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.
Page #29
MA: Yes, there are. And the most prominent mitigating factor is the reason that the current novel H1N1 Influenza outbreak worries me so.
We have spent an incredibly long time discussing the enzyme Neuraminidase over the course of this winter and I would like to take that knowledge base of yours and apply it to our current situation.
Q: Good to go.
MA: This discussion is actually less complicated than the original explanation of how Influenza replicates.
Because you already understand how Neuraminidase functions as a cleaving agent in H1N1 you will clearly be able to "see" how Neuraminidase influences sialylation and that alteration, in turn, modulates the process of HIV infection.
Because of the saturation of the species with H1N1 and the mass inoculation with H1N1 vaccine - not to mention the millions of challenges to the virus with Neuraminidase inhibitors, I would like to review with you a few potential problems.