Switching Antiretroviral Therapy, Part II
[Continued from Part I]
However, switching to a protease sparing regimen may not produce as rapid an improvement as lipid-lowering medications. At the 2005 Conference on Retroviruses and Opportunistic Infections, Leonardo Calza, MD, and colleagues reported data from a study in which 142 patients on stable HAART with well-controlled HIV were randomly assigned to either switch from their PI-based regimen to nevirapine or efavirenz, or to stay on their current regimen and add pravastatin (Pravachol) or bezafibrate (not available in the U.S.). After 12 months, triglyceride reductions in the NNRTI arms (25% for nevirapine, 9% for efavirenz) were significantly lower than those seen in the adjunct therapy arms (41% for pravastatin, 46% for bezafibrate); the corresponding reductions in total cholesterol were 27% and 10% for the two NNRTIs, and 46% and 38% for the lipid lowering drugs.
Even if switching does not bring blood lipids down to normal levels, any decrease is likely to be beneficial in terms of reducing cardiovascular risk, and may decrease the required dose of lipid-lowering medications. Yet while switching regimens and adding adjunct medications can help manage metabolic side effects, it is best to avoid the most problematic drugs and combinations from the outset, if possible, since it is often easier to prevent these conditions than to fix them later.
Protease-Sparing RegimensThe most straightforward method of addressing metabolic toxicities is to stop the offending drug(s). Because most PIs are associated with metabolic abnormalities, researchers began exploring "protease-sparing" regimens consisting of either an NNRTI plus at least two NRTIs or NRTI-only combinations. Overall, NNRTI-based regimens perform about as well as boosted PI-based regimens with fewer toxicities; however, individuals taking NNRTIs with suboptimal adherence appear to develop resistance more rapidly than those taking PIs.
In the July 1, 2001 issue of JAIDS, L. Ruiz and colleagues reported data from a prospective open-label simplification study in Spain in which 106 patients with lipodystrophy and suppressed HIV were randomly assigned to either remain on their current PI or switch to nevirapine. After 48 weeks, similar proportions (72% and 74%, respectively) maintained undetectable viral load, and CD4 cell counts increased in both arms. Total cholesterol and triglyceride levels decreased in the switch arm, but were not significantly different at the end of the study; there also were no significant differences in body shape changes. Nevertheless, participants in the switch arm reported higher quality of life, in part due to the simpler dosing schedule.
More recently, in the French ALIZE-ANRS 099 trial, reported in the March 15, 2005 Journal of Infectious Diseases and presented by Jean-Michel Molina, MD, and colleagues at the 2005 ICAAC, 355 patients with well-controlled HIV were randomly assigned to either continue their current PI-based regimen or switch to a simplified once-daily combination of ddI, emtricitabine, and efavirenz. After 48 weeks, both regimens similarly suppressed HIV (88% vs. 91%, respectively); after 36 months, 95% of patients in the protease-sparing arm still had viral loads below 400 copies/mL.
All-NRTI RegimensSeveral studies have explored switching from PI- or NNRTI-based regimens to ones that contain only NRTIs. This may be done because an individual has already developed resistance to NNRTIs or in order to preserve that class for later use. While such studies typically find that patients switching to NRTI-only regimens experience improvement in blood lipid profiles, data are mixed in terms of virological efficacy.
Some individuals evidently can do well on NRTI-only combinations. In the open-label TRIZAL study, reported by Christine Katlama, MD, and colleagues in the August 15, 2003 issue of AIDS, 40 participants with well-controlled HIV were randomly assigned to continue their NNRTI based combination or switch to an all-NRTI regimen using the Trizivir (AZT/3TC/abacavir) combination pill. After 48 weeks, virological suppression was similar in the two arms, but total cholesterol levels improved significantly in the switch group.
Esteban Martinez, MD, and colleagues reported 12-month results from the Nevirapine, Efavirenz, Abacavir (NEFA) trial in the September 11, 2003 New England Journal of Medicine (NEJM) and presented the final 36-month data at this year's Retrovirus conference. In this simplification study, 460 participants with well-controlled HIV on stable regimens containing a PI plus at least two NRTIs were randomly assigned to replace the PI with nevirapine, efavirenz, or abacavir. Patients who switched to abacavir were more likely to experience virological failure, progression to AIDS, or death than those who substituted nevirapine or efavirenz (23%, 11%, and 15%, respectively). But adverse events leading to discontinuation were more common in the nevirapine and efavirenz arms compared with the abacavir arm (19%, 25%, 9%, respectively), so overall treatment success rates were similar.
Certain individuals require the more potent activity of an NNRTI or PI, especially those with higher HIV viral loads, relatively more treatment experience, and a history of prior suboptimal therapy. Recall that in Bartlett's 2005 meta-analysis, regimens that included a boosted PI (64%) or an NNRTI (63%) suppressed HIV better than those containing three NRTIs (51%). The ACTG 5095 study, reported by Roy Gulick, MD, and colleagues in the April 29, 2004 NEJM, found that even among treatment-naive patients, the AZT/3TC/abacavir combination was less effective than efavirenz-containing regimens.
A study by Alessandro Cozzi-Lepri and colleagues published in the July 1, 2006 Journal of Infectious Diseases showed that individuals taking an all-NRTI regimen containing abacavir instead of an NNRTI or PI were 85% more likely to experience virological rebound, even if their viral load was undetectable when they started this regimen; the authors suggested that it may be prudent for such patients to switch to a more potent combination, even if their viral load is currently suppressed.
Studies have also shown that regimens combining ddI plus tenofovir may lead to early virological failure and immunological decline. Current U.S. treatment guidelines list AZT/ 3TC/abacavir as an alternative regimen only if PI- or NNRTI-based regimens "cannot or should not be used," and caution against the use of NRTI-only regimens that contain tenofovir.
Some research indicates that, far from correcting metabolic abnormalities, some NRTIs contribute to the problem; the thymidine analogs -- AZT and d4T -- are most commonly implicated. In the COMET study, patients who switched from Combivir to Truvada while remaining on efavirenz experienced reduced LDL cholesterol and triglyceride levels. Likewise, the RAVE study, described below, found that switching from d4T to tenofovir improved lipid levels.
Switching to AtazanavirFor treatment-experienced patients who need a more potent regimen, substituting the newer PI atazanavir may be a good option. Atazanavir is less likely than other drugs in its class to cause elevated LDL cholesterol and triglycerides; some studies suggest it may also raise HDL ("good") cholesterol, which is protective against cardiovascular disease. In the SWAN study, patients who switched from regimens that included other boosted or unboosted PIs to atazanavir experienced significant reductions in total cholesterol, LDL cholesterol, and triglyceride levels.
While SWAN was primarily intended to assess virological efficacy, the AI424067 trial was designed as a switch study with the aim of managing hyperlipidemia in patients with well-controlled HIV; Michael Sension, MD, and colleagues presented preliminary data at the 2005 Retrovirus conference. A total of 246 participants on stable HAART with undetectable viral load and elevated LDL cholesterol were randomly assigned to either continue their current PI-based regimen or switch to unboosted atazanavir while remaining on the same NRTIs. After 12 weeks, patients in the atazanavir arm maintained virological suppression while experiencing a 35% decrease in triglycerides, a 15% reduction in LDL cholesterol, an 18% drop in total cholesterol, and increased HDL cholesterol (they also had significantly higher bilirubin levels).
Importantly, since atazanavir, fosamprenavir, and the newest PI, darunavir (Prezista), were approved more recently, their long-term side effects in terms of body shape changes are not yet known. Another fairly new PI, tipranavir (Aptivus), has been linked with lipodystrophy even with relatively short-term use, so it is not a good candidate for switching to minimize metabolic toxicity.
Many researchers also came to suspect that lipoatrophy and other NRTI associated side effects -- including lactic acidosis, enlarged fatty liver (hepatomegaly with steatosis), peripheral neuropathy, and pancreatitis -- were manifestations of drug-induced damage to the mitochondria, energy-producing structures within the cells.
Switching NRTIsMuch research suggests that mitochondrial toxicity is most strongly associated with the dideoxynucleotides, or "d drugs": d4T, ddI, and the now-discontinued ddC (zalcitabine, Hivid). Other experts believe that the thymidine analogs -- d4T and AZT -- are the primary culprits. Either way, d4T is clearly problematic, and the d4T/ddI combination even more so. For this reason, current U.S. treatment guidelines now recommend against using these two drugs together.
Several studies have shown that switching from d4T and/or ddI to other NRTIs leads to gradual restoration of mitochondrial DNA in cells and improvements in hyperlactatemia (elevated lactic acid in the blood), lipoatrophy, and peripheral neuropathy. As noted above, switching from AZT or d4T may also improve blood lipid profiles.
Graeme Moyle, MD, and colleagues presented data at both the 2005 Retrovirus conference and ICAAC from the RAVE study, in which more than 100 individuals with moderate-to-severe lipoatrophy were randomly assigned to switch from d4T or AZT to abacavir or tenofovir. After 48 weeks, DEXA and computed tomography (CT) scans showed that those who switched experienced modest gains in subcutaneous limb fat. Tenofovir was associated with fewer overall side effects and modest reductions in triglycerides and total and LDL cholesterol; lipid decreases were mainly seen among patients who switched from d4T.
In the January 15, 2004 issue of Clinical Infectious Diseases, Grace McComsey, MD, and colleagues reported data from the open-label TARHEEL study, in which 118 patients with lipoatrophy and well-controlled HIV switched from d4T to either AZT or abacavir. After 48 weeks, DEXA scans showed increases in arm fat (median 35%), leg fat (12%), and trunk fat (18%) in the patients who switched; participants also reported that they noticed fat gains in their limbs, buttocks, and face.
Likewise, Esteban Ribera and colleagues reported at the 2005 Retrovirus conference that in the Spanish LIPOTEST study, in which 53 subjects with well-controlled HIV and lipoatrophy switched from d4T to tenofovir, facial fat thickness increased significantly, triglycerides decreased significantly, and cholesterol decreased slightly after 18 months; in addition, lactic acid levels fell significantly and mitochondrial DNA in peripheral blood mononuclear cells showed a slight increase.
Some NRTI side effects, such as peripheral neuropathy, resolve relatively quickly after the offending drugs are stopped, but lipoatrophy improves very slowly. In the MITOX study by Andrew Carr, MD, and colleagues, reported in the July 10, 2002 Journal of the American Medical Association, 111 patients with moderate to severe lipoatrophy were randomly assigned to continue their current regimen or switch from d4T or AZT to abacavir. Patients who switched experienced a significant increase in subcutaneous limb fat as determined by DEXA and CT scans, although the change was too small for them to notice. The authors concluded that at the rate of increase observed, fat loss "may take years to resolve." It is not yet clear whether some degree of peripheral neuropathy, lipoatrophy, and other manifestations of mitochondrial damage may be irreversible.
NRTI-Sparing RegimenWhile some researchers have studied NRTI-only regimens as a strategy for avoiding PI-related side effects, others have taken the opposite tack, testing regimens that contain no NRTIs.
At the 2005 Retrovirus conference, Margaret Fischl, MD, and colleagues presented data from ACTG 5116, an open-label simplification study that included 236 individuals with well-controlled HIV (although they previously had advanced disease) and no evidence of drug resistance. Participants were randomly assigned to switch from their initial three- or four-drug PI- or NNRTI-based HAART regimen to either efavirenz plus two NRTIs (78% AZT/3TC, 19% ddI/d4T) or an NRTI sparing regimen of efavirenz plus lopinavir/ritonavir. After 110 weeks, 66% of subjects who switched to lopinavir/ritonavir had viral loads below 50 copies/mL, compared with 74% who stayed on NRTI-containing regimens. Participants in the NRTI sparing arm showed a trend toward reduced virological suppression and were three times more likely to discontinue therapy due to adverse events, mainly triglyceride elevation.
These results suggest that NRTI containing regimens are superior, but toxicity profiles tell a somewhat different story. Pablo Tebas, MD, and colleagues presented data from ACTG 5125s, a sub study of ACTG 5116, at the same conference. In an analysis of 62 patients, limb fat increased significantly in the NRTI-sparing arm after 48 weeks, but decreased further in those who stayed on NRTIs. Among a subset of 46 subjects followed for an average of 104 weeks, those in the NRTI-sparing arm continued to gain limb fat, while those in the NRTI containing arm continued to lose it.
Results of another NRTI-sparing trial were presented at the same meeting by Robert Murphy, MD, and colleagues. In the ACTG 5110 study, 101 participants with lipoatrophy and well-controlled HIV were randomly assigned to either replace the thymidine analog in their regimen (24% AZT, 76% d4T) with abacavir, or else switch to an NRTI-free regimen of lopinavir/ritonavir plus nevirapine. After 24 weeks, subjects in both arms maintained virological suppression. DEXA and CT scans showed that patients in both the thymidine-sparing and NRTI-free arms experienced increased subcutaneous abdominal fat and decreased visceral abdominal fat; however, thigh fat increased only in the NRTI-free arm.
These data suggest that decisions about whether to switch to an NRTI sparing regimen should be made on an individualized basis, taking into account body weight, fat distribution, and cardiovascular risk factors.
At the XV International AIDS Conference in 2004, Joseph Gathe, MD, presented a case series of 30 patients at an inner-city clinic who were treated with lopinavir/ritonavir alone in an effort to improve adherence and reduce the cost of therapy; after 48 weeks, 67% had viral loads below 400 copies/mL.
In the open-label OK (Only Kaletra) pilot study, reported by Jose Arribas, MD, and colleagues in the November 1, 2005 issue of JAIDS, 42 patients with undetectable viral load were randomly assigned to either continue on lopinavir/ritonavir plus two NRTIs, or to stop taking the NRTIs. After 48 weeks, 81% of patients in the monotherapy arm maintained undetectable viral loads, compared with 95% in the triple-therapy arm (a nonsignificant difference). There was no evidence of lopinavir/ritonavir resistance and patients regained virological control once their previous NRTIs were reintroduced.
At the 2006 British HIV Association (BHIVA) conference this March, Laura Waters, MD, and colleagues presented an analysis of data from 35 heavily treatment experienced patients with a median viral load of nearly 55,000 copies/mL and a median CD4 count of about 250 cells/mm3 who switched from their current HAART regimens to lopinavir/ritonavir monotherapy outside a clinical trial setting. After 12 months, half achieved undetectable HIV RNA and 73% experienced at least a 1-log reduction in viral load. During the one-year follow-up period, eight patients switched again, mostly due to virological failure or immunological decline.
At the XV International HIV Drug Resistance Workshop in June, however, two teams of researchers from Abbott Laboratories reported that some clinical trial participants developed resistance while using lopinavir/ritonavir monotherapy either as first-line treatment or as part of a simplified maintenance regimen; detailed data are expected to be presented later this year.
Susan Swindells, MD, and colleagues presented data from a study of boosted atazanavir monotherapy at this year's Retrovirus conference. The 36 patients in the open-label ACTG 5201 pilot study had no history of virological failure and had undetectable viral loads while taking regimens consisting of a PI plus two NRTIs. Subjects first switched to ritonavir-boosted atazanavir plus two NRTIs for six weeks, then discontinued the NRTIs if they still had undetectable viral load. In a planned analysis 24 weeks after NRTI discontinuation, three out of 33 patients (9%) experienced virological failure (two had no detectable atazanavir in their blood, suggesting poor adherence).No evidence of genotypic resistance to atazanavir was observed, and two patients regained virological control after they received adherence counseling or their previous NRTIs were reintroduced.
While results from studies to date appear promising, monotherapy remains an experimental -- and controversial -- switch strategy. The risks and benefits of this approach are discussed in "Revisiting Monotherapy: Heresy or Revised Orthodoxy?" in the Winter 2006 issue of BETA.
At this year's BHIVA meeting, S. Mandilia and colleagues reported on an analysis of more than 22,000 individuals seen at 27 HIV clinics in the United Kingdom. Between 1996 -- the beginning of the HAART era -- and 2002, patients stayed on their first combination regimen for an average of 6.7 years. The average time on the second regimen was 4.3 years, and the third regimen lasted about the same duration, 4.2 years. About 40% of patients changed their first-line regimen due to virological failure, immunological decline, or clinical disease progression, as was the case for about 50% of those changing second or third regimens. This suggests that at least half of treatment discontinuations are due to factors other than inadequate potency, such as intolerable side effects or difficult dosing schedules.
While an expanded armamentarium of drugs has increased the prospects for finding an appropriate regimen to switch to in case of treatment failure or lack of tolerance, it remains important to select the best possible first-line regimen, because it is easier to fully suppress HIV when a person is not yet resistant to any drugs.
It is difficult to make direct comparisons among different regimen sequences -- in part because antiretroviral therapy evolves so rapidly -- but it is clear that advances in therapy have benefited people with HIV. According to a retrospective observational study of nearly 4000 patients by Fiona Lampe, PhD, and colleagues, published in the March 13, 2006 Archives of Internal Medicine, the rate of treatment failure with initial regimens fell by more than half between 1996 and 2002, with virological failure rates dropping from 28% to 12%. The authors attributed this increasing success to better drugs, a change in emphasis towards maximal viral suppression, and a general increase in adherence thanks to "accumulating clinical experience, more effective clinical management, and perhaps an increase in patients' knowledge about treatment."
In another "big picture" analysis, Bartlett and colleagues reported in the March 2006 issue of JAIDS the results of an overview of 15 randomized clinical trials assessing genotypic resistance after virological failure during first-line therapy. The combined data showed that virological success rates were highest when starting with boosted PI regimens (55%-79% success) or NNRTI-based regimens (51%-76% success) that also contained NRTIs. Patients who experienced treatment failure while taking boosted PIs developed drug resistance more slowly -- and thus retained more future treatment options -- than individuals on failing NNRTI-based regimens.
If an individual's existing regimen keeps his or her viral load fully suppressed and the CD4 cell count within a safe range, does not cause unmanageable side effects, and is easy to adhere to, there's no need to change therapy. And indeed, switching does not always prove advantageous. According to Boyle, "there's no guarantee that virological breakthrough or immune failure won't occur" with a new regimen. And many patients have switched to a supposedly superior regimen, only to develop side effects they find harder to live with. In addition, there's always a risk when switching to the newest drugs that rare or long-term toxicities or unforeseen drug interactions that were not detected in clinical trials could crop up later -- as was the case with PI-related lipodystrophy.
Mitsuyasu says it's important that patients and physicians discuss the reason for a proposed switch. He is likely to agree that a switch is a good idea if "the new drug is cheaper, easier to access, less cumbersome to use, or has fewer side effects," provided there are "no contraindications such as adverse interactions with other medications the patient is taking, or the patient is likely to be resistant due to prior therapy, or is likely to have more rather than fewer side effects than with the old drugs."
Some people with HIV -- and some physicians -- are reluctant to switch to simpler and more tolerable regimens for fear that this will limit or "use up" future treatment options. For example, some believe it's preferable to start with an NNRTI-based regimen in order to preserve the more potent PI class for later. However, as Bartlett's 2006 analysis illustrates, the general rule is that the better HIV is controlled at the outset, the longer a regimen will last before treatment failure occurs. Furthermore, the drug development pipeline is relatively full, and there is a good chance that new agents that work by novel mechanisms will become available within the next few years.
Structured Treatment Interruptions: After SMART").
Once patients and physicians decide that a switch is the way to go, it is important to ensure that it's the right one. Here, prior treatment history and drug-resistance testing can help determine whether a new medication is likely to work well for a specific person. Other individual characteristics, including cardiovascular risk factors and increased susceptibility to other toxicities, should also be taken into account. Once again, no antiretroviral regimen is "one size fits all," so it is important for HIV positive people to tell their providers which features of a regimen they find most desirable and most bothersome.
After making a switch, regular monitoring is crucial, both to ensure that HIV remains under control and CD4 counts are stable or rising, and to check for toxicities such as liver inflammation, elevated blood lipids, and blood cell deficiencies.
If a switch proves less than satisfactory, it is often possible to revert back to an older regimen. This is particularly true if the change was made to reduce toxicity. If a switch introduces side effects that prove more difficult to tolerate, an individual can usually safely switch back to the previous combination if viral load has remained suppressed. (Note: An exception is abacavir hypersensitivity; if abacavir was stopped for this reason, it should not be restarted, as this could cause a life-threatening reaction.) It may also be possible to regain lost virological control by re-intensifying a simplified regimen, especially if using a boosted PI.
If an individual's current regimen does not measure up, a switch could be the key to improved quality of life. If future advances in antiretroviral therapy continue at the same pace as they have in the past decade, people with HIV will soon have even more options for constructing regimens that provide an optimal balance of efficacy, safety, tolerability, and ease of use.
Liz Highleyman is a freelance medical writer and editor based in San Francisco.
Bartlett, J.A. and others. Minimizing resistance consequences after virologic failure on initial combination therapy: a systematic overview. Journal of Acquired Immune Deficiency Syndromes 41(3):323-31. March 2006.
Boyle, B. and others. Patients prefer simplified and well tolerated antiretroviral regimens. XV International AIDS Conference. Bangkok. July 11-16, 2004. Abstract 5815.
Calza, L. and others. Comparison between switching therapy from protease inhibitors to an NNRTI and lipid lowering therapy with pravastatin or bezafibrate for the management of HAART-related dyslipidemia. 12th CROI. Abstract 859.
Carr, A. and others. Abacavir substitution for nucleoside analogs in patients with HIV lipoatrophy: a randomized trial. Journal of the American Medical Association 288(2):207-15. July 10, 2002.
Cozzie-Lepri, A. and others. A comparison between abacavir and efavirenz as the third drug used in combination with a background therapy regimen of 2 nucleoside reverse-transcriptase inhibitors in patients with initially suppressed viral loads. Journal of Infectious Diseases 194(1):20-28. July 1, 2006.
DeJesus, E. and others. Effects of switching from fixed dose zidovudine/lamivudine (CBV) to fixed dose tenofovir DF/emtricitabine (TVD): maintenance of virologic suppression and other benefits. 45th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC). Washington, DC. December 16-19, 2005. Abstract H-517.
Fischl, M. and others. Randomized, controlled trial of lopinavir/ritonavir + efavirenz vs. efavirenz + 2 nucleoside reverse transcriptase inhibitors following a first suppressive 3- or 4-drug regimen in advanced HIV disease. 12th CROI. Abstract 162
Gatell, J.M. and others. Efficacy and safety of atazanavir (ATV) based HAART in patients switched from a stable boosted/unboosted protease-inhibitor (PI) treatment: the SWAN study. 10th European AIDS Conference (EACS). Dublin. November 17-20, 2005. Abstract PS1/1.
Glass, T.R. and others. Correlates of self-reported non-adherence to antiretroviral therapy in HIV infected patients: The Swiss HIV Cohort Study. Journal of Acquired Immune Deficiency Syndromes 41(3):385-92. March 2006.
Katlama, C. and others. Comparison of metabolic abnormalities 48 weeks after switching from highly active antiretroviral therapy containing a non-nucleoside reverse transcriptase inhibitor to Trizivir versus continued highly active antiretroviral therapy. AIDS.17(12): 1855-56. August 15, 2003.
Lampe, F.C. and others. Changes over time in risks of initial virological failure of combination antiretroviral therapy. Archives of Internal Medicine 166(5):521-28. March 13, 2006.
Martinez, E. and others. 3-year final results of a simplification trial with nevirapine, efavirenz, or abacavir as substitutes of protease inhibitors in patients with HIV infection (the NEFA Study). 13th CROI. Denver. February 5-8, 2006. Abstract 521.
McComsey, G.A. and others. Improvement in lipoatrophy associated with highly active antiretroviral therapy in human immunodeficiency virus-infected patients switched from stavudine to abacavir or zidovudine: the results of the TARHEEL study. Clinical Infectious Diseases 38(2):263-70. January 15, 2004.
Molina, J.-M. and others. Simplification therapy with once-daily emtricitabine, didanosine, and efavirenz in HIV-1-infected adults with viral suppression receiving a protease inhibitor-based regimen: a randomized trial. Journal of Infectious Diseases 191(6):830-39. March 15, 2005.
Murphy, R. and others. Switching to a thymidine analog-sparing or a nucleoside-sparing regimen improves lipoatrophy: 24-week results of a prospective randomized clinical trial, AACTG 5110. 12th CROI. Abstract 45LB.
Ribera, E. and others. Improvement of subcutaneous fat, lipid profile, and parameters of mitochondrial toxicity in patients with peripheral lipoatrophy when stavudine is switched to tenofovir. The LIPOTEST Study. 12th CROI. Abstract 860.
Sension, M. and others. AI424067: improvement in lipid profiles after 12 weeks of switching to atazanavir from boosted or unboosted protease inhibitors in patients with no previous PI virologic failure and hyperlipidemia at baseline. 12th CROI. Abstract 858.
Swindells, S. and others. A prospective, open-label, pilot trial of regimen simplification to atazanavir/ritonavir alone as maintenance antiretroviral therapy after sustained virologic suppression (ACTG 5201). 13th CROI. Abstract 108LB.
Waters, L. and others. Kaletra monotherapy -- a real-life experience. HIV Medicine 7 (supplement 1):13. April 2006. Abstract P9.
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