Dr. Cohen,

If you remember (as if I am the only on on here :)) back in November 21st I was they guy who spoke about my exposure in May 1998 with diagnosis in Oct. and Nov a VL of 1996 , CD4 of 42 percent and debate whether to treat.

On 12/21 I started that regimen (HU , d4t, DDI, and Sustiva.) I just got the new VL test back that was taken on 1/26 and am now undetectable. GREAT NEWS for me. How long can I expect to hold on to this success. I have NEVER missed a dose and don't even think about being non compliant. My doctor initially said that if I stay undectable for perhaps 6 mos. perhaps dosing on IL2 might be a possibility and perhaps stopping drugs temporarily to see reaction might be an option.

WHat do you think about this entire situation? As you know I am being treated at the U of P hospital's ID unit (and I must say a great unit and doctor).

thanks for your response.

Congrats on the great news. It is not surprising to hear - given the power of the combination you are on, and the relatively low viral load that you needed controlled. In fact, your regimen, would likely have worked well even if your initial viral load was much higher - based on the study of azt/3tc/sustiva - that combination worked impressively well when the initial viral load were over 300,000 - and substituting the azt/3tc with d4T/ddI/Hydroxyurea should be at least as good. So - how long to expect?

It is entirely possible that this regimen could work for as long as you take it. There are several reason for this confidence - in part based on news at the recent antiviral conference showing us that in some who are on similarly potent combinations, the virus does appear to be 'frozen' in time, and not mutating in a way that might it allow to some day ignore our meds. It is a bit frustrating that we don't yet have this kind of proof in combinations like yours that do not include a protease inhibitor - and this is one of the reasons that some clinicians still maintain that a PI is the most proven approach. However, others believe that the viral load results from non-PI combinations are similarly likely to work. And we should have some real info soon to put this issue to rest.

As for the two other issues you mentioned. First, IL-2. There was a bit of intriguing information presented to suggest that the use of IL2 in combination with a potent antiviral combination could make it even harder to find HIV-containing cells in the body over time. The idea is to reduce the pool of cells in which HIV is hiding - so called resting cells, that IL2 causes to wake up and die off. We don't yet have the kind of proof we need to recommend this approach yet - as we are just dealing with a few cases here and there... and we don't know if the people with these results are exceptions or the rule with IL-2. So stay tuned.

As for periodic interruptions. Once again, just a hint of information and the beginning of a new direction in research. What was reported on is a follow up by the researcher Dr. Franco Lori who first described the result of a man in Germany - the 'berlin patient'. Soon after HIV exposure, he went on a combination containing ddI, hydroxyurea, and indinavir. After his virus went below detection, he interrupted the meds, then resumed, and then interrupted again. After the second interruption, HIV has not started to regrow - now two years later. And there are a few reports of others having such similar outcomes. But there is a mystery - why is this happening? Is it starting treatment soon after exposure when HIV-directed T cells are still around? Is it the brief interruptions that 'remind' the immune system what HIV "looks like" so as to increase its focus on controlling this invader? Is it hydroxyurea and its impact on T cell function? (the latter may be a tiny bit less likely based on one case reported at this conference of a similar outcome in someone who took d4T, ddI, and nevirapine - without hydrea.) Or is this just finding that fortunate 2-3% of people who are long term non-progressors, who have the ability to control HIV without meds - and we are just now finding the exceptions to what could be the rule - that this extraordinarily successful outcome will be a rare event no matter what we do with meds, IL2, interruptions and so on?

At this point, we don't know the rules. As we are at the beginning of the story, we don't know the punchline yet. It may be that this applies to some, but not to all. It may be that measuring T cell function turns out to be helpful in learning who would benefit from this approach.

Exciting things are being done in research to further evaluate this. And you are certainly in line to join those investigations and take full advantage of this approach if it turns out to work after all...

Hope that helps. CC