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Highlights of CROI 2009

A Discussion With Pablo Tebas, M.D., Rob Camp and Bob Munk, Ph.D.

February 11, 2009

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The Body PRO is pleased to have gathered an amazing panel to discuss some of the research highlights from CROI 2009. This conference was so rich with findings that our ambitions will be modest with this panel discussion: We hope to provide here just a taste of some highlights from both a physician and activist point of view.

Bonnie Goldman: Welcome to our panel discussion on highlights of CROI 2009. Could you all introduce yourselves please?

Rob Camp: I'm Rob Camp. I'm a treatment activist and I live in Barcelona, Spain.

Pablo Tebas: I'm Pablo Tebas. I am a physician. I work in the University of Pennsylvania, although I was born in Barcelona, Spain.

Bob Munk: I'm Bob Munk and I'm the coordinator of the AIDS InfoNet Web site.

Bob Munk, Pablo Tebas, M.D., Rob Camp and Bonnie Goldman

Bob Munk, Pablo Tebas, M.D., Rob Camp and Bonnie Goldman

Bonnie Goldman: I have a long list of highlights from this amazing conference. Shall we start at HIV prevention and the exciting news of the first microbicide with some activity -- PRO 2000?1 Rob, what do you think?

Rob Camp: I think that it's good news in that it's not bad news. I think that we have to be careful that a 30% positive rate doesn't turn into people dancing in the street and throwing their condoms away.

Bonnie Goldman: I thought 30% seemed so ridiculously low. And what an odd take-home, I think the researcher said: "It's better than nothing."

Rob Camp: Well, it is better than nothing. I think that there may be some places in the world where the epidemic is so bad, that 30% actually might change the fluctuation of the infection rate.

Bob Munk: I think we have to remember to keep a different perspective when we're looking at a prevention measure rather than a therapeutic measure. We're so used to 80+% efficacy and undetectable viral loads for therapeutics, but there's a very different scale when we're looking at preventive measures.

I know I've heard 30% referred to as a real success rate if it was for a vaccine that was applied to a total population. Having said that, I think that Salim Abdool Karim, who presented these data, was rather insistent that this is something that has to be part of a range of preventive measures. It's not a stand-alone and there are certain populations for whom it could be very important. I think he used the example of a wife whose husband is a trucker and comes home every three or four weeks and she doesn't know if he's been faithful. She may not be in a position to demand condom use. If she has a woman-controlled method, even 30%, yes, is better than nothing.

Pablo Tebas: I think the good thing is that this is the first time that microbicides have shown some efficacy. That same woman can use PrEP [pre-exposure prophylaxis], so she can take a pill and reduce the risk of infection. The trials on that are ongoing. There are more than 20,000 people participating in different trials, in different varieties of pre-exposure prophylaxis with medication. They might be effective too. You can also give medication in a vaginal gel that might be effective too. Over the next few years, we will hear more and more about this type of HIV prevention. I think this was a positive finding that PRO 2000 at least showed some partial efficacy. [Click here to view Salim Abdool Karim, M.D., Ph.D.'s presentation. Click here to read an interview with him.]

Bonnie Goldman: Let's move from prevention to when to start treatment. There are two trials: One of them, presented by Mari Kitahata, M.D., demonstrated that risks were reduced if people were started on HIV treatment at a CD4 count of 500,2 while the other study, presented by Jonathan Sterne, M.D., showed that there was no benefit to starting so early.3 Pablo, what did you think?

Pablo Tebas: Over the last couple of years, as HIV medications have become less toxic and less difficult to take, and with the importance of non-AIDS-defining events happening to people with ongoing viremia, I think the pendulum has been swinging back to treat earlier.

But I don't think it's that simple. Even if we could treat everybody at 500, people have to realize that there's a commitment for life, that even the less toxic medications have some toxicity. We have to think about when is the best time to start antiretroviral therapy and I think the INSIGHT network is going to start a trial called START asking this specific question. Hopefully, we'll have an answer in a prospective randomized trial for these questions. A very expensive trial --

Rob Camp: It's a long one also, right?

Pablo Tebas: It's a long one. Some people would discuss the merits of spending so much money trying to answer these questions. Some people would say, "We already know the answer. Therapy's going to prevent some of these adverse effects." But I think doing a prospective, randomized study is the right way to get the answer. We have learned that along the years.

Bonnie Goldman: Rob, what did you think of the trials?

Rob Camp: The only thing I wanted to add about when to start is something slightly different. I went to a session about when to start in the developing world. Currently, in the developing world, it is recommended that treatment start at a CD4 count of below 200. At this session, they were trying to make the case that, if treatment is started earlier, it will prevent a lot of opportunistic diseases, as well as deaths, and the population will stay healthier.4 It may also lower the threshold rates as well and that's another important reason to at least raise treatment initiation to 350 if not higher, eventually to 500, in the developing world. I mean, it's the same thing -- it's human beings with HIV.

Bob Munk: An important thing that we can't lose sight of is that not everybody with HIV is lined up in a doctor's office trying to decide when to start treatment. There is a huge proportion of people, even in the developed world, who have not tested and they don't know their status. In terms of public health issues, this is a very important group.

We can do studies forever on 350 versus 500 with respect to when to start, but until we figure out how to get people identified when they're HIV positive, it's going to make a very limited difference.

Pablo Tebas: Absolutely. The majority of new patients that I see -- at least in my practice -- are people who show up with an opportunistic infection.

Rob Camp: Still today?

Pablo Tebas: Still today, because they belong to social groups that have little access to health care. And they present very late in the course of their disease.

Bob Munk: They have reasons not to present. I mean, they have fears about treatment, fears about disclosure.

Pablo Tebas: Fears about not having health insurance, going to a hospital. They go to the hospital only when they have a very good reason to go to the hospital.

"Should I start a patient on therapy with a CD4 count of 600?" is a question that I have very rarely faced. "Should I start the patient on treatment now or in a week?" or "Should I wait to start therapy until the genotype comes back?" are more frequently the questions that I face right now.

People present with opportunistic infections and there are data that show that if you have an opportunistic infection and you start therapy immediately, you're going to have an impact.5 That's a much more frequent occurrence in my practice than helping somebody who has a CD4 count of 600.

[Click here to view Mari Kitahata, M.D., and Jonathan Sterne, M.D.'s presentation. Click here to read or listen to their summary.]

Bonnie Goldman: Let's move on to what to start with. I know there were a lot of sessions about the NRTI [nucleoside reverse transcriptase inhibitor] abacavir [ABC, Ziagen]. Anything new?

Pablo Tebas: If anything, it feels a little bit more confusing than before. There were different studies showing different data. If people are interested, I think Peter Reiss summarized all the different issues about abacavir very well.6 [Click here to view Peter Reiss' presentation.]

There are observational data from the D:A:D cohort and the SMART cohort, which are now confirmed by a large cohort in France, that suggest that the recent use of abacavir is associated with a small increase in the risk of a cardiovascular event.7-9

In this meeting, there were presentations trying to find out why there would be an increased risk of cardiovascular events in people that start abacavir. Peter Reiss noted in his session -- and I think that's an important thing -- that there seems to be a greater risk for the people who start abacavir with no viremia than the people who start abacavir with viremia.6

So it doesn't seem that those patients who start an abacavir regimen with suppressed virus are at increased risk for cardiovascular events, at least in studies like the ACTG [AIDS Clinical Trials Group] study or the ALLRT study.10

Rob Camp: Reiss also mentioned age as a possible confounder, in that the people who were not seen to have cardiovascular problems were actually seven to 10 years younger. So maybe that also plays into why it's seen in some studies and not in others.

Bob Munk: I think it has to be put in context. What we really need to do is get infectious disease docs to do a thorough cardiovascular risk assessment of their patients. Those who have a very high cardiovascular risk with multiple factors, they may want to avoid abacavir. But for most patients, the decision about whether or not to use abacavir should be made just the same way as for every other patient.

Pablo Tebas: That is one of the most interesting things that the D:A:D study shows. In people with high cardiovascular risk -- around 15% to 20% of the total HIV population -- based on this data, you really might consider not using abacavir. For the rest of the people, the increased risk is so tiny that I don't think it should play into the equation. You should focus on preventing things that can reduce cardiovascular risk. Smoking, hypertension and hyperlipidemia are things that, if you treat or you remove them from the equation, dramatically reduces your cardiovascular risk and that's what I think people should be doing.

Rob Camp: More than one presenter said exactly that during these days -- that quitting smoking would do as good if not more than playing around with your treatments.

Pablo Tebas: Probably much more.

Rob Camp: I think that's a really important message we should try to get out -- people should consider not smoking.

Pablo Tebas: It will decrease your risk of lung cancer, which is cancer associated with HIV. Also, it will decrease your risk of osteoporosis, which is associated with HIV. You will live a better life and a more healthy life.

Bonnie Goldman: Let's move on to heart disease in people with HIV more generally, apart from those taking abacavir.

Pablo Tebas: People with HIV are at an increased risk of cardiovascular disease compared to people who don't have HIV. This is probably driven by some inflammation. There were studies showing that HIV by itself might affect endothelial function. One study at CROI I liked was from Kaiser Permanente, looking at the incidence of MI [myocardial infarction] by years. It showed that although HIV-infected patients have a higher risk of cardiovascular events than non-HIV-infected patients, during the last couple of years, the lines tend to come together. This suggests that by paying attention to traditional cardiovascular risk factors physicians are having an impact on the frequency of cardiovascular events in HIV-positive patients.11 I think that's a good thing. It means that if we act on traditional cardiovascular risk factors, we are going to drive the HIV population to where they should be.

Bob Munk: I think what this comes down to is that it's a paradigm shift for infectious disease docs. Their modus operandi is: Identify the bug and kill it. But that's not the way you deal with cardiovascular risk factors. That's not the way you deal with metabolic syndrome. This is a big shift in practice patterns and I'm not sure how we're going to achieve that.

Pablo Tebas: We're people with short attention spans and that's why we treat infectious diseases. In general, you treat people, you cure people, and you move on to the next person. In some regard, we are similar to ER [emergency room] doctors. But you're right. HIV is becoming a chronic disease. We need chronic strategies to manage the disease -- not only antiretrovirals, but other things. We need to take a more long-term look.

Rob Camp: A lot of times it's just a question of changing the hat you wear on the day for the person, right, depending on what the person needs.

Bonnie Goldman: What did you think about Jens Lundgren's presentation on behalf of D:A:D showing that PIs [protease inhibitors], particularly Kaletra [lopinavir/ritonavir, LPV/r], were more dangerous for the heart than NNRTIs [non-nucleoside reverse transcriptase inhibitors] and other drugs?8

Bob Munk: I think that fits in the same pattern. You're talking about a statistically significant signal in a large cohort study. It was important to have that reported, but when you translate that to an individual patient situation, are we talking about increasing cardiovascular risk from 2% to 3% over the next 10 years or are we talking about increasing it from 40% to 45% or 50%? That's the kind of assessment that physicians are going to have to make and patients are going to have to be aware of it. And if they're smokers, they'd better stop smoking. It's the best thing they can do to prolong their health.

Pablo Tebas: Yes. The increased risk with lopinavir was 1.4 or something like that, so if your risk is around 1%, that means that it goes to 1.4%, which is not a big change. If your risk is 10%, it means that it goes to 14%. So that may be a number that scares you a little bit more. Obviously, if you stop smoking, your risk goes down dramatically.

But the absolute risk, I think, is more important for individuals. When you have a data set with 30,000 patients and 150,000 years follow-up, any little difference is going to be significant. Does it mean it's clinically relevant? I don't know.

Lopinavir is associated with some changes in the lipid profile that might have an impact on long-term cardiovascular risk and that might be the explanation for this particular observation. But in this meeting we heard about possible substitutes for ritonavir [RTV, Norvir] that don't have the lipid effects, so we were very excited about that.12,13 [Click here to view Jens Lungren, M.D.'s presentation. Click here to read or listen to an interview with him.]

Bonnie Goldman: Let's talk a little bit about the ritonavir substitutes. How far away are they in development?

Rob Camp: Gilead just sort of publicly announced it earlier this year, so I suspect that it's probably in phase 1, maybe moving into phase 2, so we won't see it soon.

Bob Munk: I think it may be even further along than that.

Rob Camp: Yes, they're probably going to want to time it with elvitegravir [GS 9137, JTK-303] because elvitegravir, their integrase inhibitor, needs a boost and they've been using ritonavir up until now. I imagine that what they're trying to do is to at least get it approved by then, which may be mid-2010.

Bob Munk: I think it's important to clarify that these are being developed as pharmacokinetic [PK] enhancements -- that they're not really a ritonavir substitute. They're a PK enhancer. They're designed to increase drug levels of these new pharmaceutical products that otherwise would be at a sub-therapeutic level in the bloodstream.

The exciting thing about the drug is that it appears it has no anti-HIV efficacy, which may sound like a bad thing, but in fact it's a good thing because then it will not promote the development of resistance.

Pablo Tebas: Absolutely. Nobody uses ritonavir anymore as an antiviral, but the problem with using low-dose ritonavir is this: Let's say that you're starting a patient on a regimen of tenofovir [TDF, Viread], emtricitabine [FTC, Emtriva] and elvitegravir, and you use low-dose ritonavir. If you fail, the concern is, because you're using low-dose protease, are you paying a price by developing resistance to protease inhibitors such that it's going to compromise your subsequent regimens? If you have a PK enhancer that doesn't have any antiviral activity, you're not going to have that problem and that is going to level the field dramatically.

I think next year we might be talking about the studies comparing an efavirenz [EFV, Sustiva, Stocrin]-based regimen that's first line and a maraviroc [MVC, Selzentry, Celsentri]-based regimen that's first line, plus elvitegravir as the first regimen and darunavir [TMC114, Prezista] as a first regimen all because you'll be able to give a PK enhancer. I mean, it changes the field, so we will be talking a lot about different combinations with this new PK enhancer. Maybe the price of ritonavir will go down finally.

Rob Camp: That's what I was going to mention, that as an activist, I think that the issue of the ritonavir price is really important and maybe now that there will be competition, that pricing will start to go down, at least in the U.S. I know the price of ritonavir is already not quite as crazy outside the U.S.

Pablo Tebas: Then we will have probably a tablet for ritonavir, which has this not very nice formulation now that patients have to refrigerate. So I think these new drugs can change the field dramatically. And I think every single pharmaceutical company is going to start developing these for other therapies like hepatitis C drugs. It has the potential to change a lot of things.

Rob Camp: Yes, I think a number of companies are looking at it.

Bonnie Goldman: This conference had so much on non-AIDS-related complications. Anything else that stands out?

Rob Camp: The studies in themselves may not necessarily stand out. For me, it's just the realization that in fact, all of this non-AIDS stuff is happening. Whether it's connected with aging or whether it's connected simply with people living longer on treatment is not quite clear. But anyway, there are neurocognitive issues, bone concerns, kidney problems and cancers, all of which are non-AIDS-defining events that are being seen more and more commonly in HIV-infected people.

Pablo Tebas: The thing is, these studies warn us that these things happen to HIV-infected patients. We tend to think these events are occurring to our patients simply because they are alive and they're human. But it's happening with more frequency than you would expect when compared to HIV-negative people of the same age. I think we have to find out why and how we can prevent these events because they are an important cause of morbidity among patients with HIV.

Bob Munk: Yes, I think it's very telling that the studies of neurocognitive impairment showed that over 50% of patients who were studied had at least mild impairment.14 The good news is we're living longer. The bad news is we're developing these conditions that are not definitive of AIDS, but they're going along with AIDS. What we're starting to study is: Does having HIV infection accelerate these conditions? We don't know the answer to that yet. So I'm sure we're going to be seeing a lot more studies and a lot more results in future conferences in this area.

Bonnie Goldman: Finally, there were the final results from the immune booster studies of IL-2 [interleukin-2] among patients on HAART [highly active antiretroviral therapy].15,16 I don't know if anyone was following or more hopeful. I spoke with somebody today who said, "I didn't know they were still doing those studies."

Bob Munk: Well, these were phenomenal studies. I mean, from just the standpoint of the research achievement of enrolling the number of people that they did with such a large number of research centers, and then to follow them for so many years. I think the average follow-up was about seven years. This was a phenomenal scientific achievement.

The studies had a negative result, but it was a very significant result. The studies were trying to look at whether taking IL-2 and boosting people's CD4 counts led to a clinical benefit. It did not. And it very clearly did not. So the researchers said all of the improvement in clinical outcomes was due to successful antiretroviral therapy. We got a definitive answer to the question: Does boosting CD4s by using IL-2 help? The answer is no, it does not.

Pablo Tebas: They are sobering studies. I think the results of these studies will make it difficult to develop an immunomodulator. For 20 years we have been talking about immunomodulators. They did everything right in these studies. You have a drug [IL-2] that increases your CD4+ cell count, which is a surrogate endpoint that we look at when we treat patients with HIV. But in these trials the CD4 increase provided no benefit.

So if you're a pharmaceutical company developing an immunomodulator, what do you have to do? Another 4,000-person trial with clinical endpoints that is going to last seven years? It's not a very attractive proposal for anybody. So I don't know how we are going to develop immunomodulators. If I was making IL-7, I don't know what I would be thinking about, or how to develop a trial to prove that IL-7 increases CD4, that they are functional, and that they improve patients.

Rob Camp: Hopefully, one thing that they're going to do with the IL-2 studies now, with SILCAAT and ESPRIT, is go back and look at the markers that they were able to collect to see what may or may not coincide with the results we saw that may be more clinically meaningful. Because obviously these increased CD4s were what I consider empty. They were not active or useful.

Pablo Tebas: They didn't protect against opportunistic infections. If you are the FDA [U.S. Food and Drug Administration], what are you going to say? You will say, "I want to see clinical data because you are showing me the CD4 cell counts, but this is a 6,000-patient study that didn't mean anything."

Bob Munk: But I think we can't lose sight of the fact that there is very good evidence that the increases in CD4 counts following successful antiviral therapy do mean something -- for example, discontinuing prophylaxis at certain levels. So we can't lose sight of that. This does not cancel out those results, but it does suggest that simply looking at CD4 counts is not going to be enough to say, "Oh, we've restored the immune system."

Pablo Tebas: I'm worried also about the approximately 10% or 15% of HIV-infected people who are what we call "discordant." They have a virological response, but their CD4 count doesn't go up. We are evaluating interventions to try to increase the CD4 cell count in those individuals.

Bob Munk: Is that worth it?

Pablo Tebas: I don't know if it's worth it because it didn't make a difference in this trial.

Rob Camp: What worries me about this whole area is that there's no plan B; there's nothing after IL-2. In other words, there's nothing in phase 2, etc. They really have to go back to the drawing board a little bit.

Pablo Tebas: Well, but there are ongoing trials with maraviroc because there is this observation that patients who take maraviroc have an increase in CD4 cells. There is IL-7. I think people are working on this. The question is, let's say that you show an increase in CD4, what does it mean? Do you need to do a clinical endpoint trial to prove that that intervention works? Who's going to do a clinical endpoint trial? This trial cost millions and millions and millions of dollars. The company that made IL-2 quit six years ago. The NIH [National Institutes of Health] paid for the study. I mean, the taxpayers paid to do this study. I don't know if it's going to happen with another immunomodulator.

Bonnie Goldman: It's too bad, because I think discordance is still an ongoing problem. And if low CD4 counts are related to malignancies, then it's kind of imperative that we figure this out.

Pablo Tebas: Yes, we're going to have to figure out functional assays, vaccine responses or something to see if these increases in CD4 cells mean something, but we're going to have to convince the agency that that's a relevant endpoint.

Bob Munk: The INSIGHT Trials Network that did these IL-2 trials does have an extensive collection of stored samples and they are going to be examining a large number of what they're calling biomarkers. Hopefully, they will find some relevant correlations with some of them.

Pablo Tebas: Oh, the studies are important, and those samples are precious because you have clinical endpoints and you have samples from seven years and 6,000 people. We're going to learn a lot about non-AIDS-related endpoints from that cohort of individuals. It has not been a waste. I mean, we are going to learn a lot from these two trials, but it's a little bit sobering and it's going to complicate the field of immunomodulators. That's my feeling.

Bonnie Goldman: Great. Thank you so much for talking with me.


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  3. Sterne J, and the When to Start Consortium. When should HIV-1-infected persons initiate ART? Collaborative analysis of HIV cohort studies. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 72LB.
  4. Walensky R, Wolf L, Wood R, et al. When to start ART -- a policy evaluation while awaiting trial results: South Africa. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 596b.
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  6. Reiss, P. Abacavir and cardiovascular risk. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 152.
  7. The SMART/INSIGHT and the D:A:D Study Groups. Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients. AIDS. September 12, 2008;22(14):F17-F24.
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  11. Hurley L, Leyden W, Xu L, et al. Updated surveillance of cardiovascular event rates among HIV-infected and HIV-uninfected Californians, 1996 to 2008. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 710.
    View poster: Download PDF
  12. Mathias A, Lee M, Callebaut C, et al. GS-9350: a pharmaco-enhancer without anti-HIV activity. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 40.
  13. Gulnik S, Eissenstat M, Afonina E, et al. Preclinical and early clinical evaluation of SPI-452, a new pharmacokinetic enhancer. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 41.
  14. Heaton R, Franklin D, Clifford D, et al. HIV-associated neurocognitive impairment remains prevalent in the era of combination ART: the CHARTER Study. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 154.
  15. Losso M, Abrams D, and INSIGHT ESPRIT Study Group. Effect of interleukin-2 on clinical outcomes in patients with a CD4+ cell count of 300/mm3: primary results of the ESPRIT Study. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 90aLB.
  16. Levy Y, and SILCAAT Sci Committee. Effect of interleukin-2 on clinical outcomes in patients with CD4+ cell count 50 to 299/mm3: primary results of the SILCAAT Study. In: Program and abstracts of the 16th Conference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montréal, Canada. Abstract 90bLB.

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This article was provided by TheBodyPRO. It is a part of the publication The 16th Conference on Retroviruses and Opportunistic Infections.
See Also
Antiretroviral Therapy Highlights From CROI 2009
CROI 2009 Highlights: A Review of Cardiovascular Disease and HIV
CROI 2009 Newsroom


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