One of the consequences of highly active antiretroviral therapy (HAART) has been the development of multidrug-resistant HIV-1 strains. For patients infected with such strains, salvage therapy options are limited. This can be especially problematic when patients have access to the full range of antiretroviral drugs, as they do in some developing countries. In Brazil, for example, the state provides HIV/AIDS health care to all HIV-infected individuals. As early as 1991, the Brazilian Ministry of Health was providing antiretroviral drugs through its extensive public health system. Given the fact that, in many cases, antiretroviral drugs have been administered sequentially, the proportion of Brazilian patients experiencing virologic failure is assumed to be high. It has been reported that the median time to virologic failure in Brazil is approximately 14 months among treatment-naive patients. 1 Presumably, antiretroviral treatment failure rates are higher among those receiving sequential treatment than among those receiving simultaneous treatment. In an analysis of 791 samples collected in Brazil, resistance-related mutations were identified in the reverse transcriptase region and protease region in 96.6% and 58.2% of the samples, respectively. Multidrug resistance was common, with 36.8% of the samples presenting resistance to all 3 therapeutic classes. 2

It has been shown that antiretroviral-naive patients treated with boosted protease inhibitors (PIs) develop few or no primary mutations in the protease region of the pol gene. 3, 4 However, treatment failure in patients treated with unboosted PIs might be attributable to high protease resistance. One option for salvage therapy in such cases is the use of double-boosted PIs. Most of the studies addressing this issue have evaluated the use of the lopinavir/ritonavir coformulation combined with saquinavir. 5 It has also been shown that combining the lopinavir/ritonavir coformulation with amprenavir produces positive clinical results. 6 However, the adverse pharmacokinetic interaction between lopinavir and amprenavir has discouraged many experts, because lopinavir can decrease the trough levels of amprenavir. 7