Page #25
Q: Not much. It is a virus and from our lessons this winter I know that it has some similar mechanisms as the Influenza A virus.
MA: Yes it is a virus, it is called HIV. It stands for the Human Immunodeficiency Virus and is a Retrovirus.
The target cells for HIV are immune cells, called CD4+T cells, these cells help the body fight infection and disease. But they are HIV's primary target.
HIV is spherical in shape. The outer coat of the virus, known as the viral envelope, is composed of two layers of fatty molecules called lipids, taken from the membrane of a human cell when a newly formed virus particle buds from the cell.
MA: Does that sound familiar?
Q: Very much so - that sounds just like the Influenza A virus.
MA: Yes indeed it does.
Also similar is that embedded in the viral envelope are proteins from the host cell, as well as copies of a complex HIV protein (frequently called “spikes”) that protrudes through the surface of the virus particle.
This protein, known as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure in the viral envelope.
When you think back to the functions of HA and NA in the Influenza A virus, GP 120 is very similar.
The HIV glycoproteins aid in its attachment to the target cells - CD4, the primary HIV-1 receptor.
This binding exposes a site on gp120 that enables interactions with secondary coreceptors and further conformational changes. Remember how the HA in H1N1 unfolds and attaches.
Q: Yes, that is a very dramatic little trick it does.
MA: But the point is that the viral structure in both these pathogens, while differing in many key ways, is fundamentally a variation of the same form.
Q: OK I understand that, but why is it important?
MA: I believe it to be very important. But before we get back to how patterns of glycosylation of a virus can be an important factor in its virulence, would you indulge me in a bit of a sidebar?
Q: Why of course.
MA: When we had our original discussion last summer and I explained to you that I had very serious concerns about our vulnerability, as a species, to emerging pathogens you thought that H1N1 was my major worry - did you not?
Q: Yes - I assumed it was the flu - what with your log in name and such.
MA: Well, the answer is both yes and no. As with much of science - when you hear hoof beats it is normally a horse - but occasionally it is a zebra.
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.