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 PF11Ω 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.
Showing posts with label 1918. Show all posts
Showing posts with label 1918. Show all posts
2009-11-24
The Overblown Cytokine Storm and 225G from 1918
225G is not new and this "Cytokine Storm" phraseology is overblown.
The public perception of 225G and the media linkage to hemorrhagic pneumonia is new.
These Hydra Effect viral backgrounds carrying 225G within ΣPF11 are, in fact, very dangerous strains for what they are doing now and, more importantly, for where they are going . . . no question exists about that risk tendency. The only question is why hasn't the science community driven the clinical linkages to the forefront before this week? Fatal outcomes have been documented on record since July in multiple cases from Brasil.
Obverse speculation is also dangerous, especially risky when speculating based on poorly defined terms. Banter and rant occur with much vitriol and then everyone who needs the data stops listening. Few conversations are more demoralising that the ones where you have no anchor point on the major terms.
A primary topic of concern is Cytokinic Dysregulation. Reliance on inspecific phrases like "Cytokine Storm" in the media will only continue to misinform the public on a process that is far less understood than the lead investigators would like to admit.
All of which returns us to the basic categories:
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.
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?
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.
2009-08-25
Environmental Factors
Our recent research has opened the door to a new segment of correlated history on plagues that may have been incorrectly categorized as the “Black Death” in the Middle Ages. The presentation and progression in the FirstWave and SecondWave of several ancient plagues are precisely equal to Pandemic Influenza clinical outcomes. The predecessor data directly relates 5 plagues throughout the 1300’s to the 1918 pandemic.
Dr. Thomas Francis, Jr., in a seminal immune response work, On the Doctrine of Original Antigenic Sin, returns us to the history of 1485 and the "sweating sickness" of England, then onward to the 1743 pandemic called variously "Blitzkatarrh" and "the Blue Plague" precursing the 1918 speed of rapid destructive spread in the population and the effect of human skin turning cyanotic blue from hypoxia (oxygen starvation).
On a side note, we may have located the geological event, an earthquake, in the early 1300’s that created a very large inland lake in China from which a plague proceeded therewith and where other plagues have begun in the past 700 years, potentially including PF51 (as yet undeclared Pandemic H5N1) and this PF11 currently circumscribing the globe. That area of research continues to be under review though the field may lead to no new information as very little surveillance data is available to collaborate the concept.
Famines have been highly correlated to plagues throughout history. We postulate that malnourishment of metabolic qualifiers, such as Essential Fatty Acids, B vitamins and vitamin C, reduces the body’s ability to properly feedback after an initial virally-induced Cytokinic Dysregulation. The famished body is left with no nutrients / anti-oxidants to re-regulate the feedback cycle of the immune response.
Without question, the United States suffers and leads the world with a population of malnourished and yet overweight individuals due to the reliance on non-food, processed factory materials for sustenance. An overweight human is at high risk for daily leptin imbalance, a form of Cytokinic Dysregulation. The excess adipose tissue is leptin-inducing, creating a ratio error in cell-to-cell signaling. That daily chronic signaling error may exponentiate in the face of this IDRRV Influenza. Consider the combination of malnourishment with high adipose tissue in the overweight and we may see a Cytokinic Dysregulation occur that does not have the nutrients to feedback and re-regulate, leading to rapid declines and fatal outcomes. Perhaps that cycle is the causality of the high mortality and ICU admittance in Michigan among the overweight?
No one knows where this Pandemic strain is going precisely; however, the standing data lead us to draw one certain conclusion. PF11 is consistently drawing acquisitions from the current Influenza genetic reservoir, acquisitions that appear stable in producing disturbing clinical outcomes and potentially escaping the vaccine target. At this point, too few surveillance points are available to make firm predictions, but a framework may be ascertained. Under that framework, the acquisition path of PF11 suggests a movement toward a foundation of human-specific seasonal Influenza SNPs that will then continue to aggregate changes from H5N1 and 1918 descendants.
Those 1918 descendants and the H5N1 strains concern all researchers and will certainly continue to inform our investigations.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Dr. Thomas Francis, Jr., in a seminal immune response work, On the Doctrine of Original Antigenic Sin, returns us to the history of 1485 and the "sweating sickness" of England, then onward to the 1743 pandemic called variously "Blitzkatarrh" and "the Blue Plague" precursing the 1918 speed of rapid destructive spread in the population and the effect of human skin turning cyanotic blue from hypoxia (oxygen starvation).
On a side note, we may have located the geological event, an earthquake, in the early 1300’s that created a very large inland lake in China from which a plague proceeded therewith and where other plagues have begun in the past 700 years, potentially including PF51 (as yet undeclared Pandemic H5N1) and this PF11 currently circumscribing the globe. That area of research continues to be under review though the field may lead to no new information as very little surveillance data is available to collaborate the concept.
Famines have been highly correlated to plagues throughout history. We postulate that malnourishment of metabolic qualifiers, such as Essential Fatty Acids, B vitamins and vitamin C, reduces the body’s ability to properly feedback after an initial virally-induced Cytokinic Dysregulation. The famished body is left with no nutrients / anti-oxidants to re-regulate the feedback cycle of the immune response.
Without question, the United States suffers and leads the world with a population of malnourished and yet overweight individuals due to the reliance on non-food, processed factory materials for sustenance. An overweight human is at high risk for daily leptin imbalance, a form of Cytokinic Dysregulation. The excess adipose tissue is leptin-inducing, creating a ratio error in cell-to-cell signaling. That daily chronic signaling error may exponentiate in the face of this IDRRV Influenza. Consider the combination of malnourishment with high adipose tissue in the overweight and we may see a Cytokinic Dysregulation occur that does not have the nutrients to feedback and re-regulate, leading to rapid declines and fatal outcomes. Perhaps that cycle is the causality of the high mortality and ICU admittance in Michigan among the overweight?
No one knows where this Pandemic strain is going precisely; however, the standing data lead us to draw one certain conclusion. PF11 is consistently drawing acquisitions from the current Influenza genetic reservoir, acquisitions that appear stable in producing disturbing clinical outcomes and potentially escaping the vaccine target. At this point, too few surveillance points are available to make firm predictions, but a framework may be ascertained. Under that framework, the acquisition path of PF11 suggests a movement toward a foundation of human-specific seasonal Influenza SNPs that will then continue to aggregate changes from H5N1 and 1918 descendants.
Those 1918 descendants and the H5N1 strains concern all researchers and will certainly continue to inform our investigations.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
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