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This Month in HIV: Top 10 HIV/AIDS Medical Stories of 2006

January 2007

Dr. David Wohl is a clinician and researcher at the University of North Carolina In The Body's inaugural "This Month in HIV" podcast, we shine a spotlight on the top HIV medical stories of 2006. To provide a rundown, we talked with Dr. David Wohl, a researcher and clinician at the University of North Carolina-Chapel Hill and an expert at The Body's "Ask the Experts" forums.

Each year, thousands of HIV-specific study results are reported in clinical journals and presented at an assortment of HIV/AIDS conferences. But at the end of the year, which of these studies really mattered?

That's where Dr. Wohl comes in: Since 2003, he's authored The Body's annual summary of the top 10 HIV research reports of the year. In this exclusive podcast, The Body's Editorial Director Bonnie Goldman talks with Dr. Wohl about what he thinks were the most important HIV-related medical stories of 2006. If you want to stay up-to-date on HIV medicine, this is one report you won't want to miss.

We've provided an assortment of options for you to listen to or read this inaugural broadcast. You can listen to the podcast online using our player. If you'd like to listen to the podcast later or put it on your digital music player, you can download the entire 62-minute podcast in a single file or download it in three parts (Part 1, Part 2, Part 3). Not in the mood to listen to a podcast? No worries; you can read a summary of the interview or plow into the full transcript.

The End of Treatment Interruptions?

Dr. Wohl, tell me: What did you think was the number one HIV research study of 2006?

I think, absolutely, the SMART study was the number one study of the last year. It got the most buzz; it generated the most controversy; and it was one of the most surprising results we have seen from a clinical trial in HIV in a long time. This is a very straightforward study, trying to answer a question that's been there for a long time, which was: Do you need to take therapy, HIV therapy, all the time? Or can you take breaks? Can you take holidays, and decrease exposure to the HIV drugs and therefore possibly limit the problems that we see in people who get HIV therapy -- namely, the complications of drugs, which are high lipids and diabetes and perhaps liver damage. [To read more coverage of the SMART study from The Body, click here.]

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So the idea behind this was: Let's give people therapy until their T-cell counts hit around 350, stop it, and then start it up again at 250 -- versus people who just stay on therapy [the entire time]. So they randomized over 5,000 people, in 33 different countries, to treatment interrupt -- let's start it and then stop it, based upon your T-cell count -- or [in the other groups] continuously take their HIV therapy.

Lo and behold, what they found was that actually interrupting therapy, doing the treatment interruptions, was hazardous. People had more problems. First of all, more people died in that arm. Second of all, more people had the toxicities that we usually think about with HIV therapies. So this is bad news. The study was actually stopped early. So I think, on the weight on the evidence that they found, and the importance of their results, that has to be number one [HIV research story of 2006]. It teaches us that interrupting therapy, and tolerating low CD4 cell counts, in the history of bad ideas, is a pretty bad idea. [To read more about structured treatment interruptions, click here.]

But don't you think that one of the interesting things of the study was that the people who did get sick, or did die, did not have low T cells?

The way it turned out was not exactly that. It turned out that people with higher CD4 cells had an even greater risk with treatment interruptions than people who continued on therapy. That's where you saw the biggest difference, as far as bad outcomes, between the two arms of the study. In the low CD4 cell count group, both arms had people getting sick and people dying. So it wasn't that -- oh, you have a 50 CD4 cell count and you interrupt therapy and nothing bad happened to you. It did, but bad things happened to people who continued therapy, who had a low CD4 count, too. But it was the people who were doing really well -- high CD4 cell count, low viral load -- who did treatment interruptions, who suffered the worst.

Does this study end the idea of a structured HIV treatment interruption?

The notion of structured treatment interruption is not dead, but it's on life support. It's not doing well. This study really puts a chill on any notion of doing treatment interruptions. Granted, some people will say, well, the problem here wasn't so much treatment interruptions, but that they tolerated low CD4 cell counts [and] two hundred and fifty CD4 cells is just too low. Maybe if the safety net was raised a little higher, people could have done well. But, boy, it's going to be really hard to do a [treatment interruption] study now, unless you have incredible safety mechanisms built into the study.

So the take-home message is: HIV is bad, and treatment is good.

HIV is bad, treatment's good, and funny enough, cardiovascular disease, hepatic disease -- that's liver disease -- as well as kidney disease. So heart, liver, and kidney disease were more common in people who stopped their therapy -- meaning that maybe HIV itself has a role to play in these so-called complications of HIV therapy, and that actually being in HIV therapy might be better for you, as far as these are concerned. That's why it's number one.

Battle of the Titans: Kaletra vs. Sustiva (ACTG Study A5142)

What is number two, then?

Number two is a clinical trial. It's called ACTG, and that stands for AIDS Clinical Trials Group. That's a national, federally funded network of sites across the country doing research on HIV. [The] ACTG study is called 5142 and this study [was] straightforward. It pitted [against each other] the two major therapies that are listed on government guidelines for initial therapy of HIV: One is called Kaletra [generically known as lopinavir/ritonavir] and one is called Sustiva [generically called efavirenz, also known as Stocrin]. It pit them against each other in people who'd never been on therapy before.

There was a third arm, where people just took those two drugs without any other drugs. As you know, most people will take Kaletra or Sustiva with two nukes [NRTIs], such as Truvada [generically called tenofovir/FTC] or Combivir [generically called AZT/3TC]. People [in the trial] could choose their nukes in those two arms [of the study]. So there's a Kaletra arm and two nukes; there's a Sustiva arm and two nukes; and then there's a third arm of just Sustiva and Kaletra. [To read more coverage of this study from The Body, click here.]

The really interesting thing about this study was, again, unexpected results. After 96 weeks of therapy, people who got Sustiva -- a greater proportion of them -- had less than 50 copies on their HIV viral load, compared to the Kaletra group. The Kaletra/Sustiva arm together; that was sort of in between. It was significantly different between the Sustiva arm and the Kaletra arm, in favor of Sustiva.

When you look at T-cell count, however, though, remarkably the people on Kaletra and two nukes had a greater gain in CD4 cell count statistically than people on Sustiva. Both groups had increases of over 200, but there was a bit more of an increase in the people on Kaletra. Another aspect of this is the side effects. About the same proportion of people taking [either] Sustiva or Kaletra with two nukes had the same amount of side effects. It really wasn't that much of a difference between the two. When you look at really bad lipids, especially bad triglycerides, there was no difference seen at all. That's interesting because many people think that Kaletra, of all the drugs, is more likely to cause really big increases in triglycerides; [and most people think this is] much less [true with] Sustiva. But as far as high-grade triglyceride levels: We didn't see any difference between the two of them; [in fact] it was fairly unusual -- less than 6 percent of people [had high-grade triglyceride levels].

As far as [HIV drug] resistance goes: no surprise there. People on Kaletra just don't develop resistance to it that easily, even when they fail the drug, or a regimen with the drug in it. As opposed to Sustiva, where it's easier to get resistance. People who do fail it -- and remember; the majority of people didn't fail these drugs, or didn't have these drugs fail them -- but of the few who did develop resistance, you did see more resistance to Sustiva and to a nuke that they were taking, [for example,] Epivir [generically called 3TC or lamivudine]. So that's not a very big surprise.

On the whole of it, we see that these two drugs have some strengths and weaknesses, relative to each other. People are going to have to decide: "What's more important to me?" And different people will come up with different answers.

Do you think this study helps us individualize treatment choices better? For instance, if somebody is having problems adhering, then maybe Kaletra will be better, because there's less chance of resistance occurring. If somebody needs to boost their CD4 count, because they start treatment when they have a low CD4 count, they might want to try Kaletra, also.

Absolutely. I think that that's one example. Or it could be the convenience of Sustiva now -- which is included in the new one pill, once a day combination of Atripla [which contains Sustiva/Viread/Emtriva, generically: efavirenz/tenofovir/FTC]; maybe that would mean I'm willing to take the risk that if this person develops resistance, they're going to get resistance to two of the medicines in here. But it's simple and easier [than that]. A greater proportion of people [who were] taking the Sustiva got [a viral load of] less than 50. So I think, on one hand, you could look at it one way; on the other hand you could look at it a different way. The clinician and the patient have to take these [different options] and decide, well, what was more important for me in this particular study? What's better?

We're talking about two drugs that -- the majority of people do really, really well on these therapies -- and what we're talking about is actually really fairly moderate differences between the two. Not rip-roaring -- they're statistically different -- but I think both of these regimens are really good choices. But there are, again, some strengths and some weaknesses to each.

This was a government study?

It was. It wasn't funded by the pharmaceutical companies themselves. It was done by the U.S. government.

Is it really important to have a viral load of less than 50? Shouldn't the drug win if it can do that?

Yes. Having a viral load of less than 50, I think, is really important. I think the less virus you have, the longer [you have it], the better [it is]. I think that for people who have had a lot of treatment history, who've been through the wringer and are veterans of lots of different therapies, and have had a really hard time getting their viral load down; they shouldn't feel bad that their viral load isn't necessarily undetectable. But for initially starting therapy, people who have never been on therapy before, getting your viral load less than 50 and keeping it there is really the hallmark of a drug therapy that works really well.

Both these drugs got a lot of people's [viral load] down [to] less than 50. The problem is that there were some differences where, in the Kaletra arm, you saw more people get [viral loads] above 50 subsequently, or not get below 50 when they needed to. In the Sustiva arm, you saw a little bit better success. But there are counterbalancing forces that you mentioned, such as the resistance, and also the T-cell count gain that we saw with Kaletra. So on the whole, it's hard to say that one of these drugs is better than the other. They're different.

We didn't talk about side effects profiles. Kaletra has more side effects -- stomach problems -- and Sustiva has other kinds of problems. So that's another choice people have to make. What's really interesting is that, when we looked at the study, when you look at people who come off of their therapy either because of viral problems -- their viral load is not responding the right way -- or toxicity; using those both together, we saw that Sustiva was better than Kaletra, in this particular study. When you look at serious side effects, though, we didn't see any major differences between the arms.

There's going to be more data coming out very soon about this study. We may see that there's more diarrhea on one arm or more sleep problems in the other arm, as you might expect. But so far, right now, when we have only just the serious adverse events that have been presented so far, we don't see major differences between the two arms. So tolerability wise, it may come down to some of the more mild side effects that can certainly be troublesome. But the life-threatening ones: We didn't see a big difference between the two at all.

I am a little confused why this is a top ten study when the results are similar. They're both very good drugs and they both did more or less the same in the study. So it's nice that it showed that, but we kind of knew that.

"So for me, and for, I think, a lot of clinicians who are, I'm sure [thinking]: 'Should I prescribe Kaletra or should I prescribe Sustiva?' ... Now we know for sure -- this is what this one does; this is what that one does; and that's why I'm going to choose this one over that one."

I think the part that we didn't know, and why I really feel it's important is: One, we really didn't understand how these drugs would perform when compared with each other. I think that that alone is helpful. They have each been studied against other drugs and they've always come out at least on top. Nothing's ever beaten these two drugs. So when they're pitted against each other, you really have a better sense of what they're able to do. So for me, and for, I think, a lot of clinicians who are, I'm sure [thinking]: "Should I prescribe Kaletra or should I prescribe Sustiva?", the ambiguity that we had is really eliminated. Now we know for sure -- this is what this one does; this is what that one does; and that's why I'm going to choose this one over that one.

For clinicians, for the doctors, this has really been a big deal because the [U.S. treatment] guidelines say we could choose either one, but there's been no data to help us understand. Well, which one should we choose? [When] a study comes out and shows that there's some balance between the two -- well, that's research. That could be good. Then it makes us feel maybe it's okay, no matter which one I choose. I could flip a coin, and people are going to do generally well. But the key thing here is, the drugs didn't perform exactly identically. There are differences between them. We're going to find out a lot more about their differences in the next month, because there's going to be a major U.S. conference here, and the second part of the data is going to be presented. I think we're going to see even more information that could help us understand the relative differences between these two agents. So stay tuned.

Great! Now we're up to top story number three.

A Potpourri of Comparative HIV Treatment Trials: KLEAN, BMS-089 and Gilead 934

Number three is actually three studies in one. I couldn't decide. No one of these trials was good enough to be number three, so I combined three different studies to make sort of a clinical trial potpourri. I'm going to go through them very quickly.

One is called the KLEAN study -- that's K-L-E-A-N -- the KLEAN study. Snazzy name. [To read coverage of KLEAN from The Body, click here.] It also was a comparative, head-to-head trial. Again, clinicians love these [head to head trials] because they help us understand what's the best thing to prescribe to patients. It compared our friend Kaletra again, versus Lexiva [generically called fosamprenavir, also known as Telzir]. Lexiva's another protease inhibitor. It's not been as popular [as Kaletra]. It's also boosted with Norvir [generically called ritonavir], and Norvir is already built into Kaletra. So [Kaletra and Lexiva] are similar in lots of different ways. This, again, was studied in patients who were treatment naive, [i.e., they] never had been on HIV therapy before. Lo and behold, as opposed to what we saw in the study I just described: these two drugs were almost exactly identical in getting the virus down, getting the T-cell count up, in how much resistance we saw, and in their tolerability.

The big thing from this study was, a lot of people perceived that Kaletra would cause more lipid problems [than Lexiva]. It turned out there were no differences as far as cholesterol and triglycerides in this study -- between the two arms. So I think this is a very neat study. I think it was nice to see the differences, that there were no major differences at all, and that these different protease inhibitors are acting very similar. There are other data, looking at each of these drugs compared to other protease inhibitors, that show similar sorts of equivalents. I think that this whole class of drugs is going to turn out to be more alike than disalike. So that's why I like that study.

Was it this study that gave Lexiva a place in the preferred list?

It absolutely helped secure Lexiva a preferred spot on our [U.S.] government guidelines. No longer does it just list Sustiva and Kaletra; now Lexiva's there, as well.

That's a perfect segue to the second study that I'm going to mention as part of number three, and that's a study of Reyataz [generically called atazanavir], because Reyataz has also been added as a preferred agent to the public health service [U.S. Department of Health and Human Services HIV treatment] guidelines. This is a study that compared Reyataz against itself. How's that for being clever? They took Reyataz, which is usually boosted with Norvir, and compared it to Reyataz without Norvir. The idea here is that Reyataz without Norvir has been studied against Sustiva in the past, and turned out to be just as good as Sustiva. [To read an abstract of this study, click here.]

So, here, they wanted to say: What happens when you boost it with Norvir? What happens, as far as getting the virus down, and as far as side effects? The bottom line for this study as well was that there was a difference. Overall, both drugs performed rather well. But what we saw was that the people who got the boosting [of] Norvir with their Reyataz: we saw more side effects.

"We can see that triglycerides and total cholesterol actually went up significantly more in the people who got Norvir with their Reyataz [as opposed to] the people who just took Reyataz without Norvir."
On the other hand, when you look at the people who didn't get the Norvir with their Reyataz, there were a little bit more virologic failures. The last part of it was, when you look at lipids: Reyataz has been touted as a drug that is lipid friendly, as opposed to the other protease inhibitors. Well, when you take some Norvir, some of that friendliness goes away, and we can see that triglycerides and total cholesterol actually went up significantly more in the people who got Norvir with their Reyataz [as opposed to] the people who just took Reyataz without Norvir.

I think these are really helpful data for people to understand. Previous to this, believe it or not, despite Reyataz plus Norvir being a very popular therapy, we didn't have data on that combination of Norvir and Reyataz in people who'd never been on HIV therapy before. So it was really just long in coming and was refreshing to see. For people who are really interested in their cholesterol -- as many, many patients are -- it was good to understand just exactly what Reyataz plus Norvir does to lipids.

Has there ever been a study comparing Reyataz and Norvir with Kaletra?

There is a study that's going on right now. It's being sponsored by the makers of Reyataz. Again, it's a treatment naive study -- people who've never been on treatment before. I'm really looking forward to those results.

With those results available, we'll really know more. Like the other study, the 5142 study, we'll know how Reyataz rates in terms of the top preferred drugs.

Absolutely.

Because we still don't know that, right?

We don't know. I think that as you get these drugs on the preferred list, we have to understand: Which one of them might be better than another? Of course, this comes down to [the question]: Is this just us comparing apples and apples? We might be. But these are major decisions. When we prescribe a therapy for someone, this is going to maybe be for years, if not life, for some people, who do extremely well. I think it's worthwhile to have a study tell me [when] one of these preferred therapies might have some advantages over another.

Exactly. Okay. Are we done with three, and up to four?

No. The last thing on three -- and it doesn't require even as much conversation, because these are results that have been talked about before. This is a Gilead study -- Gilead 934. [To read coverage of Gilead 934 from The Body, click here. To read an abstract from the study, click here.] The study looked [at] Combivir versus Truvada when either one of them are paired with Sustiva. Now this is shifting from the protease inhibitors and the non-nukes [NNRTIs], like Sustiva, and shifting over to look at the nukes. Combivir and Truvada have been in a death battle for the last several years for market share. Really, there weren't a whole lot of data that were out there comparing the two. This study is really the definitive study. It's gone on for long enough now that we've got some really good data.

"The bottom line for this study is that both of these drugs [Combivir and Truvada] -- when combined with Sustiva -- can get the viral load down about the same."

The bottom line for this study is that both of these drugs [Combivir and Truvada] -- when combined with Sustiva -- can get the viral load down about the same. There are no major differences between the two in getting people less than 50 copies on their viral load.

The differences are that early on, during the first year of therapy, there are more side effects that you see in patients on Combivir. These are initially starting patients [treatment naive]. It's not people who have been on therapy for years and years. These are people who are just starting therapy, during the first year. [We saw] more anemia and more AZT-related side effects [were seen] in the Combivir arm than we saw in the Truvada arm. But overall, when you just look virologically, it looks better.

Immunologically, there is a bit of a bump [increase] in T-cells in people who are taking Truvada, a greater bump than we saw in the Combivir arm. But overall, I think, it's reassuring that these therapies look pretty equivalent, and that Truvada can hold its own. A lot of people complain there's not as much data about Truvada. But I think this study and other studies of Truvada, or drugs like Truvada -- Viread [generically called tenofovir] and Epivir [known generically as 3TC, lamivudine] -- previous studies of that have looked good. I think it shows us that Truvada certainly deserves its place as a preferred agent, up there along with Combivir.

So I think this is an important study. Again, with the other ones, I think this helps us understand a little bit more about how to take therapy, and how to prescribe therapy.

"So in the most strict sense -- just looking at the proportion of people who get [to a viral load of] less than 50 -- there wasn't any difference between the two drugs [Combivir and Truvada]."

There was a lot of press after the study results were released. The implication, in some of the coverage, was that if you're on Combivir you should change to Truvada because it was so much better. Is that what the study suggested?

Yes, well, it's interesting because when the study was designed, the major result that they wanted to look at, was how many people got down [to a viral load of] less than 400 copies, not less than 50. That's been a strategy that's been used a bunch of different times. When you do look at getting less than 400, the advantage goes to Truvada. But I feel we should be looking at the same sorts of things we look for in our clinic. I look for people to get less than 50. So in the most strict sense -- just looking at the proportion of people who get [to a viral load of] less than 50 -- there wasn't any difference between the two drugs [Combivir and Truvada].

So is one better than the other? I think this study shows that, again, they both are potent. There are some differences: Tolerability-wise there are some differences between the two. But, boy, it wasn't like completely blown out of the water. Combivir wasn't blown out of the water in this study. I think that people who are on Combivir and are not suffering from any of those side effects and have been on the drug for more than a year can expect not to really develop a whole [lot] of them -- should not expect to develop new toxicities related to this. So I think that I have been reluctant to switch people who are doing very, very well. That's not to say people who've been on Combivir, which is a twice-a-day medicine, haven't come into the clinic saying, "I read about this new once-a-day medicine. Can I switch over?" I have no problem switching them over.

What about fat wasting and Combivir?

I'll touch upon this in a few minutes, when I talk about another study. But in this particular study there were DEXA [dual energy x-ray absorptiometry] scans done, and those are scans that can look at fat in the body, in different compartments. It found that there was a difference between the two study arms, in that people on Combivir tended to lose fat in their arms and legs, where people on the Truvada gained some fat.

Now the rub comes in: The sponsor of the study did not build in these DEXA scans at baseline. So they don't know what people were like when they first started. The first time DEXA scans were performed were at week 48. So that means people had been on therapy for 48 weeks. Then they got another scan at week 96 of the study. So we're looking at changes that occur after week 48; that's not the cleanest way to do things. There will be another study, that I'll talk about in a few seconds, that found a very different result; that was done a little bit more rigorously.

So we still don't know. Perhaps it's the Retrovir in Combivir that might be causing the wasting.

It might be. Retrovir or AZT has been described as being responsible for fat wasting -- certainly nowhere near Zerit [generically called stavudine or d4T] -- but I think that the data are pretty mixed right now. I do think that -- and we'll talk about this again in a minute when we talk about this other study -- it also depends what you're taking with your AZT or Retrovir [generically called zidovudine or AZT]. If you're taking certain medicines, it seems to make things worse. So I think that a year ago, I would have told you that I thought AZT can cause some fat wasting. Now I'd have to qualify that a little bit, based upon some of the results we're seeing from other studies, as well.

Great. So, on to the next one?


Circumcision as HIV Prevention

On to number four. This, again, involves clinical trials. I like clinical trials because I think they help us understand how to do things. But this is not a drug clinical trial, not even a treatment strategy clinical trial; it's a prevention clinical trial. This was looking at male circumcision.

There had been some data showing that men who were circumcised seemed to be less likely to acquire sexually transmitted diseases, including HIV. This has been noticed in many parts of the world. So to help understand whether or not [circumcision] can really work in preventing acquisition of HIV, three different studies done in Africa -- one done in South Africa, one done in Kenya, one done in Uganda -- randomized men who [were] HIV-negative to get circumcised or not, and just continue. [To read an abstract of the South Africa circumcision study, click here. To read more about the Ugandan and Kenyan studies, click here.]

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Everyone got lots of counseling. Everyone was told to use condoms. Large numbers of men were enrolled. In all three studies, the same thing was found, and that was that men who got circumcised had a profound reduction in new HIV infections compared to men who remained uncircumcised. So this is just really, really, incredibly important. First, that you could even do a study where you randomized men to have their foreskin removed is notable. That three studies were able to do it, over thousands of patients, is completely just remarkable. That alone gets it on the list.

But all three studies found the same thing: [That circumcision greatly reduced rates of HIV infection]. In fact, the three studies were all halted early because of the differences that were seen between the two arms. Now, some caveats. One is: There were men who were circumcised who caught HIV. So it's not absolute protection. What we're talking about is a relative reduction.

Number two is that circumcision is not without problems. Now, in these three studies, [the operations] were done in state-of-the-art clinics, and it was done well, but real world application may be different. We certainly don't want to minimize the complications that can occur with any surgical procedure that might be done as a preventive measure, where there's not really another indication. Certainly, there can be complications. And there are a finite number of those complications. So I think those are two major things.

The third thing is that we really don't have data about how this would work here [in the U.S.]. But I think that, given the data we're seeing, and there are data that men who have sex with men in the United States who are circumcised seem also to be a little, little, little bit less likely to pick up HIV. Now, again, there are plenty of circumcised men who have sex with men in the United States and Europe who have HIV. It doesn't offer you great protection, but it might offer a little bit more protection.

"As someone I overheard said, 'We're not going to circumcise our way out of this epidemic,' but it will reduce the rate of new infections in some places."

I also think that the last thing about this is, there could be an adverse effect here, and it's not related to something happening with someone's penis; it's something that's not happening with someone's penis. That is, men who get circumcised, [may] have a false sense of security; and really, that would be a shame. You could lose completely the benefits offered by circumcision if condoms aren't used. So why get circumcised if you're going to use condoms all the time? Well, that could be a very valid question. As someone I overheard said, "We're not going to circumcise our way out of this epidemic," but it will reduce the rate of new infections in some places. If you're one of those people who got circumcised and didn't catch HIV, and you live to be an old man ... great. It worked for you.

Can you explain why circumcision is effective at reducing HIV transmission?

Why they have less risk? The mechanism? Well, I think the idea here is: What does the foreskin do? The foreskin creates a nice, warm, dark place in a part of the body that is exposed to sexually transmitted diseases. As such, it can harbor sexually transmitted diseases. [The explanation for this] also includes cells: Because cells are there [in the foreskin], because there's inflammation that can develop there. Not all men take care of their foreskins the same way, and not all men have the same type of foreskin. Not all men live in the same kind of conditions. So what you see is that there could be inflammatory cells there. Inflammatory cells are just the gates through which HIV can enter the body. There are T cells there, if there's any inflammation.

So I think that removing that foreskin creates an environment where it's a little bit less hospitable to the HIV. We've seen this with other sexually transmitted diseases. We know that this occurs.

What was the percentage that HIV infection was reduced?

About [a] 40 to 60 percent reduction, over a short term. Now, we don't have long-term data because these studies were stopped before they could complete them.

"The difference between [circumcision] and an AIDS vaccine is, this would be a horrible vaccine because the protection is just so spotty. Look, I read somewhere that maybe something like 60 percent of men in sub-Saharan Africa are already circumcised."

So right now, that's kind of the closest we've come to an AIDS vaccine, right?

Yes. The difference between this and an AIDS vaccine is, this would be a horrible vaccine because the protection is just so spotty. Look, I read somewhere that maybe something like 60 percent of men in sub-Saharan Africa are already circumcised. Widespread circumcision hasn't protected that continent, at all. So I think we have to take this all with a grain of salt. This is not going to be a major, major preventive measure. But it adds to the ones we have now.

As I point out in our article on TheBody.com: When you can count on your fingers, you can count with your ABC's what we're told works, as far as preventing HIV, it's nice to put up another finger and say, well, there's also circumcision. I wouldn't discount it as being something that can help some people, but it's certainly not going to be the equivalent, a surgical equivalent, of an HIV vaccine.

So now we're up to number five.

The Benefits of HIV Treatment and the Price Tag

Number five is an interesting study, and I think it's also a somewhat misunderstood study. What this study tried to do was understand how much it costs to treat people with HIV during their lifetime in the United States. [To read an abstract of the cost-analysis study, click here.] What these investigators did -- and these [researchers] are all people who think a lot about quality of life and cost/benefit analysis; this is sort of a dream team of people who are known for doing this kind of work. What they did is, they created a computer model of a hypothetical cohort of individuals who are starting HIV therapy. With that computer model, they can adjust things, like starting T-cell count. If we start everyone in the clinic at 200 CD4 cell count, versus starting them at 350 CD4 cell count, versus starting them when they first get diagnosed, we could see how much things would change, how [much] things would cost. They dumped into this model data from a whole bunch of different sources -- from how much drugs cost, to how many times people get hospitalized (and for how long), and how much that costs -- all these different things.

They came up with some really interesting findings, based upon how they ran this model. One thing they found is that it costs a lot to treat HIV; and that's not a surprise to anyone. But what they found especially was that, as the CD4 cell count drops, the costs increase. The costs are really built in; as you get further and further in the progression of HIV, from caring for people in the hospital, and those inpatient appointments certainly count for a lot; and there [are] more frequent outpatient appointments. People who are doing better, people with higher CD4 cell counts, they're not in the hospital as much. They are also certainly not seeing people in the clinic as much. So, the clinical cost [is less].

In fact, the fraction that is made up by HIV therapy, as a segment of the total cost, starts to diminish as people's T-cell count drops. For people with a high CD4 cell count, therapy is the big-ticket item. For people with a low CD4 cell count, that's [the cost that has] got to get a little bit diluted by all the clinical care they're acquiring.

"Based upon their modeling, the lifetime cost of treating a person with HIV who starts at around 350 CD4 cells or less was almost $400,000."

So I think that was one thing. Based upon their modeling, the lifetime cost of treating a person with HIV who starts at around 350 CD4 cells or less was almost $400,000 -- and that's including discounts on HIV medicine that are taken into consideration. So overall, that was the cost. In fact, when you look at people who start HIV therapy right after infection, even though you're treating people longer, the cost goes down. That was because people just generally are doing better; they're not going to have any of these adverse consequences that are related to progression of HIV. There's further discounting as time goes on. So that was sort of an interesting finding. [To read more about the economics of HIV, click here.]

The other thing that came out of this study that I think got some attention -- maybe unintentionally, from the investigators' standpoint -- was that to understand how much it would cost to treat someone for the rest of their life, they had to kind of "guesstimate" how long someone with HIV, starting at the levels we start HIV therapy now, would live. Their computers spit out a number of about 24 years. Now, that 24 years was based upon this computer simulation, based upon all the data we have on how people do with the current batch of HIV medicine, This is how long we would expect someone to live. It doesn't say anything about what really can happen to any one individual starting today on HIV therapy.

So I think that it's not to be looked at as -- this is the best HIV therapy can do. It's a ballpark figure of what we could realistically expect someone starting therapy today, on average, to do ... how well they will do. There's all sorts of factors that could get played into that, including how old you are when you start therapy. Certainly, someone 70 years old starting therapy would have a different life expectancy than someone 25 starting therapy. It doesn't take into account new advances that could happen this next year, or within the next five years, [which] can change that completely.

I think a lot of people have centered in on that 24 years. On the other hand, the 24 years, I think, is not a bad number. I think it shows that we have made tremendous gains over the last several years of extending people's lives. So I think that this is an important article, because it helps us understand, policy-wise, that treating HIV sounds expensive, but compared to other chronic illnesses, it's not that bad, and that people are expected to live decades -- on the order of decades, not years.

But what do you think, Dr. Wohl? Do you think that people have a normal life expectancy if they're diagnosed with HIV in 2007?

"If people come in with a little bit higher CD4 cell count ... listen to most of what I say and take care of themselves, I tell them I expect them to get old and gray, that they can live, literally, for decades."

Of course, it all depends upon how people come in. But when I see someone who is not fantastically elderly, who comes in and does not have a CD4 cell count of 50, and [does not have] PCP pneumonia [pneumocystis carinii pneumonia], or cryptococcal meningitis, or any of these horrible infections people get when they have really advanced AIDS. If people come in with a little bit higher CD4 cell count, who basically can follow through, who can come to their clinic appointments, listen to most of what I say and take care of themselves, I tell them I expect them to get old and gray, that they can live, literally, for decades.

Even if you took [these data] literally [it's not bad.] I say to someone who's 40 years old and comes into the clinic, "Look. Over the next 25 years I expect you to do great. Not that you're going to explode at year 25, but that, relatively, we can expect you to do great. What do you think's going to happen in the next 25 years? We're definitely going to see advances in care. You're going to be around. My goal is to get you around until there's a cure. So your job is to not do crack cocaine. Your job is to come to clinic and take most of your medicines." That's the kind of conversations I have. Some people I see are already in their 60s or 70s. I do tell them, "This is not going to kill you." When I see the 25-year-olds [in my office], I say, "We're going to have to work together, because we want you to be alive for a long, long time. There's less room for you to mess up. Let's get you on therapy, good therapy. Let's keep you on it for years and years and years." Again, "let's add up the decades."

Great. So it's a very positive study.

I think it's a very positive study. It doesn't cost that much, and people are getting benefits. Duh. We need to start supporting HIV therapy for everybody.


Value of HIV Viral Load in Predicting CD4 Cell Count Decline

Number six is a really technical article, and I think it was really important. I think it's going to spark a lot of conversation. The bottom line for this study is: we know that viral loads are important. They're not like CD4 cell counts; viral loads are different. A viral load's use is that it can help us understand what's the likelihood that someone's T-cell count is going to drop. When someone comes into [the] clinic, we get a viral load and CD4 cell count. If your CD4 cell count is 400, and your viral load is high, your doctor gets a little bit worried because that means that likely, over the next year or two, your CD4 cell count's going to drop quicker than someone who comes in that same day, has a CD4 cell count of 400, and has a very low viral load.

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We think about the viral load as sort of the engine that's driving the CD4 cell count decline. The more virus you [have], the worse it is. I tell my patients: foxes and rabbits. Your T cells are rabbits, your virus: foxes. The more foxes you [have], the quicker the rabbits are going to disappear. We've got to get rid of the foxes.

That was sort of the paradigm that we'd been following for a long time, sort of the model. It's based upon some data that are almost 10 years old now. Well, in this study, they looked at the viral load before people started therapy, and looked at T-cell counts in a bunch of individuals from different clinics across the country, but mostly from California.

They found [that], when you group people into big categories, the viral load does seem to predict what happens to people [in general] -- but not individual patients -- very well. What they found was that when you look at people who have a viral load that's high, and a viral load that's low: some of the people who have a viral load that's low saw their T-cell count drop really quickly. Some of the people who had a high viral load: their T-cell counts didn't drop that quickly. There was a lot of overlap between patients. For any one individual patient, the viral load didn't do very well at predicting how quickly the T-cell count would drop.

"They found [that], when you group people into big categories, the viral load does seem to predict what happens to people [in general] -- but not individual patients."

What it did is, if you took a whole bunch of patients who had a similar viral load, generally their CD4 cell count dropped at a different rate than another group of people who had a viral load of a certain amount. So if you had a group of people -- 20, 30, 40 people -- who had a high viral load, they would tend to have their CD4 cell count drop quicker than people who had -- a group of 40 patients or so -- a low viral load, on average. But when you start breaking it down and looking at individuals, that kind of falls apart. [To read an abstract of this study, click here.]

This is a really important study because this helped clinicians understand: We cannot be putting as much stock into viral load; applying the viral load that we've got, looking at groups of patients, to the one individual patient in front of us. I think that that is sort of a very, very interesting concept, and there's going to be a lot more discussion. There will be other studies that will come out from this one that I think we'll have to look at, and see if this holds up. But this is a well-done study.

The World's Best Metabolic Study: ACTG 5005s

Number seven. This gets back to the issue of body shape that we talked about before. There's another AIDS Clinical Trials Group, the ACTG national group (the U.S. government group), another trial that they sponsored, [which] looks at changes in body shape and lipids, and a whole bunch of other things in patients who were assigned to either be on a protease inhibitor, Viracept [known generically as nelfinavir], Sustiva, or a combination of the two.

Then there were also patients who were getting Combivir with those, or Zerit and Videx [generically called didanosine or ddI]. [To read more coverage from The Body on this study, click here.] There's a complicated sort of scheme of how the patients were handled in the study. But the bottom line for this particular study is: They were able to collect data, body shape data and other types of data related to metabolics, on patients over a long period of time, over 144 weeks. They were able to look at how people did, as far as their body shape.

The thing that I really liked about this study was that they looked at people who were just on Combivir -- not the Zerit and the Videx, which we know can [cause the] fat in your limbs to waste. When you just stuck with Combivir, which, like we talked about before, most people don't consider Combivir offensive to arm and leg fat (although there are some people who feel that it could, like we talked about with the Gilead study). When you looked at people who were on Combivir and the protease inhibitor Viracept: They did see decreases in their limb fat over time, whereas people on Combivir and Sustiva didn't [see this decrease in limb fat]. Now, these are not huge, huge numbers of patients, but I think it really indicates that there may be some difference between the effects you see with a drug like Combivir, depending on what it's coupled with. When it's taken with a protease inhibitor, things seem a lot worse than [for] people who take it with Sustiva.

Now, this is not just an isolated result. There had been other studies, including some from Australia. The Australians were really on top of this before anyone else was -- showing that when people took Zerit and a protease inhibitor, they had more fat waste than when people didn't take a protease inhibitor.

So I think these are important results, and they may make us qualify what we say about Combivir. As I said: I was guilty, as well, of saying, well, I think the AZT and Combivir can cause fat wasting. I'm a little bit more cautious about saying that right now. I think it's true, but I think it also depends upon what [drug or drugs] it's coupled with. [To read more about body fat changes and metabolic complications, click here.]

"No matter which [HIV] therapies they took, truncal fat -- that's the fat around the trunk, the belly -- that increased."

The other part of the study that I think is really interesting is that no matter which [HIV] therapies they took, truncal fat -- that's the fat around the trunk, the belly -- that increased. No matter if you took a protease inhibitor, no matter if you took Sustiva, no matter if you took Combivir, or you took Zerit. We saw increases in body fat in the belly, in every study that's bothered to look at body fat and look at belly fat; in specific, [every study] on people who are starting HIV therapy has found the same thing. So they all do it.

So be prepared for body fat changes if you're going to take HIV meds?

The majority of people get some weight gain. They get some return to health. Something happens. I mean, look at people, again, in the aggregate. This is not every individual. There are some people who won't [gain weight]. There are some people who will lose. There are some people who will gain. But when you look at it, groups of people tend to gain fat around their trunk.

Now, the thing we don't have is what people look like before they got HIV infected, or when their T-cell counts were really high. We know from looking at lipids that we could be fooled, that people who start HIV therapy generally have low cholesterol relative to the way that they looked before they got HIV. A lot of times, people have lost weight by the time they start HIV therapy. So this may just be a return to the average American waistline. I don't know. Those are the kind of data that would be very helpful.

But when you look differentially between different treatment regimens, we're not seeing differences. That leads me to believe this is not a drug-specific problem, this fat accumulation; this is a phenomenon that we're seeing across the board, with different therapies -- as opposed to fat wasting, where we do see differences between different regimens.

But if you start therapy and you have 500 T-cells, wouldn't this be less likely to happen? Because you're already kind of healthy.

Maybe. I think this is really interesting. One of the ways we'll see how this pans out is looking at studies of patients who start therapy soon after they're infected, like acute HIV studies. Some of those studies are conducting metabolic evaluations. That's one way we could find out right away.

"There are studies that show that aerobic and anaerobic exercise combined -- sweating, lifting weights, that kind of thing, something that you could do that's very active -- and do that frequently -- along with diet modification (appropriate diet modification), has reduced inches from around the waist."

People who take these therapies when they're acutely [very recently] HIV infected -- when just a few weeks ago they were totally fine -- and we don't see changes in body fat, that will tell us right away. But if they do [gain weight], then there's some drug-specific thing going on. There are other ways to do this, and I think your idea is really a good one. We don't have the data yet, but that would be an excellent study. If it's found to be true, it would be another motivation for starting therapy earlier, rather than later.

Isn't it true that exercise can help? It's not inevitable that you'll get a fat belly?

Well, first, the other thing I should point out is that, yes. Don't be scared, because the kind of changes we're talking about may not be undesired. This may be: "Thank God I look healthy again," not "Look at my big fat tire around my waist." That's not what we're talking [about] here. A lot of these patients didn't have anything that was so horribly disfiguring.

In extreme cases, we do see that. But most people just get a little bit -- they gain a little weight. They just feel a little better. Yes. And if it gets to the point where it's not desirable, there are studies that show that aerobic and anaerobic exercise combined -- sweating, lifting weights, that kind of thing, something that you could do that's very active -- and do that frequently -- along with diet modification (appropriate diet modification), has reduced inches from around the waist.

Brave, New CDC HIV Testing Recommendations

Number eight gets us in kind of a different realm altogether, and what I thought was very important for [studies eight and nine is that] we're looking at policy changes. The big one here is that the CDC [U.S. Centers for Disease Control and Prevention] has released revised recommendations for how people should be screened for HIV in the United States. Previously, really, HIV screening was offered to people who were considered at high risk. Either the person considered themselves at high risk, or the clinician kind of thought: "You know, maybe based on what you're telling me, maybe you should get an HIV test." You know what? That didn't work very well. The incidence of HIV -- that's new infections every year -- hasn't really changed very much, and in some subgroups [it] is increasing. So that policy was a failure. [To read more about U.S. HIV testing policy, click here.]

"I can order a syphilis test right now on anyone I want ... without getting their informed consent in writing."

A much better policy would be offering HIV [testing] much more broadly. About one out of every 300 Americans is HIV positive, one out of every 300 people living in our country. This is not some very, very rare disease. Offering testing to people as they come into their routine clinic appointments, certainly when they go to STD clinics: Those types of things make a lot of sense. I think if we make it very routine, we sort of de-stigmatize the whole idea. "Well, my doctor's offering it to everybody; it's not just me. She's not making a judgment about me. She's just deciding to test me just because that's the public policy, the public health policy." And so I think there could be some tremendous benefit.

The other part of this, though, is that to make it easier, this whole process that we go through right now of counseling people before they get the test -- getting written, informed consent, and then doing counseling after the test -- has really turned out to be, although very well intentioned, an obstacle to getting HIV testing. When you ask doctors why they didn't order an HIV test on someone, oftentimes they'll say, "Well it was just too cumbersome, and I didn't have enough time to go over it, and I thought I'd do it next time, and we forgot about it."

So the whole sort of protections, built in, might have been actually having an effect where people just weren't getting tested because it was too onerous [on the part of the clinicians]. So the guidelines say you have to certainly tell people you want to test them, and they have to have an opportunity to say, "Please don't." But otherwise, you can get an HIV test just like we order other tests right now. I can order a syphilis test right now on anyone I want who comes in to see me, without getting their informed consent in writing. This is a way, I think, to make it a little bit more level for HIV screening and screening for other diseases.

So these are important guidelines. They also recommend that everybody aged 13 to 64 in our country get tested at least once.

Do you think we'll be able to handle all the new infections that are found?

Well, for one thing, there are very few places that have implemented this. So [anyone concerned] about a big surge in HIV cases tapping out our resources [should] remain calm. There are a lot of state laws regarding HIV testing and policies -- hospitals have policies; health departments have policies -- that will have to be tackled before this can really start up. I don't think we're going to see a huge surge. If we do see, in the short term, some increase in healthcare utilization, I think it's worth it. Because in the long term, what we're hoping is [that] we'll see less new infections. So I think this is an investment in the future, where short-term expenditures will lead to long-term dividends.


Updated U.S. HIV Treatment Guidelines

Nine, again, is another policy shift. And this is the U.S. government guidelines we talked about, that recommend to clinicians what [meds] to use to start HIV therapy. [To read the U.S. Department of Health and Human Services treatment guidelines, click here (PDF).] For HIV experts who are working in the ivory towers, this doesn't have a big impact upon them. But there are a lot of clinicians out there who don't have a whole lot of patients with HIV -- maybe 10, maybe 15 -- HIV is just one of the many things that they do. They really want to keep up, and they want to do a good job, and they rely upon the guidelines to tell them what they should do. And the guidelines have really not completely kept up with clinical practice. In HIV, we tend to do things even without the full breadth of medical evidence, because we're dealing with a really important infection that could be fatal. There are a lot of data that come out all the time that don't make it into the guidelines.

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The [U.S. HIV treatment] guidelines have really caught up. The important thing about the new guidelines is [that] they've really encompassed therapies that clinicians are using now in the clinic. We mentioned it before. Besides Sustiva and Kaletra, Reyataz boosted with Norvir and Lexiva boosted with Norvir have been added to the preferred list. And any of those drugs can be taken with Truvada or Combivir. This makes the guidelines really realistic and, I think, opens the door for clinicians to have better choices and not have to justify why they are using a drug that's not on the preferred list, but that data show should work just as well as drugs that are on the preferred list.

Well, I think that's great, and I think that's to be lauded. The other thing that I really like about the guidelines are, they're really stressing that we should do resistance testing when people come into clinical care. So even though you're not on HIV therapy yet, there should be drug resistance testing done on you to make sure you didn't get infected with a resistant virus. There are increasing data that show that if you have a drug-resistant virus [HIV drug resistance] and then you start on therapy with a drug that you're resistant to, it won't work as well. So I think this is worthwhile and the guidelines are pretty clear about that.

"The [U.S. HIV treatment] guidelines have really caught up. The important thing about the new guidelines is [that] they've really encompassed therapies that clinicians are using now in the clinic."

I think the new guidelines are a breath of fresh air. They're completely revamped, as far as what they recommend for initial therapy. It's a great document, and all clinicians need to know about [it].

Do you think it helps for patients to read the guidelines?

You know, it's very technical. I think patients should be very aware of what's listed in the guidelines as preferred and not preferred; I think that is savvy. If you understand what's going on, then when a clinician tries to tell you that you should start something [about which] the guidelines say, "No way," you could ask, "Why are you starting me on this? Tell me. You may have a really good reason, but tell me why it is."

That's what you need to understand. Therapy has gotten complicated, and there are data that show that the more choices you give someone, the harder it is sometimes to make a choice. I think that people have been turned off because there are so many therapies now. Well, this makes it easy.

There's a box, and it shows Column A and Column B. If anyone's ever been to a restaurant where the menu has Column A and Column B and you have to pick two from here and one from there, you're going to get it. And that's what it takes. Look at the Column A. Look at the Column B. See what you're on. See what you're recommended to be on, and then say, "Well, that makes sense. That's what the guidelines say."

But if it doesn't show up in the guidelines, you have got to say, "Well, why not? And why am I being offered this therapy that's not listed on the preferred list?" And again, there may be a great reason; you should find it out.

We have the guidelines on The Body, so anyone can look through them. [Click here to browse through a PDF of the U.S. HIV treatment guidelines.]

Absolutely.

Okay. Number ten.

The Next Generation of HIV Meds

Number ten is, again, sort of a potpourri, and it's listed just as "New Drugs." You know, in 2006, we saw the approval of Prezista [generically called darunavir or TMC114]. That's a new protease inhibitor. It has great activity against viruses that are resistant to protease inhibitors. I think that's been a really big help. The problem is, for people who have been resistant to a bunch of different medicines, Prezista alone is not going to work; you need something to add to it.

This year we're probably going to see three new drugs -- at least three new drugs -- approved. This will include the first integrase inhibitor. Integrase is an enzyme that the virus uses to get its genetic information into our DNA, so that our cells can start making virus proteins that get assembled and made into virus that then kill the T cell. It's a very important enzyme that the virus uses to replicate and make copies of itself in our cell. We don't have any drugs right now that target that enzyme. We have drugs that target other enzymes, but not that one; this is the first one. This is the Merck integrase inhibitor [MK-0518]. [To read coverage of MK-0158 from The Body, click here.]

Number two [of the new meds] is a new non-nuke [NNRTI]. Sustiva and Viramune [generically called nevirapine] are both non-nukes. When you get resistant to one of those, you blow the other one, and there's nothing else you can do as far as that class of drug. There's a new non-nuke called TMC125 [also known as etravirine], and this is in expanded access, as are the other drugs I'm going to talk about: the new drugs. This is going to be important because it works for people who do have some resistance to Sustiva or Viramune. That's going to give a new lease on life (for that drug class) to patients who have been exposed to those drugs [and] are now resistant to them. [For more information on TMC125, click here.]

The last [of the new drugs] is maraviroc. Maraviroc is a CCR5 inhibitor. This is a drug that inhibits, that blocks, the entry of the virus into the T cells by blocking another receptor besides the CD4 receptor that's on T cells. It blocks another receptor, not allowing the virus to enter T cells.

These three drugs are all in expanded access right now, meaning that there are studies going on where people can get into them and start on those therapies if they meet the right criteria. It's basically a compassionate use program. [To read more about HIV drugs in development, click here. For more on maraviroc, click here. To learn about the expanded access program for MK-0518, click here. To learn about the expanded access program for TMC125, click here. To learn about the expanded access program for maraviroc, click here and here.]

So that's free drugs.

Free drugs. [The companies providing the medications] collect information on you, but basically [they] just want to get the drug out there. Those [expanded access programs] are at major centers, and people can look it up on the Web site, and I'm sure there will be links to it on our Top Ten list. I think they are important in that they offer a critical mass of new drugs that people can craft a salvage regimen with. By that I mean people who really do have multidrug-resistant HIV now have enough drugs where they can make a new regimen that can really work.

These drugs are all proven to be effective at reducing the virus. The good thing about all three of them is they seem to be incredibly well tolerated. We don't have a lot of data on all these three drugs yet, and some of them are moving very quickly through the approval process. The Merck integrase inhibitor [is] really well tolerated, and it doesn't seem to have any negative effect on lipids. That's really reassuring. So I think that's going to be very attractive. That's one of the [drugs] that we're really looking forward to, and it's probably going to be the first one to come out.

MK-0518, is that what it is?

MK-0518 -- a spiffy name. They'll change that to something that makes a lot more sense. And then number two is TMC125. I think that's, again, going to be very useful for some patients who have been experienced with Sustiva. I think that, again, will be something that people who are on their fourth or fifth regimen might see as being useful to them. And then the maraviroc: it's just a new class of drugs. So we'll have a new integrase class and a new CCR5 inhibitor class. That will also be an important drug for certain patients. I just think that's all very positive, and worth mentioning.

Do these drugs mean that people who are treatment experienced can expect, and hope, to become undetectable?

Sure. Sure.

"In studies where these [new] drugs [MK-0518, TMC 125 and maraviroc] have been studied in people who have been treatment experienced, a significant proportion of them [become] undetectable. And that's when they're using just this drug, plus whatever's out there. Imagine if you could combine these drugs!"

So it's changed expectations.

Yes, I think so. People lose effectiveness of therapy for a bunch of different reasons. But if people take these drugs and are able to adhere to them to the right way, to the right level, these drugs should work. In studies where these drugs have been studied in people who have been treatment experienced, a significant proportion of them [become] undetectable. And that's when they're using just this drug, plus whatever's out there. Imagine if you could combine these drugs! Now, more work has to be done about how to combine these [drugs] -- what makes sense; are there any drug interactions; any overlapping side effects. That's going to come. But I think it really holds a new lease on life for a lot of people.

So it's a very exciting time for HIV management.

Oh, it's incredible that new drugs are still coming out, and anyone who's complaining about the industry pipeline, I think, won't have much to say in 2007. It's really remarkable to me that there are still companies investing in HIV care when the market is really, you know ...

... crowded with very good drugs.

Exactly. It's not like the CCR5, or integrase inhibitor, is going to be offered to people in Asia and Africa. The market is here [in the U.S.], and Europe.

Could you briefly mention the things that you did not include in your top ten list?

Honorable Mentions

Sort of, like, what are the runners-up?

Yes, very quickly.

Very, very quickly: I think we have to take our head out of the sand and recognize that prisons are a neglected area in our consciousness when we think about HIV. [To read more about HIV and prisons, click here.] Basically, every clinician, every doctor [and] nurse, who takes care of HIV[-positive clients] is going to see someone who either has been in prison or will be in prison. About 20 percent of all the people with HIV in our country pass through a jail or prison every year. I think we have to really start paying attention to this.

"Basically, every clinician, every doctor [and] nurse, who takes care of HIV[-positive people] is going to see someone who either has been in prison or will be in prison."

There's an article in this last issue of the New England Journal of Medicine -- that's the most read and respected medical journal on the planet, and thus, by extension, the universe -- talking all about how care for HIV, and prevention especially of HIV in prisons in the United States, is really not up to par. There's an article, as well, in the Lancet Infectious Diseases -- another very important journal, lamenting about how care for people with HIV in many countries is clearly suboptimal, and how prevention just hasn't been enforced.

I think that we have to pay attention to this. There was a very interesting report about intramural -- that means spread within a prison -- HIV in Georgia. And it's clearly demonstrating that we are not doing enough to make HIV testing available in prisons, a population that already has a [high rate] of HIV. I think we have to pay attention and start doing something about this, and not ignoring it.

I think another [idea] that is worth mentioning is that there are data that people can take HIV therapy in places where they don't wear watches. There's a famous quote from over a decade ago, from, I believe, a policymaker in the U.S. government, who said, "Well, HIV therapy: How can you give it to people in Africa? They don't even wear watches to tell what time they're supposed to take their medicines." Of course, we now know that people in sub-Saharan Africa [often] take their medicines even better than [people in] Europe and the United States do. They over take their medicines, because they want the medicine, and the benefits of the medicine. There are data from Haiti that show that scores of patients, a tremendous number of patients, are taking their medicines, are doing well, and that therapy can work when rigorously evaluated over time. So I think that's just another welcome and important report.

"People with HIV can have surgical procedures that they need, and they can come out of this well. HIV doesn't usually predispose you to get bacterial infections, and those are the problems that we see after sugery."

There was another article that I think is a runner-up that we're going to have to look a little bit more closely at. You know, clinicians, HIV docs, ask all the time: "Can my patient with a low T-cell count get a surgery?" We [researchers] waffle and say, "Well, if it's over 200, they can get the surgery. If it's under 200, they can't."

There's a neat little article that shows that people with HIV can have surgical procedures that they need, and they can come out of this well. HIV doesn't usually predispose you to get bacterial infections, and those are the problems that we see after surgery. I think we can feel a little bit more comfortable saying to patients, "Yes, if you need your carpal tunnel repair; if you need to have this elective surgery, you can have it. Go for it. It doesn't matter so much that you've got HIV."

I think those are the top [articles], those are the runners-up. It was a pretty active year, and I think 2007 will be one, too!

Well, thank you, Dr. Wohl. I'm sure we'll hear a lot after people read your article, which is also going to be coming out in the next month. Thank you very much for all your insights.




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