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To: James Oscar

Page #26



Why don't we go back up to the house and I will tell you a very interesting story.

Q: Let me go to my car and get the tape recorder and I will be right there.

MA:Thank you.

The reason that I so enjoy the new math of Chaos is that I find life so full of beautiful rhythms. Most are obvious - when the bees start hanging around the garbage cans in the late summer then I know it is time to start thinking about winterizing the cabin.

Some are not.

In the 1980's I was still working in the wonderful world of nasty bugs and everyone I knew was all gaga about monoclonal antibody technology. We could literally see the magic bullet on the horizon - where a specific drug, bound to a monoclonal antibody zeroes in on its target and delivers the drug or toxin there where it is needed. ABC stuff, we were about to cure it all.

Didn't happen. But during that exchange of information I became aware of a new and strange development in the world of microbiology. In the summer of 1981 after a huge increase in requests for the drug pentaminere, a smart young lady in Atlanta reported to the CDC that there was an outbreak of pneumocystis carinii pneumonia in Los Angeles. Now this was off the chart for a rare disease cluster so it sparked my attention.

In the winter of that year PCP was being found in IV drug users. I might note that this outbreak was not considered to be caused by an infectious agent at that time.

By the summer of 1982 homosexuals, Haitians and hemophiliacs were all getting sick and contact tracing was beginning to point at an infectious agent.

However in December of 82 there was a case of a 20-month old child (who had received multiple transfusions) dying of what was now being called Acquired Immune Deficiency Syndrome - and all doubt was removed.

We had a bug.

While my research at that time was centered on DHF (dengue hemorrhagic fever) and especially the outbreaks in Puerto Rico - the new bug caught my attention and I followed the developments very closely.

During the next few years the homosexual connection became apparent and we discovered that it was not airborne.

As the disease gained a foothold in America there developed a battle about one of the most important tools in epidemiology - contact tracing.

I won't go into all the arguments but in the mid to late 80's there was stiff opposition to the medical community doing normal contact tracing (as we would with any sexually transmitted disease) in AIDS cases.

The disease had become political.

And so it was - the virus, even though it is a poorly transmitted bug, had obtained it's beachhead in the human species.



39 posted on 12/14/2011 6:10:31 AM PST by James Oscar
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To: James Oscar

Page #27



MA: And so it went. The decades have past and we have made great strides in many medical fields but this deadly HIV virus has thrived in our midst.

But that is not surprising considering that it lives to destroy our immune system and kill human beings.

I understand that bugs have no drive and no destiny, but this deadly bit of RNA frightens me.

What we have learned is not good. It hides out for years in long term memory cells multiplying and waiting for an opportunity to re-emerge and ravage the carrier.

It has actually developed numerous strategies for eluding the body's defenses and our best medications. We also know that HIV modifies the cell structure system of the host cells enabling them to enter the cells more easily.

HIV especially attacks immune cells of the T-helper type. These cells support not only direct defense against the bugs, but are also necessary for building sufficient antibodies against the invader. For this, they must rely on their mobility.

The cell structure element actin, which also gives muscles their mobility, aids in the motility of immune cells. This is necessary for immune cells to be able to establish contact with each other and combat the virus.

And now we discover that cell mobility is inhibited by the HIV Nef protein.

Nef causes an enzyme that normally has nothing to do with cell mobility to deactivate a regulator for actin regeneration. Nef therefore causes a short-circuit of two cellular mechanisms, thus inhibiting the reorganization of the cell structure element actin and the cell's ability to move. Thus, the affected immune cells can no longer fulfill their function.

MA: Do you understand how important that is?

Q: I guess that by short-circuiting the method that the immune cell uses to have good mobility the HIV virus prevents the body from mounting a good defense.

MA: Well yes, but the negative effect of Nef on the mobility of T-helper cells also has far reaching consequences for the efficient formation of antibodies by B-lymphocytes in the patient.

We often see a malfunction of B-lymphocytes in AIDS patients and now we understand why.

It is not this one extraordinary thing about HIV but the multitude of functions and abilities that gives me great pause and eventually intrigued me enough to study the mechanism of HIV virulence.

Q: I see – and that is going to bring us around to your theory on Neuraminidase isn’t it?

MA : Yes it is.


40 posted on 12/14/2011 6:11:52 AM PST by James Oscar
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To: James Oscar; ntnychik; devolve; dixiechick2000; PhilDragoo

I missed this in 2003 and I missed seeing it posted on Dec 14. I have only started reading and have bookmarked my spot to continue later.

I find it both fascinating and frightening.


229 posted on 01/27/2012 11:30:19 AM PST by potlatch (*snip*~ Having the right to be angry does not give one the right to be cruel. ~*snip*)
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