Changes in Hepatitis C Viral Response After Initiation of Highly Active Antiretroviral Therapy and Control of HIV Viremia in Chronically Co-infected Individuals

Abstract

Background: HIV seropositive individuals co-infected with hepatitis C virus (HCV) have an increased risk for liver cirrhosis. We examined the long-term effect of controlling HIV infection with highly active antiretroviral therapy (HAART) on HCV viremia among co-infected patients. Method: HIV/HCV co-infected patients who initiated HAART and were able to control HIV viremia to <500 copies/mL were evaluated. HIV and HCV viremia were measured at each time point from frozen plasma samples by using bDNA methodology. Liver function tests and CD4+ and CD8+ T cell counts of all patients were obtained at each time point. Results: Seventeen co-infected patients met criteria for study from a cohort of 156 patients. Median time to achieve an HIV viral load (VL) <500 copies/mL after initiation of HAART was 28 weeks (range, 5-225 weeks). Thirteen of 17 patients had increases in HCV VL. Slope analysis of HCV VL vs. HIV VL was -0.14 (p = .0496), demonstrating a 0.14 log increase in HCV VL concomitant with control of HIV viremia. HCV viremia returned toward baseline levels in the 16 patients who maintained HIV suppression for 6 months. None cleared HCV after initiation of HAART during this time. Alkaline phosphatase, ALT, and AST levels were not significantly changed from baseline nor correlated with change in HCV VL (p > .05). Conclusion: Control of HIV viremia may result in an early increase in HCV viremia. In this study, for every 1 log decrease of HIV VL there was a 0.14 log increase of HCV VL. The exact mechanism of this flare seen with control of HIV viremia is unknown. However, HAART alone was not able to eliminate or significantly reduce the HCV viremia in this cohort of co-infected patients.     

Prognostic Staging of Extensively Pretreated Patients with Advanced HIV-1 Disease

Abstract

Purpose: Determinants of therapeutic success are poorly characterized in patients with extensive HAART experience. Positive prognostic factors (PPFs) in the TORO trials could serve as the basis for a prognostically meaningful staging of treatment-experienced patients initiating a new antiretroviral regimen. Method: In TORO, triple-class-experienced patients with viral load (VL) ≥5,000 copies/mL received an optimized background regimen of 3-5 antiretrovirals (based on treatment history and baseline resistance testing) ± enfuvirtide (n = 995). Clinically relevant baseline PPFs that were predictive of 48-week virologic outcomes were identified via multiple regression analyses. Results: The likelihood of VL <400 copies/mL at 48 weeks (ITT analysis) was greater for those patients who had baseline CD4 count ≥100 cells/mm³ (odds ratio [OR] 2.1; 95% confidence intervals [CIs] 1.5, 3.1); baseline VL <5 log₁₀ copies/mL (OR 1.8; 95% CIs 1.2, 2.6); received ≤10 prior antiretrovirals (OR 2.4; 95% CIs 1.6, 3.4); or received ≥2 active antiretrovirals in their background treatment regimen (OR 2.3; 95% CIs 1.6, 3.3). Overall, 67% of triple-class-experienced patients who met all four prognostic criteria and received enfuvirtide achieved VL <400 copies/mL at 48 weeks vs. 43% for non-enfuvirtide patients (p < .05). Similar results were obtained when the analysis was done separately in each of the randomization arms of the study. Conclusion: Our findings provide guidance for physicians on expected outcomes in treatment-experienced patients and should be of value in their clinical management, as well as in stratifying participants in clinical trials involving treatment-experienced patients.     

Antiretroviral Treatment Regimen Outcomes Among HIV-Infected Prisoners

Abstract

Background: Despite the high prevalence of HIV in correctional settings, the duration of therapy and response to various highly active antiretroviral therapy (HAART) regimens in this setting is unknown. Method: Using a retrospective cohort study (1997-2002) of HIV-infected prisoners in Connecticut that linked demographic, pharmacy, and laboratory data, we compared HIV-1 RNA (VL) and CD4 lymphocyte responses to four treatment strategies at baseline and at the end of incarceration. Results: Using an analysis of 1,044 incarceration periods or 1,099 subjects for whom ≥6 months of continuous data were available, HAART regimens that included a triple NRTI, two NRTIs + either a PI or NNRTI, or a three-class (NRTI+NNRTI+PI) strategy demonstrated no difference in virological and immunological outcomes. The proportion of subjects who were initiated with NRTI, NNRTI, PI, or three-class regimens were 14%, 32%, 46%, and 8%, respectively. For all study groups, the mean change from baseline in CD4 and VL was +74 cells/μL and -0.93 log₁₀ copies/mL (p < .0001), respectively. Overall, 59% of subjects had an HIV-1 RNA level below the level of detection (<400 copies/mL) by the end of their incarceration. Using Kaplan-Meier curves to examine the time to change in the initial HAART strategy over the incarceration period, the three-class strategy was significantly more likely to be changed earlier than all others (p < .05). Conclusion: Although the three-class strategy was less durable, initiating HAART with any strategy resulted in similar and impressive virological and immunological outcomes by the end of incarceration, further supporting prison as an important site for the initiation and provision of effective antiretroviral therapy.     

Discordant immunologic and virologic responses to highly active antiretroviral therapy are associated with increased mortality and poor adherence to therapy

OBJECTIVE: To examine the independent association of discordant virologic and immunologic responses to highly active antiretroviral therapy (HAART) with mortality. METHODS: A population-based study of 1527 treatment-naive individuals initiating HAART used Cox proportional hazards modeling to determine the independent association of treatment response at 3 to 9 months with nonaccidental mortality. Logistic regression was used to examine associations with discordant responses. RESULTS: Viral load (VL)/CD4 discordant responses were seen in 235 (15.4%) of subjects, and VL/CD4 responses were seen in 179 (11.7%) of subjects. In adjusted Cox regression models, discordant responses were found to be independently associated with an increased risk of mortality (VL/CD4: relative hazard [RH] = 1.87, 95% confidence interval [CI]: 1.15 to 3.04; VL/CD4: RH = 2.47, 95% CI: 1.54 to 3.95). VL/CD4 discordance was found to be associated with increasing age, baseline HIV RNA load <100,000 copies/mL, baseline CD4 counts <50 cells/muL, the use of lamivudine (3TC)/zidovudine (ZDV), and poor adherence to therapy. VL/CD4 discordance was associated with younger age; injection drug use; baseline HIV RNA load >100,000 copies/mL; the use of 3TC/ZDV, didanosine (ddI)/3TC, or ddI/stavudine; and poor adherence to therapy. CONCLUSION: Discordant responses are independently associated with an increased risk of mortality and are, in turn, associated with poor adherence to therapy.     

The Significance of Low-Level Plasma HIV Viral Load on COBAS TaqMan® HIV-1 Assays for Patients with Undetectable Plasma Viral Load on COBAS Amplicor® Monitor Version 1.5

Abstract

Background: COBAS TaqMan® assay is a new HIV assay for measuring plasma viral load (VL). A significant number of patients with undetectable plasma VL on Amplicor® assay were reported to have detectable VL with TaqMan® in the study centre. Purpose: The aim of the present study was to investigate the significance of detectable VL counts with TaqMan® assay amongst patients who have had undetectable plasma VL with COBAS Amplicor® assay. Method: Observational study on patients who have had undetectable (<less than 50 copies/mL) plasma VL with COBAS Amplicor® version 1.5 assay but detectable plasma VL with COBAS TaqMan® assay between June 1, 2006 and April 30, 2007. All patients were on highly active antiretroviral therapy (HAART) for longer than 6 months before use of COBAS TaqMan® assay. Patients with detectable VL were followed up on a monthly basis until their VL was <40 copes/mL or there was confirmed new resistance to HAART using genotypic and Virco® resistance assay. Results: Plasma VL was detectable (>40 copies/mL) in 113 (14%) patients on 126 episodes using TaqMan® assay. VL was less than 500 copies/mL in 90% of those episodes. All episodes ended with VL <40 copies/mL after a median of 117 (94–143) days without change in HAART regimes. The duration of those episodes was longer than 150 days in 75% of cases. No new mutation was detected amongst specimens with detectable VL. Conclusion: Short-term detectable VL may be common with using TaqMan® assay. This phenomenon did not result in new mutations or failure of HAART in study patients in the short term.     

Monotherapy with Lopinavir/Ritonavir as Maintenance After HIV-1 Viral Suppression: Results of a 96-Week Randomized,Controlled, Open-Label,Pilot Trial (KalMo Study)

Abstract

Background: Long-term adverse events and expenses associated with HAART have led to an interest in simplified therapy. Lopinavir/ritonavir monotherapy is attractive due to its potency and high genetic barrier. Methods: This is a 96-week, open-label, randomized study to assess the feasibility of using LPV/r monotherapy in patients with undetectable viral load after being on successful HAART for at least 6 months. Subjects were randomized (1:1) to either switch from HAART to LPV/r monotherapy or to maintain their previous regimen. Results: 60 patients were enrolled. Baseline characteristics were similar in both groups. At Week 96, by intention-to-treat analysis, 24/30 (80.0%) subjects in monotherapy group and 26/30(86.6%) in the control group had a plasma viral load of <80 copies/mL. There was one virologic failure (defined as VL > 500 copies/mL) in each arm. Genotyping testing identified no resistance-associated mutations. The patient on the monotherapy arm was successfully resuppressed to <80 copies/mL after intensification with tenofovir and lamivudine. No statistically significant differences were found with regard to changes in CD4 counts. One subject in the monotherapy group discontinued due to diarrhea. Five subjects in the control group underwent regimen changes due to drug-related toxicities. Viral load from semen samples collected at the end of follow-up was undetectable on 14/15 patients randomized to monotherapy. Conclusions: Switching from various HAART regimens to LPV/r monotherapy in patients who were virologically suppressed and without a history of previous virologic failure was effective, safe, and well tolerated through 96 weeks.     

Determinants of Sustained Virological Suppression in Indigent,HIV-Infected Patients: Is Single Protease Inhibitor-Based Antiretroviral Therapy Truly Highly Active?

Abstract

Background: Effective virological suppression with HAART is dependent on strict adherence to therapy. Compliance with therapy is influenced by clinical and psychosocial factors. Method: We performed a retrospective study investigating determinants of effective virological suppression, defined as <400 RNA at 11-13 months of HAART, in an urban indigent population. The study included 366 new patients presenting for care to the Thomas Street Clinic, Houston, Texas, between April and December 1998. Median age, CD4 count, and viral load (VL) of the study population were 37.5 years, 189 cells/mm³, and 53,000, respectively. Thirty-nine percent had AIDS, 20% had cocaine-positive drug screens, and 64% were antiretroviral naïve. Two hundred and sixty-seven patients were started on HAART. Thirty-four percent showed virological suppression. Results: In multivariate analysis, adherence to HAART, care by experienced primary provider, baseline VL <100,000 copies/mL, age >35 years, and no active substance use were associated with virological suppression. Rates of virological suppression with HAART are unacceptably low in this urban indigent population. Conclusion: Low rates of virological suppression are primarily due to lack of adherence rather than late utilization of care among ethnic minorities. Single protease-inhibitor-based antiretroviral therapy does not appear to be highly active in this patient population.     

Comparison of Prognostic Importance of Latest CD4+ Cell Count and HIV RNA Levels in Patients with Advanced HIV Infection on Highly Active Antiretroviral Therapy

Abstract

The comparative prognostic importance of latest plasma HIV RNA levels (viral loads) and CD4+ cell counts among patients prescribed highly active antiretroviral therapy (HAART) has not been well characterized. Method: We assessed the prognostic value of latest CD4+ cell counts and latest viral loads for progression to AIDS or death and explored their interaction among 432 HIV-infected persons with advanced HIV who were prescribed a protease inhibitor (PI) as their first HAART regimen. Results: Pre-HAART median CD4+ cell count and viral load were 41 cells/mm³ and 126,331 copies/mL, respectively. After 12 months of HAART, the median CD4+ cell count was 154 cells/mm³; 39% of patients had a viral load of 400 copies/mL or lower. Over a median follow-up of 33 months, 109 (25%) of the 432 patients experienced an AIDS event or died. The hazard ratio for AIDS or death for those with latest CD4+ cell count <50 cells/mm³ versus ≥200 cells/mm³ was 13.9 (95% CI 6.5 to 29.7) without adjustment for latest viral load measurements and 9.5 (95% CI 4.0 to 22.5) after adjustment for latest viral load. In contrast, the hazard ratio for AIDS or death for those with viral load ≥100,000 versus <400 copies/mL was 4.2 (95% CI 2.3 to 7.7) without adjustment for latest CD4+ level and 1.2 (95% CI 0.6 to 2.4) with adjustment for latest CD4+ cell count. Conclusion: We conclude that when latest CD4+ cell count and viral load are considered separately, both are significantly related to AIDS or death; when these markers are jointly considered, the association of viral load with AIDS or death is substantially diminished. Latest CD4+ levels are more strongly related to AIDS or death than latest viral load levels in patients on HAART.     

Low-Dose Daily Subcutaneous Interleukin-2 in Combination with Highly Active Antiretroviral Therapy in HIV + Patients: A Randomized Controlled Trial

Abstract

Purpose: Previous studies with intermittent interleukin-2 (IL-2) therapy using intermediate and high levels of IL-2 have demonstrated significant increases in the CD4 + T cell count in HIV-infected patients. Intermittent regimens are amenable to outpatient use, but severe adverse events are frequently experienced with intermediate- and high-dose levels of IL-2. Therefore in this study, the effect of daily, subcutaneous low-dose IL-2 therapy on safety and immunological endpoints was investigated to determine whether immunological benefit could be achieved without toxicity in HIV-infected patients also receiving highly active antiretroviral therapy (HAART). Method: A total of 115 patients were enrolled in the trial. Fifty-six asymptomatic HIV-infected patients who had CD4 + T cell counts less than 300 cells/μL at screening and a stable HIV viral load received low-dose IL-2 (1.2 million IU [MIU]/m 2 beginning dose) once daily in conjunction with HAART (IL-2 group). Fifty-nine patients received HAART alone (control group). Results: A dramatic effect of IL-2 on the natural killer (NK) cell population was observed with mean increases of 156 cells/μL in the IL-2 group compared to 19.93 cells/μL in the control group (p < .001). Additionally, IL-2-treated patients experienced a statistically significant increase in the mean percentage of CD4 + T cells (3.52% increase) when compared to control patients (1.33% increase) (p < .001). The expanded CD4 + T cell population was primarily of the naive phenotype, with mean increases of 4.53% for the IL-2 group and 0.31% for the control group (p < .001 for between-group difference). In addition, a higher proportion of IL-2-treated patients (67%) compared to control patients (33%) achieved increases of greater than 50% in the CD4+ T cell count (p = .08). Adverse events of grade 3 or grade 4 toxicity were infrequent in the current study and were substantially lower by comparison to those in studies of intermittent dose IL-2 therapy. Also, negligible changes in the HIV viral load from baseline to final measurement were observed in both groups. A trend toward a reduced number of modifications of antiretroviral therapy was apparent in the IL-2 group when compared to control patients. Conclusion: Daily, low-dose subcutaneous IL-2 therapy in conjunction with HAART is safe and well tolerated and is effective in expanding lymphocyte cell types including NK cells and naive T cells in individuals who have <300 CD4+ T cells.     

Simplified Therapy with Zidovudine,Lamivudine, and Abacavir for Very Nonadherent,Treatment-Failing Patients

Abstract

Objective: To assess the effectiveness of a simplified therapy for very nonadherent patients who had previously failed with HAART. Method: We performed a prospective open-label study of antiretroviral-experienced patients. Dosing schedule comprised (co-formulated) zidovudine, lamivudine, and abacavir bid. Eligible patients had to have plasma HIV RNA >5000 copies/mL, previous therapy, and very poor adherence to the medication regimen. Results: Eighty-five patients were included (mean viral load, 4.4 log/mL; mean CD4, 240 cells/mL; IDUs, 78%; methadone maintenance program, 42%; AIDS, 28%). Number of previous therapies: one, 53%; two, 28%; three or more, 19%. In the intent-to-treat analysis at 1 year, 38 patients (44.7%) achieved viral load below 500 copies/mL. Adherence greater than 90% of prescribed drugs was reported in 49% of patients, adverse events were reported in 17.6%, mortality in 6%, and lost to follow-up in 26%. The factors associated with virologic failure were nonadherence (odds ratio [OR], 4.4; 95% CI 1.5-12.3), baseline CD4 cell count <200 cells/mL (OR, 3.4; 95% CI 1.3-8.9; p = .01), and more than one previous treatment (OR, 2.7; 95% CI 1.1-6.9). Conclusion: Regarding previously very nonadherent patients, this simplified combination therapy containing three NRTIs obtained satisfactory results in ART-experienced patients. However, more aggressive interventions to enhance adherence are needed to improve results.     

Comparison of Metabolic Abnormalities and Clinical Lipodystrophy 48 Weeks After Switching from HAART to Trizivir™ Versus Continued HAART: The Trizal Study

Abstract

Purpose: To analyze the evolution of clinical lipodystrophy (LD) and metabolic abnormalities in patients continuing to receive HAART versus patients switched to Trizivir? (zidovudine, lamivudine, abacavir) after 48 weeks. Method: Patients treated with HAART >6 months with plasma HIV-1 RNA viral load (VL) <;400 copies/mL and <;50 copies/mL at screening were randomly assigned to continue HAART (103 patients) or to receive Trizivir? (106 patients). Clinical LD was evaluated using a standardized patient questionnaire only at baseline, weeks 4 and 8, and then every 8 weeks until Week 48. Laboratory evaluation was performed every 4 weeks. Results: The proportion of patients exhibiting ≥1 LD symptom at baseline was 40% in the Trizivir? arm and 50% in HAART arm (difference not significant). After 48 weeks, the prevalence was 28% and 42% respectively (p = .03), and the median number of LD symptoms per patient was 2 in the Trizivir? arm and 4 in the continued HAART arm (p = .016). Median decreases in cholesterol levels over the 48-week study period were greater in the Trizivir. arm than in the continued HAART arm (–0.80 vs. –0.44 mmol/L; p < .001). Median triglyceride levels decreased in the Trizivir? arm but increased in the continued HAART arm (–0.17 and +0.01 mmol/L; p = .006). Suppression of VL was maintained in most patients with no differences between the two arms. Conclusion: A switch from "standard" HAART to Trizivir? was associated with an improvement in clinical LD and blood lipid abnormalities after 48 weeks.     

Combination Therapy With Hydroxyurea Versus Without Hydroxyurea As First Line Treatment Options for Antiretroviral-Naive Patients

Abstract

Purpose: This study analyzed whether combination therapy with hydroxyurea (HU) could be considered as first line treatment for antiretroviral-naive patients. Method: The prospective open-label study was carried out from March 1996 to May 2000. The antiretroviral treatments were treatment 1—didanosine 400 mg/day, stavudine 60/80 mg/day, and HU 500 mg/day; treatment 2—two nucleosides plus a protease inhibitor; treatment 3—didanosine, indinavir, and HU (500-1,000 mg/day). The viral load (VL) and CD4 determinations were performed at weeks 24, 48, 72, and 96. Results: The sample comprised 284 patients. The distribution of patients by levels of VL and CD4 were similar in the three treatment groups. At week 24, patients receiving T1 and T3 achieved higher percentages of undetectable VL (89% and 81%, respectively) with no significant differences (p = .127) between them. The T2 group showed a lower proportion (58%) of undetectable VL, which was significantly lower than T1 (p < .0001) and T3 (p < .0007). At week 48, the results were similar to week 24. At week 96, nearly all patients had undetectable viral load (UVL). The analysis of adverse effects showed that the T2 group at week 48 had a greater proportion of adverse effects that was significantly different from T1 (p = .0026); T3 had intermediate values with no significant difference from T2 (p = .45) and from T1 (p = .048). At week 48, T1 showed higher adherence level with significant difference from the other two treatments. Conclusion: Patients were followed for some 96 weeks and, with an intention-to-treat analysis, were found to do better virologically and Clinically in treatment groups containing HU. The combination of antiretroviral drugs with HU may be an excellent option as initial therapy because of its strong antiretroviral action, its lower rate of adverse effect, and the smaller cost as compared to other regimens.     

Immunity to Human Immunodeficiency Virus (HIV) in Children with Chronic HIV Infection Receiving Highly Active Antiretroviral Therapy

Our objective was to describe the CD4-mediated human immunodeficiency virus (HIV)-specific cell-mediated immunity (CMI) and its virologic and immunologic correlates in children with chronic HIV infection on highly active antiretroviral therapy (HAART). Twelve HIV-infected children on stable antiretroviral therapy with a median level of CD4⁺ lymphocytes (CD4%) of 25.5% and a median viral load (VL) of 786 HIV RNA copies/ml were enrolled in this study. Nine of these children were also cytomegalovirus (CMV) seropositive. Blood mononuclear cells, stimulated with HIV and CMV antigens, were used to measure lymphocyte proliferation and to enumerate gamma interferon (IFN-γ)-producing CD4⁺ cells. HIV CMI and CMV CMI were detected in similar proportions of patients and correlated with each other, although the HIV responses were less robust. HIV lymphocyte proliferation significantly increased with lower HIV VL and showed a trend to increase with higher CD4% and longer time on HAART. The in vitro IFN-γ response to HIV or CMV was not affected by CD4%, VL, or HAART. Pediatric patients with established HIV infection on HAART frequently exhibit HIV CMI despite undetectable HIV replication. We concluded that the association between HIV CMI and CMV CMI indicates that the same factors govern responsiveness to either antigen.     

Progression to AIDS or Death as Endpoints in HIV Clinical Trials

Abstract

Purpose: To assess progression to AIDS or death from month 4 after a protease inhibitor-containing regimen is initiated in a cohort of 1,281 patients. Method: We used Kaplan-Meier estimates of probability of clinical progression. RESULT: At month 4, most patients had an HIV-1 RNA plasma value below 500 copies/mL (78%) and a CD4 cell count above 300 cells/mm³ (62%). Starting from month 4, clinical progression at 1 and 2 years of follow-up was low (<3% at 1 year) in patients with HIV RNA <500 copies/mL or 500-10,000 copies/mL and in patients with CD4 between 50 and 300 cells/mm³ or >300 cells/mm³. A higher risk of clinical progression (10% at 1 year) was evidenced only in patients with poor response to antiretroviral therapy, that is, with CD4 <50 cells/mm³ or CD4 between 50-300 cells/mm³ together with an HIV RNA >10,000 copies/mL. Conclusion: In patients currently on antiretroviral therapy, clinical trials with clinical progression as endpoint are almost not feasible, except in patients with a poor immunovirological response to first- or second-line HAART.     

Early Virologic Failure and Rescue Therapy of Tenofovir,Abacavir, and Lamivudine for Initial Treatment of HIV-1 Infection: TONUS Study

Abstract

Background: To assess the efficacy and safety of the triple NRTI combination of abacavir (ABC), lamivudine (3TC), and tenofovir (TDF) in a once-daily regimen. Method: 38 HIV-naive patients (pts) were treated in a prospective open-arm study over 48 weeks (W48). Virological failure was defined as never achieving plasma HIV-1 RNA <400 copies/mL or rebound of ≥0.7 log₁₀. Results: 12/36 (33%) pts had virologic failure at W24 and 10 additional pts had HIV RNA >50 copies/mL at W12 or W24. There was a significant association between baseline viral load (VL) and virologic failure in 0%, 29%, and 64% pts with baseline VL levels <4, 4-5, and >5 log₁₀ copies/mL, respectively (p = .014). 76% of pts developed K65R and M184V/I mutations by W24, and 19% developed M184V/I alone. At W4, 86% of pts had adequate plasma C_min for the 3 drugs. 14 pts with K65R and M184V/I were given a rescue therapy with a successful outcome (<50 copies/mL; median follow-up 48 weeks). Conclusion: Convergent genetic pathway to resistance, in conjunction with lower antiretroviral potency, may explain the high rate of selection K65R and M184V mutations. These mutations did not appear to have a negative effect on rescue therapy with a variety of regimens.     

Impact of Baseline Virologic,Immunologic, and Demographic Characteristics on Virologic Responses in the Gemini Study

Abstract

Purpose: To determine the impact of baseline viral load (VL) and CD4+ cell count, race/ethnicity, and gender on response in a post hoc analysis of the Gemini study.Methods: In this 48-week study, treatment-naïve, HIV-infected participants received as initial therapy twice-daily saquinavir/ritonavir (SQV/r) 1000/100 mg (n=167) or lopinavir/ritonavir (LPV/r) 400/100 mg (n=170), each with emtricitabine 200 mg/tenofovir 300 mg daily. The proportion of participants achieving HIV RNA<50 copies/mL (primary endpoint) and median change from baseline in CD4+ cell count were compared by baseline VL (>100,000 vs ≤100,000 copies/ mL) and CD4+ cell count (>100 vs ≤100 cells/µL). The impact of baseline and demographic variables on virologic response was assessed by logistic regression analysis.Results: Responses were similar between arms (SQV/r vs LPV/r) with or without stratification. In a pooled analysis of SQV/r and LPV/r arms, CD4+ cell count >100 cells/µL (odds ratio [OR], 1.628;P = .0416), non-Thai/non-Black versus Black race (OR, 1.518;P = .0023), and non-Thai/non-Black versus Thai (OR, 0.467;P = .0046) were significant predictors of virologic response.Conclusions: Treatment groups had similar efficacy. Baseline CD4+ cell count and race/ethnicity were independent predictors of virologic response, whereas baseline VL and gender were not.