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IAS Study Summaries: An Interview with Jonathan Uy, from the University of Illinois in Chicago

July 25, 2007

Jonathan Uy, M.D.
Listen (3MB, 6.5 min.)
Welcome, this is Bonnie Goldman, editorial director of The Body Pro, and I'm here at Sydney, Australia at IAS 2007, one of the year's major HIV conferences. Right now, I'm at the poster session, where researchers are standing in front of their posters. There's nothing like hearing the results of research directly from those who actually conducted the research. It is these men and women who are transforming HIV treatment and care. In this podcast, the researchers will introduce themselves and then explain their study. I will ask a few questions after their summary.

I'm Jonathan Uy, from the University of Illinois in Chicago, on behalf of the HOPS group, poster WEPEB017. We in the HOPS have looked at the multiple other parameters as far as mortality and morbidity --

I'm sorry to interrupt, but could you explain what HOPS is?

HOPS is the HIV Out Patients Study. It's a CDC- [Centers for Disease Control and Prevention] funded prospective, database cohort study in ten HIV clinics in the United States.

Is it the largest natural history --

No. It's not a natural history [study], per se. It's not like the MACS [Multicenter AIDS Cohort Study], in the sense that it's a defined cohort that's followed. It's not a fixed cohort study like the MACS is. The strength of HOPS is that it's very representative of practice. It's sort of out there in primary care, and any of our patients in our clinics are eligible to be enrolled into it. It's more of a real world, we like to think, cohort.

Frank Palella and Ken Lichtenstein and others have done studies within the HOPS that showed that the lower the CD4 is [when] you start antiretroviral therapy, the greater your risk for morbidity, mortality, for neuropathy, for renal disease, for lipodystrophy, for all these things.

From my background, the piece that was missing, the real downside of starting antiretroviral therapy early, is the risk of developing drug resistance. Obviously, cost is [also] one, but we're not going to talk about cost now. So [let's] talk about the risk of developing resistance. Since a lot of the other analyses -- as well as a lot of other studies -- have shown that patients seem to even do better [now] even in terms of what were previously thought of as drug-related toxicities, such as neuropathy and lipodystrophy.

Our study aimed to look at the risk of developing resistance based on CD4 cell count at HAART start. We looked at all patients that we had very clear, defined, complete records for, who started antiretroviral therapy either when they when they were in the study or just before they entered started the study. We looked only at the substantive patients who [had viral loads] suppressed to undetectable. Among those who suppressed [HIV] --there were 683 patients who suppressed -- among those patients, 243 virologically failed.

Again, because this was just an observational study, we didn't have prescribed genotypes, but of those, 243 , 78 had a subsequent genotype. Of those who had a genotype at failure, the prevalence of resistance was much higher among the strata that started antiretroviral therapy [with a CD4 count] below 200 than the strata that started antiretroviral therapy above [with a CD4 count] 350. With the obvious limitation, that this is a prospective, database study with all the usual caveats, I think this is intriguing. It shows again that the benefit is starting at a higher rather than lower [CD4 count]. We hope to tease out a little more details before this goes to publication.

This is even more evidence that it's no longer a sound treatment strategy to wait until patients have a CD4 count below 200 to begin treatment. It may be that 350 is the new magic number.

Again, like with a lot of our HOPS studies, you can't make a guideline out of this. This is more evidence, not to say [that the starting point should be] 350, but, [to say,] the higher, the better.

Even 500?

We didn't look at a strata over 500, because we didn't have the numbers, but I think you see this linear increase among the three strata we looked at -- 0 to 199, 200 to 249 and over 350 -- that the higher you started, the better you did. So, again, it's indirect evidence. It's not a randomized, controlled trial. I think it's interesting that this is pretty much what we saw across all the drug classes and all the subgroups we looked at. This seemed to hold out. It's not statistically significant obviously, but we have little reason to think it's just a coincidental finding.

What were the patient characteristics? Was it mixed gender-wise, race-wise?

It's a very mixed patient population. The way we have it split up on the poster -- of the 683 patients who initially suppressed, 483 remained suppressed, and 165 failed, but didn't have a genotype and then 78 failed with a genotype.

If you looked at those who suppressed versus those who failed, it seems to be that those who stayed suppressed were more likely to be white. I don't have p-values up here. Those who remained suppressed were more likely to have MSM [men who have sex with men] as a risk factor, less likely to have injection drug use [as a risk factor], more likely to have private insurance. So your typical demographic factors that you typically associate with [HIV treatment] success, were associated with those who stayed [virologically] suppressed. This will be in the paper. We did divide among those who got the genotype, and looked at the different strata, at what the different characteristics were, but, again, I don't have that off the top of my head.

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This article was provided by TheBody. It is a part of the publication 4th International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention.