Please introduce yourself.
I'm Bob Frascino, and I am the founder and president of the Robert James Frascino AIDS Foundation. I'm an HIV specialist here in the San Francisco Bay area.
When were you diagnosed?
The virus actually found me in January of 1991 while I was performing a medical procedure on a patient with advanced-stage AIDS. I sustained a hollow bore needle stick and laceration injury and subsequently seroconverted a number of weeks thereafter, in spite of the fact that I did take AZT [zidovudine, Retrovir] as a type of early PEP [post-exposure prophylaxis] back in 1991. We didn't know a lot about PEP back then. I did take PEP but in spite of that still seroconverted. So that was in January of 1991.
And you started treatment?
I took PEP for the full six weeks and actually did not start antiretroviral treatment for a number of years. I am a clinical immunologist, and so I was following my immune status at the time, and, again, the only drugs that were available in 1991 were AZT and ddI [didanosine, Videx], and ddC [zalcitabine, Hivid] was coming along around that time. I decided not to take those drugs initially. So it really wasn't until my T-cell count started to fall around 1995, I believe, that I started taking antiretrovirals and then switched over to HAART [highly active antiretroviral therapy], which included the protease inhibitor drugs, following the Vancouver [International AIDS Conference] in the summer of 1996. I had been doing some of the research on protease inhibitors prior to that time and felt that they were worth a try, so as of the summer of 1996, I started potent antiretroviral therapy with Crixivan [indinavir] and AZT and 3TC [lamivudine, Epivir] at that time.
Were you ever on d4T (stavudine, Zerit)?
Yes. I switched over to d4T shortly thereafter when that drug came out and looked to have a higher threshold as far as resistance. [I] took d4T for a number of years -- probably five, six years or so, and had an excellent immunologic response. In other words, as far as maintaining CD4 cells, they were improving and did well as far as a virologic response suppressing viral load. So I stayed on d4T for quite some time, right through the period where we began noticing some rather bizarre and unanticipated side effects, including what we now know to be lipoatrophy.
You were beginning to see patients showing signs of this strange fat loss in their face and saw the accumulation by around 1998, 1999?
Yes, it was an interesting story. We had seen changes in the way people looked right from the beginning of the epidemic. But, of course, that was really wasting, which was really [a] loss of lean body mass, and wasting can make somebody look very cachectic and very skeletal appearing, and it's really due to uncontrolled HIV infection. We really didn't have a good control over HIV replication or HIV infection until the HAART medications came online in mid-1996. Wasting is caused by uncontrolled HIV infection and also by other conditions like low testosterone levels and poor nutrition, malabsorption, hormonal problems -- lots of different things that we were seeing early on in the epidemic.
So wasting had been there for quite some time. The news was that in 1996, when HAART therapy became widely available, there was this sort of, I guess using Alan Greenspan-speak, there was a sort of irrational exuberance over how wonderful these drugs were going to be. [For example], David Ho [Director and CEO of the Aaron Diamond AIDS Research Center in New York City] and his researchers wound up being Time magazine's man of the year that year, because he had helped bring protease inhibitors to the forefront. We really thought that by taking these drugs we could very effectively turn off viral replication to the point where we would perhaps be able to eradicate the virus. Initial projections back in 1996 were that we could eradicate the virus in perhaps three years.
So we thought, well, we will take these strong drugs no matter what they are, and no matter what they do to us, for a period of three years. We'll eradicate the virus, and perhaps we'll be cured. But, of course, that really was irrational exuberance.
As an immunologist, were you more skeptical?
No, at that point, because again, the science was catching up to the reality here. Up until 1996 we really did not have an antiretroviral that turned off viral replication effectively and for long periods of time. AZT and all these other drugs have very short-lived efficacy with lots of side effects, and here, by combining drugs, and using the newer classes of drugs, we really had something that looked very effective.
What we didn't realize, and really what probably the clinical immunologists and research immunologists realized somewhat earlier than others, was that HIV can hide in these immunological sanctuaries where drugs really can't get to them. HIV is actually a bit smarter than we originally thought it was. Even though we can turn off viral replication in many places in the body, because HIV can hide, and because it is immunologically protected -- being a retrovirus -- we really cannot eradicate this stuff. There are some very long-lived cells in the body where HIV can hide completely protected, and as long as we take these drugs, maybe we can keep the virus from reproducing. However, if we were to stop these drugs, the viral replication comes back with a vengeance, and this is what we learned.
So the thought was that these immunologic long-lived cells could live maybe 60 years, and so we would have to take these drugs not for three years to really burn out this virus in a human; we'd have to take them for perhaps 60 years, and this was obviously disheartening to those of us who were on the drugs, thinking that perhaps we would be off of them and cured in a matter of years. We're now looking at having to use them lifelong. And along this time -- this was during the 1997-1998 period, when the immunologists were discovering this -- along this time, we also started noticing these rather bizarre physical changes, and the thought was: Could this be related to the drugs? But we didn't know.
It didn't make sense that it would be wasting?
It didn't make sense that it would be wasting. In fact, it wasn't wasting. We could actually measure lean body mass, and we could see that people were -- their lean body mean was actually getting somewhat better. We were also getting better at treating things like hypogonadism with supplemental testosterone. We were getting better with nutrition. People's appetites improved. We were getting better at regulating hormonal problems. So the wasting was going away, because we were controlling HIV better. Again, one of the primary causes of wasting would be uncontrolled HIV infection.
We were now controlling HIV infection, so the wasting was actually going away, but people's shapes were beginning to change. We didn't understand it at first, and this became this sort of term that we called "lipodystrophy," which I think, unfortunately, is a bad term. We started talking about lipodystrophy and fat redistribution, and it turns out that those are, we know now, probably not accurate terms, in that it wasn't so much a case of fat redistribution -- where we were thinking that fat from the arms and the legs and the buttocks and the face was going over and being deposited in the back of the neck in the buffalo humps or in the stomach, in what we used to call Crix-belly or protease paunch.
We were thinking that fat was going from one place and being deposited in another place and that it was all part of the same syndrome, and we called that lipodystrophy. In other words, the fat was not going where it was supposed to go. We know now that's really not the case. It's really two separate things going on. There's lipoatrophy, which is the loss of the subcutaneous fat, the fat just underneath the skin, and it's seen most frequently in the arms and the legs and the buttocks and the face. That's lipoatrophy.
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