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Old 01-26-2010, 11:06 PM   #1
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Join Date: Dec 2009
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Default Swineflu : The next wave

As most people think that the Swine-Flu has come and gone, this post can easily be branded as a panic mongering without cause. Well, let me then say that some people are not well aware of the biological mechanisms at play with this H1N1 pandemic.
History has proven that the Influenza virus infection is occurring in waves. The first wave of the H1N1 Spanish Flue pandemic had been very mild, only to come back 6 months later with devastating consequences.
So the first wave (with many ripples) of our current H1N1 pandemic has come and gone also without causing too much trouble. The second wave is expected to hit in March/April with a new, “improved” version of the virus.
While the virus is regrouping and brewing, let’s get ready for the second wave.
Last year I posted some info about the virus and its deadly effects, the Cytokine Storm, on another forum. There some people had the opinion that a good diet and rest will fight the virus off.
It is very important to understand what really happens during an infection, especially in view of recent developments. These new developments i will explain at the end. But first the old post:

We will have to look honestly at the current situation (Nov 2009) with the H1N1, the symptoms and possible ways how to beat the virus.
The international medical community is very adamant to release details about the flu symptoms, due to reasons which might become obvious. But for an effective fight we have to identify the symptoms of this viral attack and that very early. Any info on early symptoms are valuable, it doesn’t matter how gruesome they might be.
Prepare for the unexpected:

First: Facts
It is now official: The virus has changed and has adopted a genetic sequence (Receptor Binding Domain D225G), that is the same the 1918 flu had:


As the name said, the change will give the virus the ability to bind as easy to a new host as the 1918 flu.
Therefore it can be reasonably assumed that the infection rates will be the same as 1918. Maybe even higher, due to vast increased human mobility.
I learned that in 1918 approx. 30% of the world-population was infected, but the mortality-rate was low (about 2%). Still more than 20 Million people died. In the Ukraine the hospital admissions of people with ARI (acute respiratory infection) have a fatality rate of from 5% to 10%. But that’s for the “harmless” strain.
So how about the mortality-rate of the mutant strain? Here are some preliminary results:


Analysed were 10 samples, of which 4 were fatal cases. In all fatalities mentioned in this article, the virus had the D225G mutation, and only in those ones.
That indicates a much, much higher fatality rate for the new strain. This might be a result of the “improved” receptor binding, which meant higher rate of infection.
It locks like we are in for a VERY rough ride…

Obviously the medical community is unprepared for this onslaught. And they know it:

So we are more or less left to help ourselves. This thread is great in doing that, and let me contribute my 2 cents.
My approach will be the worst case scenario. That’s to wake up even the hopeful believers in “good diet and rest”. We are facing a tiger without the window in-between, and any mistake made will be made only once. Because the nature of this disease is unforgiving and deadly.
It looks like that there is a specific characteristic to the viral attack: The more hyperactive the immune system is, the more dramatic is the outcome - more fatalities. Kids have a very strong immune response…
Although it is always mentioned, that there were “underlying health conditions” in the infected kids in question, this looks like a smoke-screen to me. It is maybe supposed to hide that the more healthy you are, the more likely you are going to die.
.. which would be very bad news, because it would mean that the common avenue to boost the immune system will only result into a higher probability to go down.

So, what to do? Vaccination, some will say. But it looks like as if vaccination does not affect the new strain, the vaccine fails (see link above).
Vaccination would make things even worse, because the vaccine “boosts” also the immune system, through the toxic squalene. Then the hyperactive, “boosted” immune system runs into the virus, while being affected by the squalene poisons – a fatal double whammy. Maybe that’s why they are so interested to get us all vaccinated, even the (humane?) CFR people…

I hope that I am wrong, and if so, then please post and correct me.
But if not, what to do?
It looks like a typical CATCH 22 situation. (I really like the film)

It is very difficult to find data on that in the internet. It looks like there is a general consensus throughout the international medical community NOT to disclose medical details. This looks not like an organized gag-order, but has obviously more to do with a (only human) response to the FRIGHTENING NATURE OF THE DISEASE. But the info that seeps through is just terrifying:

The mutant virus goes deep into the lung and starts there its destructive work. Doctors will often do only a nasal swab for testing. While the patient will test negative for the virus, it is busy down in the lung.

So what is happening in detail: The mutant virus can survive higher temperatures and is therefore going deep into the lungs into the area of the fine Alveoli, where the oxygen-to-blood-transfer is done via a very thin membrane:

and zoom...

Lets look at the hypothetical case of Mr. John Doe:
The “prepared” Mr. Doe is walking the street, thoroughly protected by tight clothing, gloves and a really good filter-mask. A microscopic drop, containing the virus, attaches itself to any fine tissue at the eyes. The virus enters the body of Mr. Doe through this gate.
The mutant virus travels deep into the lung and starts there its destructive work. The infection of Mr. John Doe starts in the beginning like an ordinary flu-infection: Fever, maybe nausea etc..
Mr. John Doe will enter a

Systemic inflammatory response syndrome (SIRS).

(SIRS, I don’t like you !)

Mr. Doe feels that something is not right, and as a precaution gets himself tested for swine flue. The doctor will do only a nasal swab for testing. And while Mr. Doe will test negative for the virus, it is busy down in the lung.

The immune systems white blood cells will react to this infection by releasing Cytokines (a messenger substance), which will attract more white blood-cells to fight the virus. These cytokines-releases are normally well regulated, just enough to call for the help required.

The patient Doe enters the stage of SEPSIS.

Up to now everything is normal, but then….

In this case there is a massive pathogenic attack on the way. So something somehow goes wrong:
- Either the white cells fail to initiate a pathogenic recognition of the virus, which would start the fight against it. Instead the cells will call for more help by releasing more cytokines.
- Or the onslaught is so massive that it somehow triggers an unproportional (extreme and massive) cytokine response from the white cells. For that the virus has to have an extremely high rate of reproduction, which might be the case here.
Anyway, the result is: An ongoing massive overproduction of cytokines, with no check and balance in place. The mechanism that triggers this response is not clear. It is called a CYTOKINE STORM (CS).

What is a cytokine storm and how severe are the symptoms?
In 2006 a new substance called TGN1412 was tested, which caused a CS in the test persons. Here is what happened:


By now the patient Doe will have entered the next phase: Septic Shock

As the cytokine-production goes over the roof, even a layman can now recognize that something goes very wrong. The cytokines opens the blood vessels, so that plasma and blood can enter into the body-texture and –organs. The thin membrane of the Alveoli becomes porous along with other membranes. The blood pressure will sink rapidly, because of the capillary leakages.
Sometimes an “acute alteration in mental status” of the patient is observed. In other words, the patient faints and/or gurgles nonsense.
Now the able doctors will recognize that the patient Doe has entered the phase of a


with a

Systemic Capillary Leak Syndrome (SCLS)

Patient Doe will be admitted to ICU.
But now the lungs have started filling up with fluids:

Please notice the dark areas at the periphery. Thats were the Alveoli are.
And within only 6 hours it will look pretty bad:

The dark areas are liquids in the lungs.
The blood pressure collapses because of the drain of fluids.
To stabilize the blood pressure, the patient Doe will receive (a lot of) fluid by intravenous means. But that fluid will immediately leak out into the body-organs and -tissue. As the patient will receive up to 40 liters of fluid (or more), the body will swell and become unrecognizably bloated. At that stage some Does will go into cardiatic arrest, but not our Doe. He is already unconscious, but his body still fights.
Depending on the scope of the capillary leakage the lungs will be filled with either blood-plasma or blood-cells plus plasma.
This pumping-up of the whole body inhibits the flow of oxygen and nutrition to the vital organs (Ischemia). Patient Doe will of course get help through a respirator. And while others will die of intrapulmonary haemorrhage necrotizing pneumonia, our Doe is still on it. As the lungs are no more functional and the CS is still running, the patient Doe will now enter into the stage of

Multiple Organ Dysfunction Syndrome (MODS)

The kidneys, lungs, heart, liver etc. are starting to fail. That’s where the story of our patient Doe ends fatally.
But wait, I forgot: As the CS is an immunological reaction to an infection which can not be overcome by conventional means, the doctors will give the patient immunosuppressors in order to overcome at least the unregulated cytokine production. The result is a very weak, bloated patient with a suppressed immune system and a multiple punctured body. It’s where secondary infections like Staphylococcus Aureus et al are entering the playground to finish up the undone.
It’s a horrible death.
So this is a CYTOKINE STORM. So, to be clear: Whatever is done, either the CS hits Doe or the secondary infections. A real CATCH.

Oh sorry, I forgot to nail the coffin. As posted earlier:


Quote: “Because cytokine inhibition does not protect against death, therapies that target the virus rather than the cytokines may be preferable.”
It means that even if patient Doe survives the CS, he still has to get rid of the fast multiplying virus.
It’s a real CATCH 22.

It’s a horrible death.

Here a pic of a fatal case of SCLS/MODS. WARNING: GRAPHIC IMAGE!!


The light bluish skin is a result of anaemic blood, blood without oxygen. It’s the Cyanosis Blue of 1918.
You can see the blood in the lungs protruding from the mouth.

That’s the answer to why we have a mum throughout the medical community. The truth is so devastating, that nobody wants to admit it in public.
Yes folks, as cruel as it seems: That’s what some of us are in for…
Still thinking about sauerkraut and a good digestive rest?

Last edited by bashi; 01-27-2010 at 01:32 PM.
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