March 8, 2010
This is part two of a two-part interview discussing highlights from CROI 2010 related to antiretroviral therapy for HIV-infected patients. Part one focuses on antiretrovirals in development; part two focuses on already-approved antiretrovirals, the question of when to initiate antiretroviral therapy and the evolution of the CROI meeting itself. You can use the table of contents below to quickly jump from section to section.
Table of Contents
Myles Helfand: From drugs in development, let's move on to drugs that are already on the market. What kind of research was presented here at CROI regarding recent efforts to improve existing treatment options for patients?
Joel Gallant: Probably the most important one was the eagerly awaited results of ACTG 5202. This may have been the most confusing presentation at CROI, not because the presenter did a bad job but because, again, they were forced to combine a lot of data into a 10-minute period. This was a study that looked at two things. It looked at Epzicom [abacavir/lamivudine, ABC/3TC, Kivexa] versus Truvada [tenofovir/emtricitabine, TDF/FTC], and it looked at Sustiva [efavirenz, EFV, Stocrin] versus boosted Reyataz [atazanavir, ATV]. Since there were two comparisons, there are four arms: You have Truvada/Sustiva, Truvada/Reyataz, Epzicom/Sustiva and Epzicom/Reyataz. It's a complicated study design.
We had already heard, in Mexico City in 2008, the results of an interim analysis, where the DSMB [Data Safety Monitoring Board] recommended that the patients with a viral load of above 100,000 copies/mL be unblinded as to their nucleoside assignment, because the Epzicom was underperforming. There was a higher rate of virologic failure in that group of patients with high viral loads, and it was suggested that they switch over to Truvada. That's the last we heard, and nobody understood why that had happened. We were all waiting to see the final results.
As you could imagine, in any study comparing four different regimens, with the size of the study, there are going to be a lot of different nuances. The bottom line for me is that this was probably, I think, the first clinical trial that showed that a boosted protease inhibitor [PI] could be as effective as Sustiva. So, in terms of virologic efficacy, boosted Reyataz and Sustiva were pretty much the same. That was true, whether you looked at [whether either drug was taken with] Epzicom or Truvada.
The other thing that I thought was interesting: I think most people assume that because Epzicom didn't do as well as Truvada in the high viral loads, we would see some inkling of that in the lower viral loads -- that we would say, "Well, maybe the differences weren't as big, but Epzicom would still not be as good as Truvada at low viral loads." In fact, that really wasn't true. At the low viral loads, you couldn't see any sign of that earlier failure that we had seen at the high viral loads, making it still very puzzling why we saw that in the earlier analysis.
But there were some differences, mostly favoring Truvada, and that had to do with safety and tolerability. If you looked at the time it took before you got to a significant safety event, if you were taking Epzicom with Sustiva you were more likely to develop one of those events than if you were taking Truvada/Sustiva. It didn't seem to affect the ones who were on Reyataz.
There was also a shorter time to treatment modification if you were on Epzicom, with either Sustiva or Reyataz. Now, a lot of that was probably because of [abacavir (ABC, Ziagen)] hypersensitivity: They weren't doing HLA-B*5701 screening in this study. So you could argue that kind of a difference wouldn't apply today, where we screen people and they don't develop hypersensitivity reactions.
And then, finally, there were greater lipid changes with Epzicom versus Truvada. And there were greater lipid changes with Sustiva. So if you were on Epzicom and Sustiva, it was kind of a double hit, because you had the two drugs that caused the most lipid changes.
On the other hand, the lipid changes that were seen were not affecting the cholesterol HDL [high-density lipoprotein] ratios. So some would argue that, even though there are differences, it's probably of marginal clinical significance.
There are all sorts of other comparisons we could look at, but it gets pretty tricky. I guess one that I should mention, too, is that if you did fail on Sustiva, you were more likely to develop resistance than if you failed on Reyataz. And that's not surprising; we saw that in [ACTG study] 5142, when Sustiva was compared with Kaletra [lopinavir/ritonavir, LPV/r].
So, lots of little nuances here, but I think there are at least some conclusions we could draw from this.
Myles Helfand: This is a dizzying number of different conclusions. Some of them are potentially conflicting. Adverse events on efavirenz versus atazanavir; high viral load being worse for Epzicom than for Truvada, but not so much at lower viral load levels.
We've got these four or five different regimens that could potentially work really well for first-line therapy. Do you need to literally go to a chalkboard and work out a chart where you're laying out, "OK, so these are all the pluses of this regimen; these are all the minuses"; and then weigh positives and negatives with many different regimens before you make a decision? Or can we somehow simplify this?
Joel Gallant: I think that's what we have guidelines for. Maybe I have a bias, in the sense that I'm on the [U.S. Department of Health and Human Services] guidelines panel [for the treatment of HIV-infected adults and adolescents]. But I think the guidelines panel does this job for you. They sort out the data, and they come up with some recommendations that I think are quite reasonable.
Obviously, the panel will need to go and look at 5202, and a number of the other studies presented at CROI, to make sure that changes aren't required. But I actually think, personally, that the list is a pretty good list right now, for preferred regimens, and that the 5202 results support the current list.
So the current list of preferred regimens is: Truvada plus either boosted Reyataz, boosted Prezista [darunavir, TMC114], Isentress [raltegravir, RAL] or Sustiva (in which case it's Atripla [efavirenz/tenofovir/emtricitabine, EFV/TDF/FTC]). Those four regimens, I think, are the right ones to reach for. But they won't be the right ones for all patients, and that's where you go to the alternative list, which is also a good list of regimens.
Myles Helfand: That's actually maybe a point worth emphasizing: The word "alternative" can be, I think -- and maybe has been -- misconstrued by portions of the clinical community to mean, well, maybe you should avoid these drugs. But it seems like what you're saying is, if the preferred drugs work really well, the alternative ones work really well, too; they may just not be the greatest ones to use, because you've got better.
Joel Gallant: Yes. I think the point that the guidelines make is very important. It says the "alternative" regimens may be preferred for some patients. So, for example, if you have a patient with kidney problems, then none of those preferred regimens may be the right choice [due to tenofovir's association with nephrotoxicity], and an Epzicom-based regimen may be preferred for that patient. It doesn't mean you're using a bad regimen. It's kind of saying, if all else is equal, you would pick a preferred regimen; if there is no reason not to pick a preferred regimen, you would pick one of them. But a pregnant woman should be on Kaletra [instead of efavirenz], for example. Somebody with kidney disease should not be on tenofovir. So there are lots of reasons to go to the alternative list. And they are perfectly acceptable regimens. Most of them have shown good efficacy, and it's just an issue of maybe some tolerability differences, and things like that.
Myles Helfand: So, moral of the story, as the biased representative: study the guidelines.
Joel Gallant: Yes, absolutely. And I would say, too, that when you look at the guidelines, don't just look at the tables. People tend to think of the guidelines as a few tables that tell them what to do. But, boy, things are getting complex, and especially the "when to start" question -- where, within the guidelines panel, there are differences of opinion. If you read the text, I think you really will learn a lot, and get a better sense for the nuances and subtleties of what we're recommending.
Myles Helfand: That may or may not be becoming more clear as a result of research presented at this conference, which we'll get into shortly.
Moving on to other drugs that are part of our first-line armamentarium: There were new data presented at CROI on darunavir.
Joel Gallant: Darunavir is already approved for both treatment-experienced and treatment-naive patients. It's now a preferred first-line PI at the dose of 800/100 once a day, with ritonavir [RTV, Norvir] boosting, based on the ARTEMIS data. But the package insert, the FDA [U.S. Food and Drug Administration] label, says that for treatment-experienced patients, you should use the original POWER study dose of 600/100 twice a day.
Everybody, I think, has assumed that although the label says "treatment experienced," what really matters is whether patients have PI resistance -- and, perhaps specifically, darunavir resistance. In my own practice, a patient may get the once-a-day regimen even though they are treatment experienced, if I know that they don't have resistance to darunavir.
This study set out to prove that, presumably so they could get their label changed. They took patients who had treatment experience, but no darunavir resistance, and they randomized them. They randomized them to either the once- or twice-a-day regimen. What they found was that the results were the same for the two arms.
The problem with the study is that, in fact, most of these people had no PI resistance at all. That's kind of what happens these days; when people fail PIs that are boosted, they tend not to have resistance. So again, this study was really comparing once a day versus twice a day [in PI-naive patients]. So it's no surprise that they would do just as well on once a day. But nevertheless, at the very least, it could lead to a change in the label to say that you would use this for patients with no PI resistance, or patients with no darunavir resistance. That would help a little bit.
Myles Helfand: Is there anything that's particularly new here? Presumably, even though it wasn't necessarily approved [for this use], I'm assuming at least some clinicians were already prescribing once-daily darunavir [in treatment-naive patients].
Joel Gallant: I would hope so. It just doesn't make any sense to go strictly by whether they are treatment experienced or not. I understand that the FDA had to do it that way, because that was the way the ARTEMIS study was set up. But from a scientific standpoint, what you care about is whether they are resistant to darunavir or not.
For me, the interesting part of this study was really the lipid results. There was a very significant difference, favoring the once-a-day arm, in cholesterol, LDL [low-density lipoprotein] cholesterol and triglyceride elevations. People on twice-a-day [darunavir] had quite a lot more -- almost double the amount of lipid elevations.
We've questioned whether the differences among PIs are due to the PI itself, or to the amount of ritonavir, or both. In this case, you can't be sure, because one group is getting 1,200 mg of darunavir and the other is getting 800. But I think the more significant difference is that one group is getting 100 mg of ritonavir and the other is getting 200. I suspect that that's what's really driving this difference, which I think supports the idea that we should be using 100 mg of ritonavir unless we have a good reason not to. In a naive patient, there's almost never a reason not to use a regimen that includes only 100 mg of ritonavir.
Myles Helfand: When is there a point in twice-daily dosing of darunavir/ritonavir?
Joel Gallant: There is a point for treatment-experienced patients. For those with PI resistance, that's definitely the dose to use. But what I think it tells us is that -- at least these lipid changes suggest to me that -- the guidelines are correct in narrowing the list of preferred PIs to boosted atazanavir and once-a-day boosted darunavir. Because why would you use a regimen where you had to use 200 mg of ritonavir unless there was a good reason? Why not use the lowest possible dose of a drug that clearly elevates lipids?
Myles Helfand: From here, let's move into a topic that I suppose has been growing in its urgency over the past couple of years, or at least has received a large amount of renewed attention: the idea of latent HIV reservoirs, and what happens when a person is on fully suppressive therapy over many years, but yet still appears to be developing potential complications, apparently related to HIV. There were a number of studies presented at CROI that examined the idea of taking suppressive therapy and further intensifying it with another drug, with the idea of maybe drawing out some of that latent HIV.
Joel Gallant: Well, there are two ideas around intensification. One is to try to improve CD4 response, and the other is to further suppress viral replication. So, for example, we had the ACTG study looking at maraviroc [MVC, Selzentry, Celsentri] intensification in people who were suppressed on antiretroviral therapy, but were having poor CD4 responses. And the hope was that, because maraviroc had been shown to have what appeared to be an independent effect on CD4 count, this would improve things. But in fact, it was pretty much a negative study: There were some people that seemed to benefit but, for the most part, there was no clinically significant gain in CD4 count.
That leaves us still not knowing what to do with patients who have poor CD4 responses. Although it's not much help to those patients, I would say that this further emphasizes the critical importance of starting people [on antiretroviral therapy] early, because then they won't get into that situation.
The other type of intensification [we saw presented at CROI] was raltegravir. There was a twofold rationale for this. One was, again, looking at CD4 increases. There had been a little hint of CD4 improvement with earlier raltegravir intensification studies. That was not seen with these [studies at CROI, in which raltegravir intensification] didn't seem to make much of a difference in CD4.
The other idea was to see whether you could take people whose viral loads were under 50 copies/mL, but not under 1 -- in other words, they have some low-level viremia in that 0 to 50 range -- and further suppress it. The idea there being that maybe it's better to have a viral load of less than 1; maybe that would reduce inflammation and immune activation. But also because, from a pathogenesis standpoint, it would tell us whether or not there is ongoing replication of HIV despite therapy -- and that's a really important question.
Most of these studies have not shown any change. You take a person whose viral load is, let's say, 20, and you give him raltegravir, or other drugs. In almost all of the studies, we've seen no difference. What that probably indicates is that there really isn't viral replication going on. This low-level viremia that we see is probably not a function of replication, but a function of release of virus from reservoirs. That's good news, in the sense that we really are suppressing patients' viral replication with the therapy we have. But it perhaps also tells us that we're not going to be able to deal with eradicating reservoirs just with antivirals alone.
Myles Helfand: How long can reservoirs continue to release particles of HIV?
Joel Gallant: Probably as long as they exist. I don't think that the release of these particles is a bad thing; it's not doing any harm. It's just a sign that these reservoirs exist. These aren't viruses that are going on and infecting new cells, and replicating. The real issue is how we eradicate HIV from the reservoirs, not so much how we stop them from releasing virus.
Myles Helfand: As a whole, then, what does this tell us about the nature of latent infection and the power of intensification to really do anything of benefit?
Joel Gallant: I think it says that the way to deal with latent infection is not antiretrovirals, at least not the ones we have now; that we've already done the best we can do at suppressing the virus; and that if we're going to eradicate HIV, or if we're going to try to achieve what Dr. [Anthony] Fauci calls "functional cures," it's not going to be by giving more drugs. It's going to have to be by something that activates latent cells, wakes up the reservoir, or provides some sort of improved anti-HIV immunity. We've done about as much as we can do, in terms of viral suppression.
Myles Helfand: Anthony Fauci, who is the head of NIAID [U.S. National Institute of Allergy and Infectious Diseases], which is a major funder of U.S. HIV research, seems to be thinking in the same direction. He actually announced at this conference that NIAID was going to be focusing its efforts much more on issues related to prevention -- particularly vaccine development -- and eradication, perhaps at the sacrifice of research that focuses on existing treatment.
Joel Gallant: Yeah. You can see the bright side, and the dark side. I mean, who knew that in 2010 we would hear that NIAID was going to really focus on eradicating or curing HIV? For so long, the idea of eradication or a cure was just kind of pie-in-the-sky, and people didn't really talk about it seriously. Now they are, which is great.
Who could predict that we would be really downplaying the role of treatment? The implication is, well, treatment is good enough now, and it's time to move on. Maybe that's correct, in terms of having the greatest impact on the epidemic. But for people who have HIV, obviously treatment research is very, very important to them. So it's a good news/bad news sort of thing.
Myles Helfand: Yeah, exactly. I think it's a tough pill to swallow, no pun intended, for people who are living with HIV, particularly in light of the past couple of years in which we have seen growing signs of people with HIV developing a range of complications, particularly ones -- cardiovascular disease, inflammation, bone disease, CNS [central nervous system] issues, cancers -- that appear to develop at an earlier age than people who are HIV uninfected.
There was a good amount of research that was presented about all of these things at CROI. But the question is, how much of that [research] is going to actually continue?
Joel Gallant: Yeah. That's a very concerning question. I think that's really what's hot right now, is trying to figure out whether this so-called premature aging -- and I say so-called because I don't think it's necessarily a single phenomenon; it may be a collection of multiple phenomena going on at once -- but I think the question is, to what degree do we prevent that with HIV therapy, versus how much of that is going to happen regardless of therapy. I think that's one of the big unanswered questions. There's no question that people do better if they are on therapy than if they're not. But do we completely eliminate the risks by putting people on therapy?
I think the answer we're beginning to see is no, that there are still things that happen, even when you're treated. And we desperately need to continue to research those issues if we're going to begin to see these long-term complications over decades of therapy.
Myles Helfand: What did the research at CROI tell us that's new in those areas?
Joel Gallant: I'm very interested in the whole when-to-start question, and I'm a pretty big advocate of starting people early, even to the point of just starting everybody with HIV on therapy. I think the data at CROI supported that concept, for the most part.
We saw a number of studies that looked at the issue of the CD4 count, including the nadir CD4 -- the lowest that you've had -- and correlating it with the development of certain complications. So, for example, from the large CHARTER study, which was looking at neurologic complications of HIV, they found that your neuropsychological performance on specialized testing was a direct function of the lowest CD4 count that you've had. So if you started out with a low CD4 count -- even if you're on therapy and doing well now -- you have a poorer neuropsychological performance than if you started with a higher CD4 count. Other, smaller studies had shown that before. But I think that's of critical importance in saying that we really need to not be waiting for people to develop low CD4 counts before starting therapy.
There was a group that looked at arterial stiffness as a proxy for atherosclerosis and, again, found that the nadir CD4 count was associated with arterial stiffness. So that the idea is that if you wait too long [before starting treatment], you begin to develop coronary artery disease.
Then we saw that nadir CD4 count was associated with a higher risk of fracture in the HOPS cohort.
So everything just keeps telling me that we need to get away from this emphasis on immunosuppression -- the old idea that, well, as long as you keep your CD4 above 200, you'll be fine. Or you could change that to 350. I think what we're seeing is that HIV does bad things to you, regardless of what your CD4 count is. And we may not see those differences right away, but I think over time, these studies are telling us that it's not good to have viremia, and that we should be focusing as much on suppressing viral replication as we do on preventing immunosuppression.
Myles Helfand: We're just three months removed from the latest iteration of the U.S. DHHS [Department of Health and Human Services] treatment guidelines for HIV-infected people. That most recent update included an adjustment to the when-to-start recommendation. Now the recommendation is that if you're between 350 and 500, you should start therapy. Although, in what may have been a first for the guidelines, they actually specifically state that the panel was split over the when-to-start issue.
Does the research presented at CROI, and other research that's come to light over the months since those guidelines came out, do they just add to the amount of evidence that may further sway members of the panel in the future to go more towards, "You know what? Maybe we should start therapy even higher."
Joel Gallant: First, let me just spell out what the guidelines say now. Everybody agrees that you should start below 500. The split there was only about whether people felt that it was a strong or a moderate recommendation. It was just a split on emphasis. Below 500 is where we recommend therapy overall.
But then half the panel felt that we should recommend therapy above 500 -- in other words, at any CD4 count. The other half of the panel didn't think that was wrong, necessarily, but they just felt that it was more optional. So that was where the split was.
But I interpret this to say that the guidelines now support treatment at any CD4 count, but just with a different sense of urgency, based on where your CD4 is. If it's very high, then it's less urgent. The lower it gets, the more urgent it is. And I certainly think that the stuff presented at CROI only supports that.
I can't say whether it will cause a change in the guidelines. I think that most likely the when-to-start issue will take a rest for a little while, before coming out with yet another revision so quickly. But I certainly think that the stuff we heard is supportive of what the guidelines panel came up with.
Myles Helfand: There were some other presentations at the conference on life expectancy and mortality, and how they relate to CD4 count also, no?
Joel Gallant: Yeah. There had been a nice study a while ago from the Aquitaine cohort in France that basically said that if you achieved a CD4 above 500 and you had an undetectable viral load, and you maintained this for, I think it was, five or six years, your life expectancy was essentially going to be that of the HIV-negative French population. That's a study that I cite a lot to my patients, because so many of these life expectancy things, they'll kind of say, well, overall, you can expect "this many" years of life lost if you have HIV. I don't find that very helpful to an individual patient, because it includes the data from people who don't take their meds, who have hepatitis C -- all sorts of things. And if my patient isn't like that, then they can't really use those data to look at their own expectation. Whereas I think if you narrow it down, as the Aquitaine cohort did, to patients who are doing really well, I think that's very useful.
At CROI, we saw data from the ATHENA cohort, which is the cohort from the Netherlands, which modeled life expectancy for patients who were treatment naive and without AIDS 24 weeks after diagnosis. And again, they found that their life expectancy was around 53 years, which is essentially the same as uninfected controls in the Netherlands.
The French data and the Dutch data say that you can have the same life expectancy [with HIV as without it], under the right circumstances. The question then is: Will your quality of life be the same? Or will you be plagued with complications of aging at a younger age than HIV-negative people? And that's, I think, where the real question lies.
Myles Helfand: As a clinician, how do you talk to your patients about that kind of thing? How do you answer the, "How long will I live? And how well will I live?" questions?
Joel Gallant: I tend to tell patients that if you are starting therapy; and if you're good at taking therapy, you're not missing doses, you're not becoming resistant; and we can get your CD4 count up, that you can expect to live a normal life and die of something other than AIDS. Of course, I can't predict somebody's life expectancy. But I can probably tell them, "You're not going to die of AIDS."
The real question, as I said, is to what degree HIV-related complications will affect your life, even though you're doing well from an HIV standpoint. My own opinion is that if you start early enough, at a high CD4, you can probably avoid a lot of those complications. But what I don't know is whether you can avoid them all. I think that's the real hard question right now, the one we need to deal with the most.
So much of our data come from the practices of earlier years, where we did wait a long time to start therapy. If we started everybody with high CD4 counts -- and that's assuming we can find them at those counts and get them into care -- perhaps we would see fewer complications. That's my hope, as an optimist. But clearly, there is some residual inflammation and immune activation going on, even in people who are fully controlled. So we can't promise people that everything will be just as it would if they were HIV negative.
Myles Helfand: I also imagine there's a certain amount of realism that needs to play into that discussion that you have with a patient who may have been recently diagnosed. Because I think, as probably many of the clinicians who are listening to this could attest, a pretty large number of people aren't diagnosed until they already have CD4 counts that are low enough to have brought them into a clinic or hospital to get tested for something.
Joel Gallant: Yeah. That's the thing we've got to fix. There's all this talk about "test and treat." Let's test everybody and treat everybody. But it was, what, four years ago that the CDC [U.S. Centers for Disease Control and Prevention] recommended routine testing for the whole population. And we have not come very close to doing that in most parts of the country. In fact, in some states, it's still illegal to follow those recommendations.
We have got to do something about this. It's got to be more on the radar screen of people doing primary care, people doing urgent care, emergency room care. We've got to start testing people before they become immunosuppressed. Because so many of these benefits of early therapy are really not even available to such a large percentage of people who are positive, just because they don't get tested soon enough.
Far more important than the question of when to start is: How do we get people diagnosed? And then, if we do that, then how do we get them into care? How are we going to expand HIV care and expand payment for HIV care, to be able to accommodate the patients that will be coming in as a result of testing?
Myles Helfand: Are there answers to those questions? There were a couple of presentations at CROI that talked about antiretroviral therapy as prevention. And I know that here in the U.S., federally funded research is examining a test-and-treat style program in both Washington, D.C., and in part of New York City. But as you said: It's been four years since the CDC recommended routine testing for all adults and many teens, but it's still not happening on a very broad scale. How much of that is related to funding? How much of that is related to inertia -- the tendency for things at rest to stay at rest? How much of it is that stigma about HIV is still pretty bad in the United States, not to mention the rest of the world?
It's a lovely idea, and it's great that it's being investigated. But people are still debating whether global warming exists.
Joel Gallant: And evolution, and landing on the moon, yeah.
Myles Helfand: So how realistic is it?
Joel Gallant: I think that routine testing is realistic. But when I talk to doctors who are friends of mine who aren't in the HIV field; they will be telling me about a case, and I'll say, "What's the HIV status?" "Well, I don't know." I say, "Well, don't you know about the CDC recommendation in 2006? You're supposed to know all your patients' HIV status." "I am?"
It isn't out. They don't know. Unfortunately, maybe we need to have some teeth in this. We need to have some kind of -- you know, link it to state funding. Or some really highly, well-publicized case of a huge lawsuit against a physician for failing to diagnose HIV would get this into the attention of clinicians.
It's partly patient awareness, but I think it's mostly in the hands of clinicians to be implementing this in their practices. In emergency rooms, it's tricky, because obviously they have got a lot of other stuff going on. There is [also] some funding, some financial, aspect to the testing in emergency rooms.
But certainly, in a clinician's office, where you're drawing blood anyway, and you're just checking off a bunch of boxes for blood tests, and all you have to do is just tell the patient, "I do this kind of testing, and I include HIV," and you check off the boxes; that's not really a funding issue. It's just an issue of having it, being aware of it.
You brought up the issue of antiretroviral therapy as prevention. There was this incredible study at CROI looking at discordant couples in Africa. They found that only one transmission occurred among couples where the positive partner was treated, versus 102 transmissions in the couples where partners weren't treated. And that one transmission that occurred, it occurred in somebody who had just started therapy a few weeks ago.
It's an incredibly valuable form of prevention, probably better than anything else we have, including condoms and circumcision and abstinence and everything. It's yet another reason why we have to be finding these patients and getting them into care.
Myles Helfand: We've talked about the testing part of it. But what you've just gotten into is the treatment part of it. And globally, obviously, there are still issues with treatment access, which would limit this. But even in the United States, I would imagine that, for a clinician -- I mean, you probably have a lot of patients who are maybe not thrilled with the idea of starting treatment. So what do you tell them if they maybe aren't psychologically ready to start treatment? What do you tell them to try to convince them that it's a good time to do it?
Joel Gallant: Well, I talk to them about the guidelines. I talk to them about the evidence that we've been discussing. I talk to them about the issue of prevention. If somebody's got a CD4 above 500, I talk to them about these things. I don't push it too hard. But as a CD4 gets lower, I get a little more pushy about it.
But I think getting people into care is the biggest, first step. At least they know they are positive. Hopefully they are not transmitting HIV, and hopefully the fact that they've even come to see me means that they believe in medical care enough to consider therapy when it's really necessary.
I think that, for so many years, people have had this idea that HIV is a disease that you don't treat right away. So that's in everybody's mind. They know that. And I think it's going to take a while to change the mindset of people towards an idea that HIV is a disease you treat unless you have a really good reason not to. That's going to take some education, on the part of clinicians, on the part of patients, so that they won't be so surprised when they come in and they're diagnosed, and you say, "Let's talk about treatment."
But we'll get there. If you have TB [tuberculosis], you don't go to a doctor and say, "What do you mean, I need treatment?" You know that you're going to have to be treated. And I hope HIV will eventually be seen in the same light.
Myles Helfand: We have just swept through a lot of different studies covering a broad range of issues that are, to varying extents, related to antiretroviral therapy. How did the year's premier HIV research meeting stack up, compared to previous meetings? From a clinician's standpoint, what are your main takeaway messages from this year's CROI?
Joel Gallant: That's a good question. For years, I've been going to conferences. And my expectation is that I'm going to come back and I'm going to have a bunch of information about randomized, controlled clinical trials comparing antiretroviral therapy that will advance the field and help us know better how to treat patients. That's really been my focus, and it's been how I evaluate a conference: How many randomized, controlled trials did I hear about? How many new drugs did I hear about?
I think over the last few years, I've had to change that emphasis and realize that a conference can be a good conference even though it doesn't have a whole bunch of randomized, controlled trials. The field has changed and there are other things to learn about. So in that light, I think this was a good meeting. I think that we heard a lot of interesting stuff about complications of both HIV and HIV therapy. I think we heard more supportive data for the idea that HIV is a disease that should be treated. I think we learned more about the role of antiretroviral therapy as probably the best preventive approach that we have -- which is yet another reason to be treating HIV. And we learned, for better or for worse, that we can't necessarily assume that the drug pipeline will just continue to pump out new drugs, so we have to use the ones that we have very carefully and wisely.
I think that the conference helped to support what's going on in the guidelines right now, which was gratifying. So I think it was a pretty good meeting.
Myles Helfand: Dr. Joel Gallant is a professor of medicine and epidemiology at the Johns Hopkins University School of Medicine, and he's one of the top clinician-researchers in the United States. Dr. Gallant, thank you very much for taking the time to walk us through the antiretroviral therapy highlights of CROI 2010.
Joel Gallant: My pleasure, Myles.
This transcript has been lightly edited for clarity.
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