Replies

Page #62

MA: No I am not. I believe, and this is only my belief - not science, that the virus is on the verge of a complete breakout of its current behavior and will soon change both its transmission vector and its virulence.

The nuts and bolts of what precipitates this transformation are not clear to me and, in truth, we may never know the answer to that question.

Q: Ma if you are not sure how it changes then how can you be so certain it will be dangerous?

MA: Well, it is not so black and white as you make it. What I believe is that it will change. It will go airborne and it will become quick and deadly. When it makes that magic mutation that gives it the ability to ride the water droplets expelled in a cough or sneeze to the lungs of a healthy person - not only will it have found the mechanism for rapid transmission but the mutation will also set in motion a very different chain of events from what we know now.

When the new HIV virus arrives in the lungs of a new patient there is the great potential for a positive feedback loop to be established between the new invader and the host's immune system. At the arrival of the new pathogen, cytokine will signal the body to send T Cells to fight the infection. The T cells, upon being stimulated by the cytokine will begin to produce even more cytokine.

This is the normal reaction and happens all the time. But we have a real problem don't we?

Q: HIV lives on T cells?

MA: Yes of course. So now we have the feedback loop. T cells rushing to the lungs where they are infected with new virus and more and more cytokine being produced by the body. The result is called a "Cytokine Storm". The lungs begin to fill with fluids and immune cells. The result is sudden death. When this event takes place in the lungs, it can kill a healthy young person in less than 48 hours. We learned this lesson in the 1918 flu outbreak.

Q: So the hardy virus can jump from lungs to lungs and once there put in motion a very serious reaction that will kill you rather quickly. Is that about it?

MA: Just about, the only addition I would add is that once the new bug creates this "soup" in the lungs - with each cough or sneeze this deadly pathogen is sent on an airborne journey looking for a healthy lung to infect..

Q: OK, I see all that and I understand why you have been so concerned about doing anything that might increase the chance of the virus mutating.

But, what I don't really see is this - Say it happens as you say, somewhere in Russia or China the virus is successful in breaking out and infecting a patient, his family and even some health care workers - wouldn't it quickly be quarantined and controlled? Even SARS can be contained.

MA: Yes were there to be an isolated breakout and the proper barrier nursing techniques could be initiated, then the prognosis would be for containment. But that is not to be the case.

Q: I don't understand what you mean.

MA: There is a very unusual phenomena in the world of Virology called "coincidental spontaneous mutation". We use this term to describe an event where the same mutation breaks out in multiple locations in the same time frame.

The causality of this event is highly debated but the phenomena is well documented.

Q: Recently?

Page #63

MA: Very recently. In 2009 there was an event that occurred concerning the H1N1 novel virus that should have sounded the alarm bells for all those who are watching these pandemics.

There was a mutation of the H1N1 virus that occurred in Brazil, China, Japan, Mexico, Ukraine, and the United States. The mutation is called H1N1/D225G.

This mutation directly attacks the lungs, causing swelling and hemorrhage. Symptoms include progressive over 38C temperatures, breathing difficulty, a dry cough producing blood, and destruction of lung tissue starting in the lower lungs. Time from onset of symptoms to death was 4-7 days.

When we performed post mortems we found the lungs were blackened, as if burnt, perhaps related to lung hemorrhage.

Both the D225G marker, a so-called ‘domain changing receptor’, and the symptoms listed above seem to link this variant to the Spanish Flu Pandemic of 1918.

The multiple coincidental spontaneous mutations were so startling that some people believed we had seen a test run of a biological agent. That was not true.

What we experienced was soon repeated again when clusters of Tamiflu resistance patients appeared in Wales and North Carolina. These patients all acquired an identical change in the H1N1 virus - yet lived a world apart.

It is not a new phenomena. There have been many reports, historically, about bugs acquiring resistance seemingly overnight. Again, the mechanism for this type of event are completely unknown to us. There are so many things that occur in our physical world that seem bewildering - yet commonplace.

That is the great joy of science, to reach into that unknown realm and search for those natural rhythms that are just beyond our understanding.

Q: I don't know what to say. I had no idea such a thing was even possible. But it makes the hair on my neck stand up when you talk about the effects the mutation has on the lungs. Is that what happened in 1918?

MA: Well we have to be careful about overreaching but yes something very similar to this event. That bug killed the young and healthy with impunity. Once again, in a cytokine storm the more robust your immune system is - the more devastating the feedback loop.

Q: It is almost like we are, step by step, building up to your vision of the HIV mutation. All these events are so similar to what you postulate.

For the first time MA, I am a little frightened.

MA: And why is that?

Q: I suppose because before this discussion your theory seemed just too far fetched to make any sense. But when you frame the outbreak with all this in the background - it is just a bit too real for me.

I am in the position of having read your writings stretching over nearly a decade and it is impossible to forget how prescient you have been on so many issues. That worries me when your predictions begin to make not only reasonable sense but have a small ring of truth.

MA: Ring of truth?

MA: Well, it is not so black and white as you make it. What I believe is that it will change. It will go airborne and it will become quick and deadly. When it makes that magic mutation that gives it the ability to ride the water droplets expelled in a cough or sneeze to the lungs of a healthy person - not only will it have found the mechanism for rapid transmission but the mutation will also set in motion a very different chain of events from what we know now.

When the new HIV virus arrives in the lungs of a new patient there is the great potential for a positive feedback loop to be established between the new invader and the host's immune system. At the arrival of the new pathogen, cytokine will signal the body to send T Cells to fight the infection. The T cells, upon being stimulated by the cytokine will begin to produce even more cytokine.

This is the normal reaction and happens all the time. But we have a real problem don't we?

Q: HIV lives on T cells?

MA: Yes of course. So now we have the feedback loop. T cells rushing to the lungs where they are infected with new virus and more and more cytokine being produced by the body. The result is called a "Cytokine Storm". The lungs begin to fill with fluids and immune cells. The result is sudden death. When this event takes place in the lungs, it can kill a healthy young person in less than 48 hours. We learned this lesson in the 1918 flu outbreak.

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February 15, 2012

I was emailed the following information listed below from Spain. The email explained to me that there was a study released in December of 2011 which explained how the mechanism of this event has now been discovered.

After some really hard concentration (thank you again MA for all the lessons) I understand what they are saying. Here is the bullet points and URLS.

1. HIV has a gene TAT (Tat stands for "Trans-Activator of Transcription)

2. Tat vastly increases the level of transcription of the HIV dsRNA. Before Tat is present, a small number of RNA transcripts will be made, which allow the Tat protein to be produced.

Tat then binds to cellular factors and mediates their phosphorylation, resulting in increased transcription of all HIV genes, providing a positive feedback cycle. This in turn allows HIV to have an explosive response once a threshold amount of Tat is produced, a useful tool for defeating the body's response.

http://en.wikipedia.org/wiki/Tat_(HIV)

SHORT VERSION - THE HIV GENE "TAT" ARRIVES IN EARLY INFECTION, HIJACKS THE BODY'S CELLS AND ONCE A CRITICAL MASS OF TAT IS PRESENT CREATES AN EXPLOSION OF HIV VIRUS.

3. Three months ago a group of Spanish researchers discovered that:

BACKGROUND: HIV-1 Tat protein has been shown to play multiple roles in the pathogenesis of AIDS; however, there is no information currently available on its effects on adipose tissue alterations. We have studied the effects of Tat on SGBS adipocytes to gain insight on its role on the development of lipodystrophy.

METHODS: SGBS preadipocytes were exposed to Tat during and after differentiation. Acquisition of adipocyte morphology, expression of gene markers of adipogenesis and inflammation, release of adipokines and cytokines to the medium, and glucose uptake were measured. The action of Tat on tumour necrosis factor (TNF)-α-regulated messenger RNA expression was determined in differentiated adipocytes. The capacity of rosiglitazone, resveratrol and parthenolide to influence the action of Tat was also assessed.

RESULTS: Tat treatment reduced the number of SGBS preadipocytes that acquired adipocyte morphology. It also led to repression of adipogenic gene expression and induced the coordinate expression and release of proinflammatory cytokines in human adipose cells. Moreover, combined treatment with Tat and TNF-α produced an additive effect on the repression of adipocyte genes. The observed effects of Tat on gene transcription in adipocytes were due, in part, to TNF-α that was secreted as a consequence of intracellular exposure to Tat.

CONCLUSIONS: Tat impairs adipogenesis in human SGBS preadipocytes and increases the expression and release of proinflammatory cytokines. Positive crosstalk between Tat and TNF-α contributes to the anti-adipogenic and proinflammatory effects. HIV-1 Tat protein may play a role in the adipose tissue alterations that ultimately lead to lipoatrophy and systemic metabolic disturbances observed in HIV-1-infected patients.

http://www.ncbi.nlm.nih.gov/pubmed/22301094

SHORT VERSION - THE EXPLOSION OF TAT IN EARLY INFECTION HAS A SECONDARY EFFECT. IT CREATES AN ENHANCED RELEASE OF CYTOKINE.

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So........ MA's theory about an HIV infection in the lungs has a clearly defined mechanism to explain the deadly Cytokine Storm reaction she predicts.

This leaves only the last element of her theory yet to happen - HIV develops the ability to survive in water droplets of a cough or sneeze.

I hope she is wrong.