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As CROI 2007 drew to a close, we asked Judith Aberg, M.D., Principal Investigator, AIDS Clinical Trial Unit and Director of HIV, Bellevue Hospital Center at New York University to discuss what she felt was the most interesting research presented at the conference.

What do you think were the most important presentations at CROI 2007?

Well, I think probably the most important [discoveries] are the new antiretroviral drugs that are going to be available. I think both the Merck [& Co, Inc.] integrase [MK-0518, raltegravir] and the Gilead [Sciences, Inc.] integrase [GS-9137], now, are going to give our patients other options that they didn't have before. I think the data, was pretty impressive with the Merck integrase, in particular, with 77% of experienced patients that had a lot of [HIV drug] resistance achieving undetectability -- i.e., viral load suppression. [Click here and here to view these studies. Click here for coverage of these presentations.]

We have maraviroc, the new [Pfizer, Inc.] CCR5 entry inhibitor, as well. [Click here and here to view studies of maraviroc presented at CROI 2007.] Our patients are going to have more options than they've had in the past year. I think if you think about what's going to now be available through expanded access [programs], we have the integrase inhibitor, we have the CCR5, and now TMC125 [etravirine] coming out. [Click here to view a study of TMC215 presented at CROI 2007.] It's a whole new paradigm.

Isn't this the first time since 2003 that we've seen so many new drugs at one time?

Yes, we've got three new drugs. I mean, TMC125, of course, is a non-nucleoside [NNRTI], and it's not a new class; but the other two are new classes of drugs. So, more options for our patients.

Anything else that caught your interest at the conference?

Well, you know, I have an interest in metabolic complications. I think the ACTG 5142 data, suggesting that there was more lipoatrophy with the efavirenz [EFV, Sustiva, Stocrin] arm, compared [to] the [ritonavir]-boosted lopinavir [LPV/r, Kaletra], is interesting. I just want to note that it's not that patients actually develop more lipoatrophy; they return down to baseline, more or less, whereas there was improvement in the boosted lopinavir arm.

I think we need to explore why that is, because we haven't had any thoughts before that efavirenz was associated with mitochondrial toxicity. Some questions that come to mind for me [are]: Is this morbid inflammatory response (because we don't see as much of a CD4+ [cell count] increase with efavirenz as we do with boosted lopinavir)? Is it somehow related to inflammatory markers? You know, what's really the story behind that? Because this is the first time we have ever seen something like this. I don't think we have enough information at this time.

Certainly, efavirenz is a very potent drug. In most of the studies that we've seen, you know, it's become the gold standard. I don't want people to think because they see this that they shouldn't be using efavirenz. That's the wrong message. People need to take a step back. We need to figure out what's going on with those DEXAs [dual energy X-ray absorptiometry] before we make any further comments about it.

When do you think we're going to get to see new data on that? I guess at IAS [International AIDS Society Conference] in Sydney?

Yes -- I don't know. I haven't really had a chance yet to talk to the team.

To read or listen to more interviews with HIV clinicians about what they felt was the most important research presented at CROI 2007, click here.