cytokine Storm and 225G from 1918

225G is not new and this "Cytokine Storm" phraseology is overblown.

The public perception of 225G and the media linkage to hemorrhagic pneumonia is new. 

These Hydra Effect viral backgrounds carrying 225G within ΣPF11 are, in fact, very dangerous strains for what they are doing now and, more importantly, for where they are going . . . no question exists about that risk tendency.  The only question is why hasn't the science community driven the clinical linkages to the forefront before this week?  Fatal outcomes have been documented on record since July in multiple cases from Brasil.

Obverse speculation is also dangerous, especially risky when speculating based on poorly defined terms.  Banter and rant occur with much vitriol and then everyone who needs the data stops listening.  Few conversations are more demoralising that the ones where you have no anchor point on the major terms.

A primary topic of concern is Cytokinic Dysregulation.  Reliance on inspecific phrases like "Cytokine Storm" in the media will only continue to misinform the public on a process that is far less understood than the lead investigators would like to admit.

All of which returns us to the basic categories:

• What we do know?
• What we don't know?

What we do know?

Now that 225G matched clinical data is available, however limited, a potential correlation is being drawn on lung tropism. The standing bench studies, including the Palese and JKT team collaboration in 2006, detailing variant tropism based on differential HA reception at α2-3 and α2-6-linked sialic acids evaluated correlative to aa225 lend evidence to the concept of deep lung involvement though the experiments were conducted by varying permutations of aa190 and aa225 on 1918 variants.  Whereas, we stand in 2009 with quite different genetics that require cross-validation prior to citation with applicability to PF11.

Tissue type targets are compelling studies and this particular superarray protocol may prove even more useful on PF11 than 1918 samples.  We note that though 1918 and PF11 now share 190D and 225G, that all 1918 public sequences show 206S.  206T continues to emerge and conserve regionally in PF11.  All 225G bearing strains after April show 206T, except the July CatNS1706 and the undated Vladivostok01.

Reproducing the glycan microarray procedure with the contemporary and ideal dataset including Brasil and Catalonia may bring a tigher focus onto today's issues.  We couldn't ask for a more balanced set of control factors with Catalonia offering sequences less than one week apart demonstrating both important pairings: 206S/225G and 206T/225G . . . a bench review made to order.

We also do know that a proper immune response, that is a timely and regulated innate immune response, is not occurring in certain of these patients. When the n +1 generations of the virus progeny begin to lyse the host cells, that failure of innate immune function to have responded early leads to an undetected and massive viral load due to the rapid replication trait of PF11. The cell detritus and the density of moving viral particles elicit a host-driven, limited “self-destruct” series of events because the multiple levels of early detection parameters have been bypassed leaving the core essentially defenseless.

What we don’t know?

Much of what we need to know today about Cytokinic Regulation is yet to be studied. 

The systems of feedback loops are extensive with individual effectors often having multiple functions, in some cases, opposing functions.  So please bear in mind that we are looking into an instantaneously self-modifying system that not only self-revises the systemic parameters, but recruits and removes players in the middle of the game and then encourages them to change sides without even changing jerseys.  And to top the difficulties, Heisenberg applies.  Tighten down the screws to look at one molecule and his best friend will no longer stand anywhere near him, though they were conversing with verve before we attempted to measure.

That disclaimer in place, you may still note important aspects of proper cell-to-cell signaling systems from the following discussion as you keep in mind that the presentation is highly compressed for educational purposes.

Though Cytokinic Dysregulation is occurring in most PF11 cases at some level of interchange, the 225G and 225E strains may potentially interfere at a more profound level with the early innate response by amplifying the PF11 conserved effect of the NS1 paired Glutamates at aa96 & 97 that constrains the IFN synthesis instantiation cycle by binding TRIM25, an early catalyst to RIG-I ubiquination.  Influenza bench researchers don’t know exactly where the failure is occurring or at which combination of cell-to-cell signalers in PF11 or the PF11 225G strains.  Until those identification studies are designed, undertaken and reproduced, discussion at this point is stark hypothesis based frequently on the speaker’s sheer lack of present research content mastery. Apparently, saying “I don’t know?” and then returning to the bench to design and gather a proper foundation of data is a skill rarely encouraged in our “Science for Hire” era.

Our team is unimpressed that the wider science community, with such broad analytical skills and exceptional equipment, relies on pseudo-explanation, this cloud of diversion, by invoking the “Cytokine Storm” phrase.  More than 20 well-characterised and 100 identified distinct molecular signal functions are at work in the early immune response, including cytokines, but not limited to that class of communicators.  Tagging a term for PR purposes is much simpler than tagging a molecule for tracking, but you received your instruments because you can think, not for your ability to improvise inventive talk.

Think.

Eighty billion dollars in research should arrive at a better answer with higher specificity and actionability than the blanket “Cytokine Storm” tome.  Data and procedure discover Facts.  Anything less is purely Public Relations.

Our team continues to hold an opinion that we first described in 2006 concerning Cytokinic Dysregulation and the NS1 protein of Influenza.  Succinctly, the viral ability to suspend innate immunity for up to two days post-infection, as characterised by Mount Sinai this year, prevents the early and required pro-inflammatory Cytokinic Response to viral detection.  That blunting, taken in conjunction with detailed studies around adaptive immunity, may result not only in failure to clear the virus from some patients in a timely fashion, but also in failure to produce a useful quantity and competence of memory T-cells and Ab.  The early failure to clear a rapidly replicating virus like H5N1 or PF11 results in a frank trauma to the immune system when the first generations of viral progeny lyse their host cells after being undetected and flood the tissues with virii and toxic cell detritus.  That disorderly surge of human and viral proteins en masse activates a late and cascading pro-inflammatory response that frequently fails to down-regulate properly.

This explanation is contrary to "pop" science reports that a normal and robust immune response over-generates cytokines and attacks self indiscriminately.  We hold that, by the time the virus has lysed thousands of cells and released millions of virii, that most adjacent tissue areas are "fair game" for immune response due to toxic cell detritus and viral travel.  That flooding of antigen and waste matter, widespread and instantaneous to the immune system, may further interact with some virally induced derangement of the alternative pathway of complement and generate the intensive up-regulation of signaling, pro-inflammation cascades and the resultant tissue damage described in the clinicals as DIC, DAH and ARDS.

Ergo, the findings of massive tissue damage on necropsy is the result of a failed early innate immune response, not a normal robust response.  A normal, properly up- and down-regulated robust innate response clears infection in more than 90% of various infections (viral, fungal and bacterial) and proceeds to generate Ab in short order via the adaptive arm of immunity.

When viral hosting cells properly detect intrusion, flag themselves for apoptosis (cell death) and are then assisted by cytotoxic T-cells, the injection of fragmentins via perforin "tubes" induces an endogenous apoptotic program literally cutting DNA into 200 base multimers (fragments) and eventually condensing chromatin.  That organised molecular result is far less inflammatory and far more useful for antigen identification than the disorderly outcome of a virally "exploded" cell.  Now you can see why proper genetic expression during each phase of this programmed cell death guarantees a lower pathology than the chaotic and toxic outcome of lytic host cell destruction resulting from viral NS1-induced, delayed genetic expression. 

A confluence of PF11 traits (failed early detection, multi-tropism and rapid replication) against the host-pathogen interface may force a limited "self-destruct" in the host upon eventual detection in an attempt to save the organism.  That limited "self-destruct" is not the desired outcome of a normal and robust immune response, but occurs due to a failure of the immune system to detect and respond early in the process.

Timing matters. 

Individual viral genetics and individual host immune genetic expression are primary effectors that must no longer be discounted under the clouds of some nebulous "Cytokine Storm" or Mysterious Mutation.

Cytokinic Dysregulation is wider than immunity. 

Johns Hopkins School of Public Health estimates that half of all Americans suffer from chronic illness.  150 million in one country.  Cytokinic Dysregulation is a very real situation occurring daily in the lives of a significant group of chronic illness sufferers as a component of asthma, chronic joint damage, digestion tract insult, diabetes, endocrine dysfunction, vascular inflammation of undisclosed cause, detoxification pathway insult (renal/hepatic), immune dysfunction, obesity and numerous sub-clinical, but accumulative pathologies.  Each of these suffering individuals is at an increased PF11 risk based on the types and levels of cell-to-cell signaling failures across their systems.

So let's stop talking about this overblown "Cytokine Storm" and begin candid discussions with specificity about causality.


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.

Hemorrhagic Pneumonia: CDC Issues Alert to Physicians for Heightened Surveillance

This report is preliminary and will be reviewed for corroboration as the official documents become available.

Although confirmation is not yet complete on this item, the American CDC has apparently issued an alert to physicians concerning hemorrhagic pneumonia in the United States.  The North Carolina Medical Society has published a description of the CDC alert and has identified a reporting point in their state. 

The PF11 viral reservoir is extending and revising in important areas concerning trait enhancements.  Since the early part of the pandemic, this viral reservoir has exhibited exceptional abilities to damage the human body due to Influenza Flux; however, we may now be moving into deeper water if this alert is validated.  While no one may say exactly where this virus is going, we are able to track the genetics and the human clinical outcomes correlated to those genetics.

Deep lung involvement appears to be supported as a trait enhancement via the D225G polymorphism on the viral Hemagglutinin.  225G is not a new incursion into ΣPF11, but now paired with 206T is becoming a higher concern.  The US and Mexico demonstrated 225G with 206S early in the pandemic.  206T, as predicted, has now become fixed or consensus in many geographies.  Recent studies on the Ukraine, Russia, China and Norway show 225G in the Hemagglutinin to be circulating alongside the dangerous 225E and the wildtype 225D bearing strains.

Heightened surveillance is being required from the medical community while the general public is receiving communications with an alternate message?  Moms and Dads will want to get ahead of this issue by gathering accurate and complete information as soon as possible.  PF11 will be with us for a long time.

Gather and Solve.

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.

TamiFlu Resistant Cluster of 4 at Duke Medical Center, North Carolina, US

As the thirteenth TamiFlu Resistant sequence was released publicly by Italy demonstrating a hypermorphic progression to another novel strain, the Duke University Medical Center contemporaneously described a group of patients acquiring PF11 Influenza in an isolated ward of their hospital.  Four of the patients from this isolated ward were found to be infected with a TamiFlu Resistant strain.  Transmission is suspected and may be verified by publication of all sequences from that ward over a time period covering two weeks prior, during and two weeks after the event.  Three of the four patients had fatal outcomes (75%).

Antiviral resistance has now been documented in 50 instances, when investigated, including North America, Europe and widely across Asian countries.  The 13 sequences that are available are, for the most part, incomplete for research into cross-segment linking of Hemagglutinin (HA) polymorphisms correlative to the antiviral-resistance conferring H275Y Neuraminidase (NA).  Investigators are left at bare benches staring into empty beakers waiting for catalyst. 

The resistance marker is now found on numerous backgrounds potentially demonstrating an ability to travel as a silent sub-species.  Up to this current stage of the pandemic virus progression, this resistance trait, in several cases, appears to arise in an individual as the prominent super-infection (co-infecting silent H275Y PF11 strain) based on some unidentified characteristic of the individual's host-pathogen meshing, including immune dysregulation or other existing Cytokinic Dysregulation morbidities.

Publication of the remaining 37 sequences, including the Duke University Medical Center clinicals from this prestigious research institution, may benefit worldwide understanding of the efficacy and longevity of currently promulgated mediation measures for PF11.

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.

Ukraine Expected to Surpass 1 Million Infections in Only 10 Days; the U.S. took 10 weeks.

A day in the Ukraine is like a week in the United States . . .

for Pandemic Influenza spread, that is.

On October 29, the Ukraine officially reported an uptick in Influenza-like-Illness (ILI) and a surge in hospitalisation.  Concomitant deaths were reported from hemorrhagic pneumonia and four doctors were soon included in the fatality pool.  The situation was recognised and immediate action was taken.  Very early in the process, a nationwide alert was issued and the situation came under central management.  In mere days, the healthcare infrastructure was stressed and supplies were exhausted.  Resources have been redirected and escalations continue.  Citizens are cutting their own clothing to make masks.

Tomorrow will mark 10 days since that spark. 

Based on the most recent daily case increases trending upward from 32% to 37%, we expect the Ukraine to surpass one million reported infections by Saturday afternoon, November 7, 2009.  If the reporting trend continues with the weekend and the rates hold, just under 1.2 million cases will be cataloged.  We cannot speculate if a report will be made publicly available on Saturday.

The official reports from the United States indicated that 1 million infections were reached in late June 2009, 10 weeks after the initial sparks of PF11 began to ignite the populations and burn through the major cities.

The Ukraine progression defines a new method for PF11.  In the early phases of any catalyst event, all statistics are suspect, but the trending is often useful.  Official numbers, upon some minor calculations, demonstrate that the daily increase in hospitalisation and deaths is rapidly climbing.  Yesterday the increase in daily hospitalisations was 20% and today the increase is 37%, almost a doubling in day-to-day velocity.  Yesterday the increase in deaths was 17% and today the increase is 42%, more than a doubling in day-to-day velocity. 

Data reporting cut-offs are always at issue in these early inflows, but over the next two weeks an exacting pattern will be defined.  Researchers must be given access to the raw data to determine causality and vectoring.  A significant library of samples has been received and sequenced in a prestigious European coordinating laboratory.  No data at this time has been released. 

Timeliness is essential when a virus has marched to 1 million suspect cases in only 10 days in one country of less than 50 million people.  1 of 50 ill across 10 days.  Clinical and environmental data matching the sequences will be critical to deduce and weight the parameters driving this regional escalation.  Those who will writeoff these flashpoints as medical infrastructure failures and sub-standard housing problems endemic to the third world are not intellectual Titans.  A pandemic is by definition unpredictable in phase shift timing and degree.  To discount this Ukrainian surge in suffering to poverty is simply academically irresponsible in a pandemic era.  These data points requested, if made public today, may save the lives of many in the area and exponentially more in the coming months around the globe.

The Ukraine is bordered by the countries of Russia, Belarus, Poland, Slovakia, Hungary, Romania and Moldova.  The southern area of the Ukraine is involved in several bird migration routes being bordered by the Black Sea.  Sequence examination of late summer specimens from these bordering areas and Eastern Europe demonstrates a trend equal to the United States with a significant Hydra Effect and substantial Antigenic Diversity delivered via Influenza Flux.  US sequences certainly match and even advance the polymorphisms in Eastern Europe and these border nations.

Our studies clearly demonstrate a one to three week lag at maximum in transport time and acquistion into new geographic areas of trait-enhancing genetic material within ΣPF11.  The stage is already set with similar sequences existing in most parts of the world.  225E has continued to penetrate in dozens of nations and is a factor in our present working hypothesis for this Ukraine spark. 

If the Ukraine has variant genetic specimens, the information is primary to world health.  Singapore was recently courageous enough to release 600 sequences that widely demonstrate movement in the reservoir.  Only an immediate evaluation of the full dataset of Ukrainian sequences and matched clinical information will provide countries the opportunity to prepare if this incident does mark an inflection point or catalyst event in the pandemic.

Is the US only one cold winter week from the situation today in the Ukraine?  Is the base of Pandemic 2.0 now widening in countries that have some point of susceptability?  If so, the landing strips are presently in place for these new polymorphisms to land on the existing PF11 strains in every basic geographic area of the world. 

We may all be one week from seeing a million new cases in our homelands or, worse yet, watching 2% of our population stricken in only 10 days. You do the math for your nation and then decide if we need data transparency and academic honesty.


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.

Use Low and Slow Exposure to Make Hungry Antibodies Fast

We produced this article on 2009-05-03 for members of our community in response to questions surrounding the then epidemic which soon became PF11.  The information remains useful as a general guide though the Hydra Effect is more pronounced today.

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As the number of PF11 infections increase within a community, the average newest-exposed or most recently exposed individual in the population will have multiple and, more importantly, persistent viral exposures, significantly more than the individual effect early in the pandemic.

As an epidemic grows, the NEI (Newest Exposed Individual) and their naïve immune system will initially be presented with a substantial particle count from a multitude of variants.  The virus will have made moderate adaptations to the new host, humans, and may, therefore, be more capable due to Influenza Flux.  Many labs have now demonstrated that passage of a novel virus through a new host and / or new host tissue type will lead to selection for host-matching genetics.  Upon this more substantial initial exposure, the NEI’s immune system will naturally have an immediate requirement to mount an innate response and, if successful, to subsequently mature a separate line of antigen-matching B cells for each variant strain of community Influenza (PF11 Hydra Effect).

A separate and important consideration today is that much of the population is immune depleted due to genetic damage and may be missing significant feature functionality in the cell-mediated and humoural responses.  Any heavy taxing may overwhelm the system of the immune-suppressed.

As the boundaries shrink between the non-exposed and the exposed, we may see a higher death rate among the NEI population because their Multiplicity of Exposure and total intake of infective viral particles will be high and variant.

We’ll now examine the idea strictly on a particle count example that is tempered for ease of communication.  These numbers, though simplified, are conservative.

Early in any epidemic, presume that exposed individuals get 1,000 particles to start an infection.  Later individuals will have at least a dozen of their close community who are infected, thus, 12,000 input particles.  Influenza delays and partially disables innate response, so 12,000 input particles is far worse than the small number may seem.  The synergy of 12,000 initial virions attacking a body may have a stultifying effect on immune response, especially on a delayed or late stage immune response. Twelve thousand particles each entering 1,000 on the copy machine within each infected cell may result in twelve million virions circulating freely in one replication cycle, certainly in less than a day. 

Your body is doing a lot of heavy lifting for an unappreciative guest.

Bear in mind that even the early specimens from ΣPF11 have been found to replicate 1,000 times faster in mammals than standard H1N1 Seasonal Influenza, so our very simplified example is vastly underplayed from the reality of what actually occurs in the human body.  Now that the trait-enhancing genetic marker of PB2 E627K has been identified across several geographies in this reservoir, we can expect the additional increase in replication speed to become fixed.

I’m not so sure that anyone’s humoural response can make the required 12 million antibodies for the dozens of genetically variant inputs that will be part of that initial 12,000 particle exposure, at least not in a useful timeframe.  Due to proximity and transport requirements, the NEI may need to make 60 million or more antibodies to accomplish neutralisation of that initial 12 million Influenza variants.  A properly regulated, innate immune response will always be the driving factor in successful clearance of an IDRREAV like PF11.

Then you have the Elimination challenge.  Without an early and powerful macrophage and inflammatory up and down-regulating process, any Cytokinic Dysregulation due to delayed cell-mediated immune response may leave the tissues filled with plasma and the small blood vessels effectively clotted closed, setting off another chemokine cascade to flood the system with anti-clotting agents (DIC).   A well-timed and even response is essential so that elimination may occur on a manageable schedule.

Remember that three phases must be fulfilled sequentially to clear any toxin or pathogen from a biological system.

1. Detect
2. Destruct
3. Eliminate

Failure to operate at maximum potential during any stage means practical failure of the entire system.

Initial exposure reduction may be noted as the most important factor in reducing Influenza severity in a previously healthy host individual.  Slow and Low Exposure protocols ensure that your NEI (n+1) are provided the greatest opportunity for survival and reduced severity.  Communities will fail or succeed in this pandemic based on their Multiplicity of Exposure.  In this pandemic, choices made by each individual may have long-term health implications for that individual and for their community.

How do we establish a Slow and Low Exposure protocol?

In the event of a rapidly replicating Influenza virus, a community’s highest priority must be on social distancing to reduce the number of exposure episodes and the per exposure viral count.  A prominent secondary priority must be to supply the community members with the materials, catalysts and protective time umbrella necessary to make genetically accurate antibodies in a sufficient count to neutralise and defeat those new strains of Influenza.  These two priorities when executed in tandem will create the Low and Slow exposure that allows members of a community to make accurate antibodies fast.

Everyone will eventually be exposed, though not everyone will display outward symptoms.

Each exposed and infected individual becomes a risk at some point to others in the community due to viral shedding.  The initial symptomatic host (index = n) within a community (family, workgroup, school, day care, etc) will be forced to rely almost entirely on innate immune function to overcome a rapidly replicating virus.  A weak innate response puts that individual in the unenviable position of being a rapid viral shedder.  The first exposure in a community is a sentinel to the others.

On the other hand, any subsequently exposed individuals [(n + 1), family members, professional peers, fellow students, et al] may have another route if they are properly managed and supplied.  If the remaining community (n+1) is following hygiene and social distancing protocols to reduce total exposure episodes and viral concentration (per exposure infective particle count), those members may discourage the rabid community burn and promote a Low and Slow Exposure.  Given the additional time due to the lower total infective particle input, the immune systems of the (n+1) individuals may have the opportunity to produce an array of vibrant antibodies before the virus manifests an extensive reproductive cycle and attains the minimum viral count required to produce interior spread and outward host symptoms.

An early and robust innate response to PF11 may be followed by an equally broad antibody build.  That early response, in sufficient numbers, controls the virus in the host and reduces viral shedding, limiting further community illness.  The antibody build, if competent, provides an additional memory function for that individual’s future exposures to genetically matched viral assaults.

Everyone will be exposed.  Work for safety in your community by making your exposure Low and Slow to build hungry antibodies fast.



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.

Can My Child Be Re-Infected If They've Already Suffered from Pandemic Influenza H1N1?

Georgia Mother and Her Children Infected Twice with H1N1

Many cities around the world are reporting re-infections, including US geography in and around Georgia and New York.

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Does an antibody set from a previous infection protect me?  Not always.

Under what conditions do my antibodies protect me?  An antibody response is very protective if timely, in high quantity and matched to the intruding virus.

Viral strains change and PF11 is changing rapidly on the areas that the human body uses for recognition.  If you were trying to identify a villain that you only saw once from the rear, then you’d have to use the clothing as your key. The villain knows that you only saw his clothes and not his face.  Will the criminal change clothes?  Yes.  Will this virus? Yes.

For some reason, people have been led to believe that “getting” PF11 now will be an iron-clad protection from later versions of the disease.  Medical professionals seem to rely on this thinking though their training demonstrates otherwise.  We do have a new Influenza season every year and they do see many patients more than one time in a season.   They do create a new vaccine every year and that vaccine does fail to match or fail to seroconvert much of the time.  They do know that Influenza is variable, but they don’t realise just how variable because they haven’t taken the time to study the ΣPF11 genetic sequences.

We received a response from a friend who is a medical professional noting that her child had been exposed from an extended family member, developed symptoms and appeared to have fully recovered.  We rejoiced that they had been spared significant suffering, but were concerned about the triumphant tone of the message.

Busy people sometimes do not regard the facts well unless the facts fit into their busy schedule.  In fact, busy people sometimes fail to put their own knowledge to work in their own families?  A virus like PF11 does not care about your schedule.

We responded with facts about this particular unprecedented pandemic:

Are you doing anything to ensure that all of you are developing a robust antibody response over the next 21-30 days?  Remember that due to weakened host immune responses a strong percentage of people who are exposed will not seroconvert to a fully protective antibody profile.  Even an individual who does build a basic profile will face future PF11 specimens that have escaped the antibody profiles in that individual host and host family.  That future specimen could occur in less than a month from the initial infection due to the observed PF11 enhanced genetic acquisition trait and the ample circulating diversity in any single geography.  I refer you to the Three Time Loser in 1918.  If the host is traveling, then multiple exposures to variant antigens are ensured.

Maintaining a properly regulated innate immune function is extremely important even after an individual appears to have successfully recovered from the initial exposure cycle.  The antibodies created, if they do seroconvert a protective set, can only be called into action via the initial innate immune response.  The virus must be recognised by the body before any adaptive immune response will be mounted.  A properly regulated innate immune response serves that detection function, acting as a coordinator, determining if matching antibody exists and calling it into action.  Secondarily, a significant count of children and young adults are on file as having appeared to recover and then relapsing to become fatal cases.  This PF11 virus may quiesce the immune system at any phase, early or mid-stream.  The relapse potential is a fact with this viral reservoir.

Influenza Flux between swine, bird and man creates a mismatched host-disease interchange that is highly variable in outcomes.


Succeeding in Round 1 against this virus is great, but now the virus knows that you can block a left jab and will try something new.  As PF11, under the cover of cold weather, learns more about the North American hosts, PF11 will exploit the weaknesses just as the reservoir did in South America in July and August with more than 1,000 deaths in Brasil alone.

Diligence in the Round 2 will determine our success.  You are in a 15 round endurance match.  This virus is well-trained and well-stocked in his corner.  Will we stay on our toes and move one step ahead of the virus or will we rest on our heels leaving our chin exposed for the knockout punch?

Each adult will decide for themselves, but remember that the children are dependent on the adults who head their families and their communities to decide for them.



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.

US Passes Thousand Death Marker prior to Influenza Season with 1,197 Confirmed Deaths

1,197 Confirmed Pandemic H1N1 Deaths before the Influenza Season begins in the United States and we stopped testing and officially recording most cases in early July, more than 10 weeks ago.

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.

E627K from July Discovered Retrospectively, Tied to Vacation Island off the Netherlands in Diabetic Patient and Adolescent Female

Though the sequences have not been released, the team at Erasmus MC in Rotterdam has done us all a great service by providing an early report of 627K in the Netherlands. 

The multiple cases all vector from visits to a popular vacation island between July 13 and August 9.  Two of the cases do not appear to be related via direct contact, potentially indicating an endemic and silent spread of a minor PF11 population carrying the human-fit virulence factor 627K in a sub-clade that may match the major circulating sub-clade there but for the Lysine recombination.  Ten of twelve (83%) sample specimens from this geography fall into this sub-clade indicating the potential for dominant circulation in that area.

As this release of information via Promed is very limited, additional evalution and insight will require amendment and revision to this article as the matter is clarified on several accounts, including specification of the E627K sequence count and the various ratios confirming the certain Hydra Effect demonstrated in the study population.

In our reading, 4 distinct cases are discussed in the Osterhaus release. Which two of the four are described as having the E627K is questionable and will determine the H2H transmission assumptions.  The researchers may have mentioned “two patients” because the family contact and the younger sister may have been directly evaluated by them in a clinical setting?

• Male Diabetic who may have shared activities with ill female camper, onset 2009-08-09
• Female camper, onset after returning home 2009-07-20 
• Female family contact of ill camper, onset after camper returned on 2009-07-20
• Younger sister of female family contact, onset 2009-07-23

This highly interpretive post is preliminary based on inconclusive language in the press release.
No mention is made of the correlating PB2 virulence of aa701N and aa703K at this time in the information released.  We suspect these to be absent due to the non-fatal clinical outcomes; however, confirmation would be useful.

As the samples were examined retrospectively, little new observational evidence will be forthcoming.  Rational projections due to this 627K mid-Summer emergence in the Netherlands and the late May emergence in Shanghai71T could cause us to expect a geographically-dispersed, wild-type sub-population carrying this virulence factor.

Tenacious sub-clonal evaluation of current sequences in the United States will likely indicate mixed peaks at the PB2 residue coding for the Lysine at 627.



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.