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.
Page #28
Q: You said that you "understand that bugs have no drive and no destiny, but this deadly bit of RNA frightens me." Why is that?
MA: Because it is so different and it is so extremely targeted.
Most of science involves making accurate observations and correctly interpreting the data.
Well when you objectively look at HIV you see a very odd critter. In the quarter-decade that we have been fighting this virus there is only one impression that any serious researcher can reach:
And that is that HIV is swiftly evolving to avoid the body's immune defenses - in fact it is rapidly changing to compensate for even small human variations.
Take the human leukocyte antigen (HLA) genes. These proteins act as a signaler against intruders. The proteins present little pieces of HIV to the body's T cells, which then seek out the virus and kill it.
However there are variants of HLA genes that are far better at combating HIV than others. And when we see a population where there is a favorable variant of HLA such as HLA-B*51 then we see the virus quickly mutate to a state that can resist the HLA-B*51.
In Japan over 2/3rds of the infected population has the resistant HIV variant because the population pool has a large percentage of HLA-B*51 carriers. But in other parts of the world where the HLA variation is not present or is different – then it is a different virus variation that dominates the infected populace.
In other words this little critter keeps shifting very rapidly to make certain that it continues with it’s grim job of killing humans – of all races, of all regions and of all beliefs.
This is evolution at "warp speed" and it is not pretty.
MA: There is no dispute about this bug. It targets humans with a devastating attack on the immune system, specifically helper T cells.
After it has decimated the helper T cells, the immune system cannot signal B cells to produce antibodies or Cytotoxic T cells to kill infected cells.
Also after depleting the Helper T cell population, the body can no longer launch a specific immune response and becomes susceptible to just about everything.
Our memory T cells are rapidly infected and destroyed in the mucus membranes of our tissues during the first several days after HIV infection. And they are largely never restored.
This sad list just goes on and on...
It is hunting us and it is winning. Twenty five million people are dead, another 33 million are infected. If this were a highly infectious disease then these numbers would be very different.
Knowing that, we can never assume that this fast-mutating bug will not become more virulent. Also we might, as good practitioners, ask if there are any known factors that influence HIV virulence.
Q: I assume that there are.