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CROI 2008: Boston, Massachussetts; February 3-6, 2008

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The Body Covers: The 15th Conference on Retroviruses and Opportunistic Infections
CROI 2008 Highlights: An Interview With Joel Gallant, M.D., M.P.H.

February 6, 2008

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Dr. Joel Gallant has been treating people with HIV since the beginning of the pandemic. He's also a leading HIV researcher and a professor at Johns Hopkins University School of Medicine in Baltimore, Md.

Can you give us your take on the most interesting research presented at CROI 2008?

I'm going to have to speak from my own perspective of being interested in treatment. There was a lot of stuff about prevention that we can talk about, too, but I'm focused more on treatment.

Reyataz Versus Kaletra for Initial Regimens

Joel Gallant, M.D., M.P.H.
Joel Gallant, M.D., M.P.H.
One of the most [important] clinical trials was the CASTLE study, which is the first head-to-head comparison of Kaletra [lopinavir/ritonavir] with boosted Reyataz [atazanavir] -- that is, Reyataz, given with Norvir [ritonavir].1 We have been using a lot of boosted Reyataz over the years, but without any big study really demonstrating that it was as effective. We finally have that study, and it really looks like it's fine. Both drugs did very well.

But there were some advantages of Reyataz, specifically in terms of side effects like diarrhea and nausea, and it had a little bit less of an effect on cholesterol and triglycerides. The data really are telling us that all these boosted PIs [protease inhibitors] were great. You don't pick one because it's stronger. You pick it because maybe you like the side effects better or it has fewer pills or different doses. But they all seem to work very well.

What I think people in the audience may not understand is that sometimes drugs are not approved for first-line use, but they are used anyway. That's very common. A lot of drugs are not used for what they are approved for.

In the U.S. that's true, because once that drug is approved, we can use it "off-label," if you will. We don't have to use it for the approved indication. In some countries, they do, so they are very much restricted by the local country's approval mechanism. But for us, we've been able to use boosted Reyataz [for intial therapy]. In fact, it's been listed as a preferred regimen in the guidelines,2 even though it hasn't had that FDA [U.S. Food and Drug Administration] indication.

Truvada Versus Epzicom for Initial Regimens

Were there any other first-line therapies that were looked at?

There was the HEAT study, which was the first head-to-head comparison of Truvada [tenofovir/FTC] with Epzicom [abacavir/3TC, Kivexa].3 These are both nucleoside [nucleoside reverse transcriptase inhibitor (NRTI)] backbones that were combined with Kaletra. There's been a lot of debate over which of these is better. The bottom line is: They both look fine. They both look great. They did a great job.

There was no difference in terms of the effectiveness of either one. In terms of side effects, the things you would expect would be hypersensitivity with the Epzicom [because of the Ziagen (abacavir) that's a component of this drug] and kidney issues with the Truvada. But we really didn't see much of either.

They weren't doing HLA-B*5701 screening, the way we would do now, so obviously they did have a little more hypersensitivity in the Epzicom arm.

There wasn't much in the way of kidney problems with the Truvada. We had a little bit, but less than 1 percent. There was a little bit better cholesterol and triglyceride profile with Truvada than Epzicom. But for the most part, they both look good.

Ziagen/Epzicom and Heart Attack Risk

Did you have a new perspective on Epzicom because of the D:A:D study from Europe?4

It was interesting, because only a week or two ago, the DHHS [Department of Health and Human Services] guidelines in the U.S. changed2 -- Epzicom and Truvada are now the preferred nucleoside backbones, and Combivir [AZT/3TC] has been demoted to an alternative. Everybody thought that made perfect sense. The European guidelines had just made that change, as well.5 Then along came the HEAT study that I just mentioned, showing that those are both good combinations. So everybody's happy.

Next the D:A:D study comes along.4

D:A:D is a big observational cohort study that's really been doing a lot of work on looking at cardiovascular complications of HIV treatment, things like myocardial infarction, or heart attack, and lipid changes. They set out to look at the nucleoside component of therapy, to see if that made a difference. Their suspicion, their hypothesis, was that people who were taking thymidine analogs, like AZT [zidovudine, Retrovir] and d4T [stavudine, Zerit], would be at a higher risk for heart attack because those drugs increase cholesterol.

What they found was that that wasn't the case. In fact, it was abacavir that increased the risk and, to a lesser degree, ddI [didanosine, Videx] -- abacavir being Ziagen and a component of Epzicom. They found what they called a 90-percent increase in risk, which sounds horrible, but keep in mind that the numbers of heart attacks were very, very low. You're talking about a 90-percent increase over a very low number.

Nobody has any idea how abacavir would do this, if it does. Keep in mind that this is an observational study. In other words, people weren't randomized to take abacavir. They just were looking at whatever people happened to be taking. So there's a lot of room for what we call "selection bias."

As an example, if somebody was on a protease inhibitor and their cholesterol went up and they developed coronary artery disease, the doctor could have said, "I've got to get them off this protease inhibitor to protect their heart." So the doctor switched the patient to Ziagen and then the patient had a heart attack. Maybe it was the protease inhibitor's fault, not the Ziagen. It just happened to be that people were more likely to be on Ziagen if they had these problems. That's an example of selection bias.

The investigators tried to control for that as best they could, with various statistical methods. But you can never completely eliminate that bias.

I don't think we know right now whether this is a real risk of Ziagen and Epzicom, or not. We need to keep an open mind. We need to look at this further and see whether it is. It's certainly not a reason for people to panic and rush out and stop or change their therapy at this point. If there is a risk of a heart attack from this drug, it's small in comparison with the risk of smoking cigarettes or sitting on the couch eating potato chips. You have to be realistic and put this all in perspective.

If you had a patient who is worried about the results of the study and has heart disease, would you take him or her off of Ziagen?

Viread [tenofovir], or the combination of Truvada, is certainly also a great choice. If somebody was really worried about it, I'd be happy to switch them to Truvada, provided that there weren't kidney issues. If somebody has problems with their kidneys, then they are definitely better off on Ziagen or Epzicom. But if there aren't any kidney issues, then you could certainly use Truvada instead of Epzicom, and there would be no problem there. But I doubt that I'm going to recommend that to my patients. I would certainly listen to my patients if they were concerned about the issue.

I see. So you're not going to be proactive.

I have to say, the most common nucleoside regimen that I use in practice is Truvada, because it doesn't require the testing of HLA-B*5701 and it has excellent data.6 If I have a patient on Epzicom, it's usually for a good reason. It's usually because, for whatever reason, they can't take Truvada. Maybe they have kidney issues, or something like that.

Most of the people I've got on Epzicom probably need to be on Epzicom. That may not be true for all physicians. Some are much more commonly using Epzicom.

I don't know whether this single study should change their practice, or not. It's hard to say. Again, it's an observational study and I think that is its weakness. On the other hand, it's a very powerful observational study, with huge numbers of patients, and has produced some very good studies from the same cohort in the past, so we have to look at this. But I think the jury's still out on whether this is a real risk or not.

I guess it's wise to warn people who are currently taking Ziagen or Epzicom that they should not stop taking their drug if they're worried. They should discuss this with their physician.

The risk of stopping your drug is far greater than any risk of heart problems could ever be. Again, this was a huge study: thousands of patients. They didn't see very many heart attacks. It's just that they saw more with abacavir.

Right, 33,000 patients.

Yes. We're talking about a very small number of events. The relative risk may have been there, but the absolute risk is very low.

HIV/HAART and Heart Disease

There was a bunch of presentations at the conference about the general risk of heart disease in older patients with HIV. Could you comment on that?

Obviously, our patients are getting older, and we hope they'll keep getting older. They are already at higher risk for heart disease, just by aging. But there's always been evidence that HIV itself can increase the risk of heart disease and some of our treatment can increase the risk of heart disease, if it affects cholesterol. There were interesting findings from the SMART study.7 You remember: The SMART study was the study where they randomly assigned people to either continue therapy or to stop and then restart when their CD4 count dropped.

One of the early observations from the SMART study was that people who stopped therapy were more likely to have heart attacks. When these results came about everybody thought, that doesn't make sense. It should be the other way around! People on therapy should have more heart attacks because of the cholesterol changes.

But it wasn't that way. So people have been looking for a reason for why stopping therapy would increase the risk of heart attacks. One thought was that maybe, when your viral load goes up, you develop inflammation or immune activation. That could cause coronary plaques to form.

One of the presentations today looked at a lab test called D-dimer, which is a test that's used to measure how easy it is for your blood to form clots.8 Having a high D-dimer level is associated with clotting more easily. That's not a good thing, because clots in your coronary arteries are what cause a myocardial infarction. What they found was that in the SMART study, when you stopped therapy, your D-dimer level went way up. The more your viral load went up, the higher the D-dimer level went up.

This suggests that what's happening is that, as HIV drugs keep your viral load suppressed, they are also keeping this D-dimer level down. They are making it harder for you to form these bad clots. Then, when you stop therapy, that clotting risk returns.

This raises another whole question. Presumably it isn't just stopping therapy that increases your D-dimer level, but probably also not being on therapy at all. We have long had data that people who are untreated with HIV are more likely to develop clots in their veins.9 Certainly people with dialysis catheters are more likely to clot those things off. This may have to do with this easier clotting in untreated HIV. It raises this whole question of: When should you start therapy? Should we be starting earlier because of these issues? It hasn't been answered yet, but it's an intriguing concept.

Wouldn't this be compounded if you already have a genetic risk for heart disease?

Possibly. There are a number of risk factors for heart disease, some of which you have no control over, like your genes and your gender. Others you do have control over, like smoking, high blood pressure, diabetes and high cholesterol. So if you have a strong family history of heart disease, or if you have some of these other risk factors for heart disease that you haven't modified, then having untreated HIV could be another factor that increases your risk.

What should a 22-year-old, recently diagnosed with HIV, feel about these kinds of numbers and worries? Are they the population that's being discussed? Or is it really just the older population of HIV-infected people?

A 22-year-old is much less likely to get into this kind of difficulty because, presumably, they have far fewer risk factors for these issues. I think we're only beginning to talk about this now because our population is aging, and they'll be getting into the age where these things can happen.

I think that for people of any age, there is evidence that it's better to have treated HIV than untreated HIV. It's better to have an undetectable viral load than a detectable viral load.
I think that for people of any age, there is evidence that it's better to have treated HIV than untreated HIV. It's better to have an undetectable viral load than a detectable viral load. We haven't yet gotten to the point where we're going to say everybody should be treated, no matter what. But theoretically that could be true. Right now, we sort of compromise, and we say that if your T cells are below 350, then you should be treated. But I don't think there's an upper limit. I think you could argue that everybody's better off having a suppressed viral load.

Cancer and HIV

Were there any presentations of interest on cancer and HIV?

The focus is now moving away from the so-called AIDS cancers, like Kaposi's sarcoma [KS] and lymphoma, and moving to looking at the non-HIV-associated cancers. We're finding that some of them, in fact, are HIV associated; that if you have a low CD4 and a high viral load, you're more likely to get not just lymphoma and KS, but some of these other cancers.10 Again, this is another reason why you want to be treated for HIV, rather than letting your CD4 count get low.

Hepatitis C and HIV

What about hepatitis C? I know they are seeing a lot more sexual transmissions of hepatitis C in people with HIV.

We're all waiting for these newer, better drugs for hepatitis C, and hoping that they're coming along. We are seeing sexual transmission. It's not common, and it appears to be associated with rougher sex, and sex that may involve blood contact. But, we're certainly seeing it.

It also appears that, if you are acutely infected with hepatitis C, you have a much better chance of being cured if you get treated right away than if you wait and let it turn into chronic hepatitis C. Patients and clinicians need to be aware of this. If you have people whose liver tests are going up for no good reason, make sure that you test for that, using PCR [polymerase chain reaction] testing to make that diagnosis, so you can get people on treatment right away.

HIV Drugs in Development

It's been an odd conference, because there aren't a lot of new drugs being discussed. There's just one CCR5 inhibitor being discussed.11,12 Compared to recent HIV meetings, this one has been subdued when it comes to new treatment options.

Yes. We're in a lull now, after the veritable avalanche of new drugs from last year. We had so many new ones that came out, up till Intelence [etravirine, TMC125] was just approved in the last couple of weeks. I don't think we're going to see a lot of new approvals anytime soon. The drugs that we have coming, while they have their advantages, aren't necessarily drugs that will offer something to people who have failed the current ones.

For example, elvitegravir [GS 9137], the new Gilead integrase inhibitor, has cross-resistance with Isentress [raltegravir, MK-0518].13 Vicriviroc [SCH 417690; SCH-D], which is the next in-development CCR5 inhibitor, is not going to work if you've failed Selzentry [maraviroc, Celsentri], because this failure means you have X4 [CXCR4]- or dual/mixed-tropic virus. Thus, you won't respond to a CCR5 inhibitor.14

It may be a while for more HIV drugs to be developed. That's why I think it's going to be so important that we use these drugs well. If we start seeing the emergence of resistance to integrase inhibitors, we're not going to have a lot of options to fall back to.

Were there any new targets being looked at at this conference?

People are looking at new types of entry inhibitors, including small molecule entry inhibitors that could be taken orally.15 There's still some hope; there's hope for the maturation inhibitor bevirimat [PA-457].16

Isn't there also a study about using a drug intravenously once a month?

Yes, there have been several. There's the Tanox drug, known as TNX-355, which has been looked at. That's usually given every one to two weeks.17

Isn't there also a Tibotec drug?

Yes, there's a Tibotec NNRTI [non-nucleoside reverse transcriptase inhibitor] called TMC278 [rilpivirine] that they are hoping could be given once a month by infusion or injection.18 That would be very exciting, and could have implications for things like pre-exposure prophylaxis, as well.

HIV Prevention

So there's some excitement about new drugs. Anything else?

The big downer at this meeting is the prevention news. As exciting as treatment news is, the prevention news just continues to be depressing. We had the failure of the HIV vaccine this year.19 Circumcision looks good in preventing HIV in men, but it doesn't seem to be helping the female partners in Africa, when men get circumcised.20

Then there was the failure of the first vaginal microbicide recently.21 Now, at this meeting, we heard that treating people with acyclovir [Zovirax] doesn't help to prevent HIV transmission, as well.22

That's the herpes drug.

Yes. It's not that these herpes drugs directly suppress HIV. First of all, they keep you from having genital ulcers, which are a great way for HIV to get in. We also know that having herpes activates your HIV replication. So the hope was that by using that kind of a drug you would decrease spread, but it didn't seem to work.

The real hope now is in specific microbicides that contain active anti-HIV drugs and PrEP, or pre-exposure prophylaxis, where you actually give drugs to people who are HIV negative and try to keep them from getting infected. Of course, condoms are still a good idea.

In the HIV testing arena, there seems to be decreasing use of condoms and an increase in unprotected sex among, at least, men who have sex with men.23

Yes. It's concerning. I think people have lost their fear of HIV. Of course, it isn't the same disease it was 20 years ago. It's not as scary. But still, who wants to have a chronic disease? I still think preventing HIV is better than treating it. I think we need to still focus on that.

There's a lot of talk now at the U.S. Centers for Disease Control and Prevention of directing the message of prevention towards people who are HIV positive, rather than negative. Directing it at people who are negative has not worked very well. People who are negative do incredibly dumb things.

I think we need to focus on people who are positive, and get the message out that "the disease stops with me." I used to hear that a lot in the '80s and the early '90s; people came in and they said, "This stops with me. I'm not spreading to anybody." I don't hear that so much anymore, and I'd love to hear that again.

Do you think methamphetamine is part of that story?

Oh, yes.

Are you seeing it a lot?

You couldn't design a better drug for spreading this epidemic than crystal meth -- a drug that enhances sex, enhances your ability to have lots of sex, and completely takes away all judgment and inhibitions. It's just made for this. I'm seeing a lot of HIV transmission, including transmission of resistant virus that's directly linked to crystal meth.

Smoking Cigarettes and HIV

To wrap up: There might be news coming out of the conference about cancer, or about heart disease, but most patients really don't have to worry. Could you put that in perspective for people?

All of these things are so tiny and miniscule in comparison with the risk of not treating your HIV. It's a luxury that we can focus on things like heart attacks. When you think back to before 1996, we would have loved to talk about your risk of future heart attack back then, because people were dying every day. It's great that we can now focus on these long-term complications, and try to prevent them.

Despite these occasional glitches and pieces of bad news, our drugs are getting safer and safer, and easier to take.
At the same time, despite these occasional glitches and pieces of bad news, our drugs are getting safer and safer, and easier to take.

Frankly, when I look at my patient population of, say, 250 to 300 people, of course I have a few people who are dealing with a lot of these issues. But most of them are not. They are doing great, and they're working, and feeling good. They frankly don't have to spend much time thinking about their HIV, when they take their pills once a day. I think things have really improved.

I've heard that one of the biggest lifestyle changes somebody with HIV can make to reduce his or her risk of heart disease is to stop smoking, because such a great percentage of people with HIV smoke.

Yes. Smoking dwarfs all other risk factors. When you think about protease inhibitors increasing your cholesterol, the risk that that causes is miniscule compared to the risk of smoking. The day you stop smoking you lower your risk significantly for heart disease.

If I have a patient who smokes, but is worried about his or her protease inhibitor, then we have to have some kind of a common sense talk. Because smoking is such a big risk for heart disease -- not to mention stroke, lung disease, cancer, and all sorts of other problems you don't want to have.

OK. So, a pretty good conference, you would say?

Yes. I would say it's a pretty good conference. Hopefully, we'll have maybe more exciting stuff at future conferences, and better news on the prevention front. But at least in terms of treatment, things are going very well.

Great. Thank you very much.

Thank you.

This transcript has been lightly edited for clarity.


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    View poster: Download PDF
    View slides: Download PDF
  2. Panel on Antiretroviral Guidelines for Adult and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health and Human Services. January 29, 2008; 1-128.
  3. Smith K, Fine D, Patel P, et al. Efficacy and safety of abacavir/lamivudine compared to tenofovir/emtricitabine in combination with once-daily lopinavir/ritonavir through 48 weeks in the HEAT study. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 774.
    View poster: Download PDF
  4. Sabin C, Worm S, Weber R, et al, and the D:A:D Study Group. Do thymidine analogues, abacavir, didanosine and lamivudine contribute to the risk of myocardial infarction? The D:A:D study. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 957c.
    View poster: Download PDF
  5. European AIDS Clinical Society (EACS). Guidelines for the clinical management and treatment of HIV infected adults in Europe. December 2007.
  6. Arribas J, Pozniak A, Gallant J, et al, and the Study 934 Team. Three-year safety and efficacy of emtricitabine (FTC)/tenofovir DF (TDF) and efavirenz (EFV) compared to fixed dose zidovudine/lamivudine (CBV) and EFV in antiretroviral treatment-naive patients. In: Program and abstracts of the 4th International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention; July 22-25, 2007; Sydney, Australia. Abstract WEPEB029.
    View poster: Download PDF
  7. El-Sadr W, Neaton J, for the SMART Study Investigators. Episodic CD4-guided use of ART is inferior to continuous therapy: results of the SMART Study. In: Program and abstracts of the 13th Conference on Retroviruses and Opportunistic Infections; February 5-8, 2006; Denver, Colo. Abstract 106LB.
  8. Kuller L and SMART Study Group. Elevated levels of interleukin-6 and D-dimer are associated with an increased risk of death in patients with HIV. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 139.
  9. Klein SK, Slim EJ, de Kruif MD, et al. Is chronic HIV infection associated with venous thrombotic disease? A systematic review. Neth J Med. April 2005;63(4):129-136.
  10. Bruyand M, Thiebaut R, Lawson-Ayayi S, et al, and Groupe d'Epidémiologie Clinique du SIDA en Aquitaine (GECSA). Immunodeficiency and risk of AIDS-defining and non-AIDS-defining cancers: ANRS CO3 Aquitaine cohort, 1998 to 2006. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 15.
  11. Zingman B, Suleiman J, DeJesus E, et al. Vicriviroc, a next generation CCR5 antagonist, exhibits potent, sustained suppression of viral replication in treatment-experienced adults: VICTOR-E1 48-week results. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 39LB.
    View slides: Download PowerPoint
  12. Zingman B, Suleiman J, DeJesus E, et al. Vicriviroc in combination therapy with an optimized ART regimen for treatment-experienced subjects: VICTOR-E1. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 795.
    View poster: Download PDF
  13. DeJesus E, Cohen C, Elion R, et al. First report of raltegravir (RAL, MK-0518) use after virologic rebound on elvitegravir (EVT, GS 9137). In: Program and abstracts of the 4th International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention; July 22-25, 2007; Sydney, Australia. Abstract TUPEB032.
  14. Tsibris AMN, Sagar M, Su Z, et al. Emergence in vivo of vicriviroc resistance in HIV-1 subtype C: role of V3 loop and susceptibility to other CCR5 antagonists. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 870.
  15. Pett S, Emery S, MacRae K, et al. Safety and activity of SCH532706, a small molecule chemokine receptor 5 antagonist in HIV-1-infected individuals. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 38.
    View slides: Download PDF
  16. Adamson C, Waki K, Ablan S, Salzwedel K, Freed E. Viral resistance to the HIV-1 maturation inhibitor bevirimat in the context of a protease that confers resistance to protease inhibitors. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 859.
    View poster: Download PDF
  17. Norris D, Morales J, Gathe J, et al. Phase 2 efficacy and safety of the novel entry inhibitor, TNX-355, in combination with optimized background regimen (OBR). In: Program and abstracts of the XVI International AIDS Conference; August 13-18, 2006; Toronto, Ontario, Canada. Abstract TUPE0058.
  18. van't Klooster G, Verloes R, Baert L, et al. Long-acting TMC278, a parenteral depot formulation delivering therapeutic NNRTI concentrations in preclinical and clinical settings. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 134.
  19. Robertson M, Mehrotra D, Fitzgerald D, et al. Efficacy results from the STEP study (Merck V520 protocol 023/HVTN 502): a phase II test-of-concept trial of the MRKAd5 HIV-1 gag/pol/nef trivalent vaccine. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 88LB.
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  20. Wawer M, Kigozi G, Serwadda D, et al. Trial of male circumcision in HIV+ men, Rakai, Uganda: effects in HIV+ men and in women partners. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 33LB.
  21. Doncel G, van Damme L. Update on the CONRAD cellulose sulfate trial. In: Program and abstracts of the 14th Conference on Retroviruses and Opportunistic Infections; February 25-28, 2007; Los Angeles, Calif. Abstract 106LB.
  22. Celum C, Wald A, Hughes J, et al and HPTN-039. HSV-2 suppressive therapy for prevention of HIV acquisition: results of HPTN 039. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 32.
  23. Stall R, Friedman M, Marshal M, Wisniewski S. What's driving the US epidemic in MSM. In: Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections; February 3-6, 2008; Boston, Mass. Abstract 53.

Reader Comments:

Comment by: (mailed you a note) Thu., Jul. 24, 2008 at 3:38 am EDT
Dr. Gallant, I have mailed you a note. What about stem cell research and HIV? We know that some people can not replicate HIV due to unique lack of specific enzimes. Are we thinking out of the box? I have done some research on this matter and will make an appointment with you to discuss it. Also I suggest we look at Serostim very closely for mangering specific long term side affects.
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Comment by: Tue., Jul. 8, 2008 at 9:55 am EDT
it was really very useful in real practice, and moreover, practically discussed
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Comment by: Clayton O. Barbour, II, MD Wed., May. 14, 2008 at 8:24 pm EDT
Given the limited options of nucleosides in our antiretroviral therapy we need to be cautious in the rush to judgment regarding the association of abacavir and didanosine with cardiovascular events proposed by the DAD cohort. Medical providers need to know if this observation is true or an aberration secondary to unrecognized extrinsic factors in this non-randomized cohort. I have to admit to some skepticism when the purported findings from this cohort do not match with my clinical experience. My personal observation indicates that the use of abacavir or didanosine, as a component of HAART, is a marker for treatment experience. Treatment experienced patients during this era of HAART statistically had a greater risk for virologic failure, with associated inflammatory response, and immune activation which could be predisposed to cardiovascular events.

Frequently, treatment experienced individuals were treated with abacavir after failing a thymidine / lamivudine regimen paired with a PI or NNRTI. These individuals with resistant virus have a greater risk of virologic failure on subsequent regimens. Such individuals were often, unfortunately treated with sub-optimal HAART regimens as new agents became available between 2000 and 2005. Thus, abacavir, prior to the availability of tenofovir, was frequently paired with the newest PI in these successive failing regimens. These individuals often experienced intermittent success, followed by subsequent failure of partially suppressive regimens. This resulting intermittent viremia would be accompanied by immune activation. Immune activation is associated in elevated d-dimer, CRP, and other inflammatory markers associated with cardiac adverse events. This has been suggested as the potential cause of the increased risk for cardiac events identified in the SMART trial of structured treatment interruption, which demonstrated an approximate 1.6 fold increased risk of fatal/nonfatal cardiovascular events.
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