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.
2009-10-08
Can My Child Be Re-Infected If They've Already Suffered from Pandemic Influenza H1N1?
Georgia Mother and Her Children Infected Twice with H1N1
Many cities around the world are reporting re-infections, including US geography in and around Georgia and New York.
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Does an antibody set from a previous infection protect me? Not always.
Under what conditions do my antibodies protect me? An antibody response is very protective if timely, in high quantity and matched to the intruding virus.
Viral strains change and PF11 is changing rapidly on the areas that the human body uses for recognition. If you were trying to identify a villain that you only saw once from the rear, then you’d have to use the clothing as your key. The villain knows that you only saw his clothes and not his face. Will the criminal change clothes? Yes. Will this virus? Yes.
For some reason, people have been led to believe that “getting” PF11 now will be an iron-clad protection from later versions of the disease. Medical professionals seem to rely on this thinking though their training demonstrates otherwise. We do have a new Influenza season every year and they do see many patients more than one time in a season. They do create a new vaccine every year and that vaccine does fail to match or fail to seroconvert much of the time. They do know that Influenza is variable, but they don’t realise just how variable because they haven’t taken the time to study the ΣPF11 genetic sequences.
We received a response from a friend who is a medical professional noting that her child had been exposed from an extended family member, developed symptoms and appeared to have fully recovered. We rejoiced that they had been spared significant suffering, but were concerned about the triumphant tone of the message.
Busy people sometimes do not regard the facts well unless the facts fit into their busy schedule. In fact, busy people sometimes fail to put their own knowledge to work in their own families? A virus like PF11 does not care about your schedule.
We responded with facts about this particular unprecedented pandemic:
Are you doing anything to ensure that all of you are developing a robust antibody response over the next 21-30 days? Remember that due to weakened host immune responses a strong percentage of people who are exposed will not seroconvert to a fully protective antibody profile. Even an individual who does build a basic profile will face future PF11 specimens that have escaped the antibody profiles in that individual host and host family. That future specimen could occur in less than a month from the initial infection due to the observed PF11 enhanced genetic acquisition trait and the ample circulating diversity in any single geography. I refer you to the Three Time Loser in 1918. If the host is traveling, then multiple exposures to variant antigens are ensured.
Maintaining a properly regulated innate immune function is extremely important even after an individual appears to have successfully recovered from the initial exposure cycle. The antibodies created, if they do seroconvert a protective set, can only be called into action via the initial innate immune response. The virus must be recognised by the body before any adaptive immune response will be mounted. A properly regulated innate immune response serves that detection function, acting as a coordinator, determining if matching antibody exists and calling it into action. Secondarily, a significant count of children and young adults are on file as having appeared to recover and then relapsing to become fatal cases. This PF11 virus may quiesce the immune system at any phase, early or mid-stream. The relapse potential is a fact with this viral reservoir.
Influenza Flux between swine, bird and man creates a mismatched host-disease interchange that is highly variable in outcomes.
Succeeding in Round 1 against this virus is great, but now the virus knows that you can block a left jab and will try something new. As PF11, under the cover of cold weather, learns more about the North American hosts, PF11 will exploit the weaknesses just as the reservoir did in South America in July and August with more than 1,000 deaths in Brasil alone.
Diligence in the Round 2 will determine our success. You are in a 15 round endurance match. This virus is well-trained and well-stocked in his corner. Will we stay on our toes and move one step ahead of the virus or will we rest on our heels leaving our chin exposed for the knockout punch?
Each adult will decide for themselves, but remember that the children are dependent on the adults who head their families and their communities to decide for them.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
Many cities around the world are reporting re-infections, including US geography in and around Georgia and New York.
---
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.
2009-10-07
US Passes Thousand Death Marker prior to Influenza Season with 1,197 Confirmed Deaths
1,197 Confirmed Pandemic H1N1 Deaths before the Influenza Season begins in the United States and we stopped testing and officially recording most cases in early July, more than 10 weeks ago.
For additional background on the clinical and epidemiological observational facts concerning Pandemic Influenza H1N1, please refer to the Table of Contents for PF11 Trends & Issues, Mid-Term.
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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