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

Georgia Mother and Her Children Infected Twice with H1N1

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

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

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

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

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

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

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

We responded with facts about this particular unprecedented pandemic:

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

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

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


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

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

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



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

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

What human outcomes has PF11 demonstrated in these Early Waves?

Last Updated 2013-05-30

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)
• Heart Attack, Stroke and Pulmonary Embolism, 34 year old Athletic Male
• Acute Necrotizing Encephalopathy (7F) Comatose 8hr post ER release, Brain Dead Day 2 [PubMed, pdf]
• Acute Necrotizing Encephalopathy (4F) [pdf] with Sequelae
• 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.  pH1N1 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.