Pandemic Influenza Trends and Issues

What Can Happen in 30 Days with Pandemic Influenza?

2010-07-27T01:19:00.018-05:00

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

2009-11-24T23:02:00.012-06:00

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

2009-11-23T05:14:00.012-06:00

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

2009-11-22T22:59:00.002-06:00

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.

2009-11-06T23:49:00.020-06:00

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

2009-10-08T11:14:00.022-05:00

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?

2009-10-08T05:44:00.015-05:00

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

2009-10-07T11:17:00.004-05:00

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

2009-09-29T18:04:00.028-05:00

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.

How Long Will the Pandemic Last?

2009-09-25T04:24:00.032-05:00

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, PF11_β, and a future tipping point, PF11_Ω, for ease of discussion. Let's agree that we must progress beyond that future event of PF11_Ω before the Pandemic will dissipate. (Glossary)

The distance between PF11_β and PF11_Ω 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 (PF11_β) and the metropolis of Worst (PF11_Ω). 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_>Ω, 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.

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

2009-09-24T01:29:00.010-05:00

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.

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

2009-09-15T19:13:00.020-05:00

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.

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

2009-08-29T17:31:00.015-05:00

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.

PF11 Trends & Issues, Mid-Term, Table of Contents

2009-08-25T14:46:00.009-05:00

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.

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

Environmental Factors

2009-08-25T04:21:00.011-05:00

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.

Where is PF11 going?

2009-08-25T03:38:00.020-05:00

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.

What is the Nation Level Response to PF11?

2009-08-25T03:27:00.006-05:00

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.

What part of our population is affected by PF11?

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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 GF_λ ). 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. GF_λ 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. GF_λ 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 GF_λ 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.

What human outcomes has PF11 demonstrated in these Early Waves?

2009-08-25T02:13:00.044-05:00

Last Updated 2011-09-08

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)
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. PF11 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.

What features does PF11 engage inside a human body?

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PF11 moves fast, wears camouflage and is comfortable operating in almost any terrain.

At our institute, we categorise FirstWave PF11 alongside the H5N1 and the 1918 pandemic strains as an Interferon-Deranging, Rapid Replicating Virus strain (IDRRV). The similarities between PF11, today’s Avian Influenza H5N1 and the 1918 strains are quite unappealing, but must be communicated. The SecondWave viral strain cannot be characterised until we see a stable genotype in the coming months because this present virus is persistent in acquiring new genetic material. Although most Influenza-suspect pandemics / plagues that we’ve reviewed in history demonstrate marked clinical differences in the first and second waves, we prefer to measure rather than speculate on this “once in a century” event. Science measures. Measurement may only occur during or after an event.

This virus carries the genetics for extreme illness, sudden death and long-term sequelae (complications) for survivors . . . and PF11 has connections to advance genetically. The circulating strains have clinically demonstrated a destructive multi-tropism (6 major human tissue types at last count), an ability to temporarily deactivate the immune system (interference of a required early cytokine-mediated process) and a swift speed of replication. By having a “head-start” on the body after immediately blunting the immune system and then using the added feature of rapid reproduction, PF11 initially gains a solid grasp in the throat and lungs.

Then the multi-tropism, like H5N1 and 1918, gives the PF11 virus an ability to attack multiple organ systems individually or simultaneously creating a wider battleground inside the host than a typical immune system can manage, culminating at times in a fatal outcome. Many patients demonstrate no fever until after they have deeply progressed (50% - Chile, 33% - Mexico), showing that the first warning signal for Influenza may not occur. The virus has the binding ability to enter many types of organs and has now been documented as using the bloodstream for transport.

What is FirstWave PF11 doing today?

For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.

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

Why should I care about Pandemic Influenza H1N1?

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In the absence of a viable solution to a known future event, logic holds that we will work to Prevent the Event.

Today, we are each facing a potential high impact event. Our team has focused an extensive research project on Pandemic Influenza for 5 years, examining pandemics / plagues, measuring the available facts and associated data on the clinical and epidemiological outcomes and identifying mediation measures that predict success while spotlighting those that allow failure.

Our team, as of this writing, recognises a clear set of signals correlating to our predicted trajectory of a high-impact, pandemic influenza viral march. Investigation of daily genetic and clinical reports, including individual close scrutiny of many rapid deaths among the young, demonstrates a present trend matching numerous historical plagues. You have heard by now about the 1918 Pandemic, but you may not have grasped the weight of a plague so culturally impacting that the Influenza death count among service age young men was a primary factor in ending the World War.

In our estimation, a triple reassortment, multiple recombination-based Pandemic Influenza H1N1 (PF11) was less expected than an H5N1 Avian Influenza spread. However, the PF11 results appear to be very similar in many individual clinical outcomes to H5N1. Moreover, PF11 is much more concerning due to the rapid geographical spread and the suggestion of viral fitness-inducing conservation in the genetics, mimicking the 1918 Pandemic strain that killed 50 to 100 million people globally and destroying 70% of the population in some locations.

Our careful examination of the viral traits and the human biological response strongly suggests that the primary mediation measures (anti-virals and vaccines) being implemented today at the national and international level will be recorded in history as scientific errors when the post-pandemic data is reviewed. Our trusting children, the primary risk group, are known to not respond well to TamiFlu. A review study released last week in the British Medical Journal indicates that the complications from using TamiFlu in children outweigh any minimal benefit. Non-pharmaceutical interventions (NPI) that were proven in our country during 1918 and across the span of history are being downplayed or openly denied today. Those very same NPIs were recorded as essential in many response plans from 2004 until their recent redaction during the early phases of PF11.

Historical data proves that reducing caseload and spread early in a pandemic dramatically decreases future virulence and death peaks for many reasons including denying the virus the wide foothold necessary to recombine and strengthen. Our present national response is guaranteed to increase early peaks, established by mathematical models and observational data to produce a larger future death count. Reliance on faith in a vaccine that will arrive too late, match too little and seroconvert too few is removing focus on more practical actions that can be taken now to reduce the peaks early in the SecondWave.

We appear to have much to learn yet? Would the abundant observational facts assist?

If you care to continue reading, in this blog you will learn facts about PF11 relating to human biology, individual outcomes and population effects. Virulence, pathogenicity and transmissibility will be profiled at those three levels.

For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.

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