Use Low and Slow Exposure to Make Hungry Antibodies Fast

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

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

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

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

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

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

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

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

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

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

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

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

1. Detect
2. Destruct
3. Eliminate

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

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

How do we establish a Slow and Low Exposure protocol?

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

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

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

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

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

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



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

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