Eric S Daar

Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States

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Publications (163)979.2 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: In this article, we examine the effectiveness of a variety of HIV diagnosis interventions in recently HIV-diagnosed men who have sex with men (MSM). These interventions use the preventive potential of postdiagnosis behavior change (PDBC), as measured by the reduction in the number of new infections. Empirical evidence for PDBC was presented in the behavioral substudy of the Southern California Acute Infection and Early Disease Research Program. In previous modeling work, we demonstrated the existing preventive effects of PDBC. However, a large proportion of new infections among MSM are either undiagnosed or diagnosed late, and the preventive potential of PDBC is not fully utilized. We derive empirical, stochastic, network-based models to examine the effectiveness of several diagnosis interventions that account for PDBC among MSM over a 10-year period. These interventions involve tests with shorter detection windows, more frequent testing, and individualized testing regimens. We find that individualized testing interventions (i.e., testing individuals every three partners or 3 months, whichever is first, or every six partners or 6 months, whichever is first) result in significantly fewer new HIV infections than the generalized interventions we consider. This work highlights the potential of individualized interventions for new public health policies in HIV prevention. Copyright © 2015 Elsevier Inc. All rights reserved.
    Annals of epidemiology. 01/2015; 25(1):1-6.
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    ABSTRACT: Efavirenz and abacavir are components of recommended first-line regimens for HIV-1 infection. We used genome-wide genotyping and clinical data to explore genetic associations with virologic failure among patients randomized to efavirenz-containing or abacavir-containing regimens in AIDS Clinical Trials Group (ACTG) protocols. Virologic response and genome-wide genotype data were available from treatment-naive patients randomized to efavirenz-containing (n=1596) or abacavir-containing (n=786) regimens in ACTG protocols 384, A5142, A5095, and A5202. Meta-analysis of association results across race/ethnic groups showed no genome-wide significant associations (P<5×10) with virologic response for either efavirenz or abacavir. Our sample size provided 80% power to detect a genotype relative risk of 1.8 for efavirenz and 2.4 for abacavir. Analyses focused on CYP2B genotypes that define the lowest plasma efavirenz exposure stratum did not show associations nor did analysis limited to gene sets predicted to be relevant to efavirenz and abacavir disposition. No single polymorphism is associated strongly with virologic failure with efavirenz-containing or abacavir-containing regimens. Analyses to better consider context, and that minimize confounding by nongenetic factors, may show associations not apparent here.
    Pharmacogenetics and Genomics 11/2014; · 3.61 Impact Factor
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    ABSTRACT: Antiretroviral therapy (ART) is associated with improved kidney function; however, the nucleotide reverse transcriptase inhibitor (NRTI) tenofovir disoproxil fumarate (TDF) has been associated with decreased kidney function and proteinuria.
    Journal of acquired immune deficiency syndromes (1999). 09/2014; 67(1):36-44.
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    ABSTRACT: It is uncertain whether HIV-1 antiretroviral exposure and clinical response varies between males and females or different race/ethnic groups. We describe ritonavir-enhanced atazanavir pharmacokinetics in relation to virological failure, safety and tolerability in treatment-naive individuals to investigate potential differences.
    Journal of Antimicrobial Chemotherapy 08/2014; · 5.34 Impact Factor
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    ABSTRACT: The relationship between efavirenz use and suicidality is not well-defined.
    Annals of internal medicine 07/2014; 161(1):1-10. · 13.98 Impact Factor
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    ABSTRACT: Host and viral factors influence the HIV-1 infection course. Reduced Nef function has been observed in HIV-1 controllers during the chronic phase, but the kinetics and mechanisms of Nef attenuation in such individuals remain unclear. We examined plasma RNA-derived Nef clones from 10 recently infected individuals who subsequently suppressed viremia to less than 2000 RNA copies/mL within one year post-infection (acute controllers) and 50 recently infected individuals who did not control viremia (acute progressors). Nef clones from acute controllers displayed lower ability to downregulate CD4 and HLA class I from the cell surface and reduced ability to enhance virion infectivity compared to those from acute progressors (all p<0.01). HLA class I downregulation activity correlated inversely with days post-infection (Spearman's R= -0.85, p=0.004) and positively with baseline plasma viral load (Spearman's R=0.81, p=0.007) in acute controllers, but not in acute progressors. Nef polymorphisms associated with functional changes over time were identified in follow-up samples from six controllers. For one such individual, mutational analyses indicated that four polymorphisms selected by HLA-A*31 and B*37 acted in combination to reduce Nef steady state protein levels and HLA class I downregulation activity. Our results demonstrate that relative control of initial HIV-1 viremia is associated with Nef clones that display reduced function, which in turn may influence the course of HIV-1 infection. Transmission of impaired Nef sequences likely contribute in part to this observation; however, accumulation of HLA-associated polymorphisms in Nef that impair function also suggests that CD8+ T-cell pressures play a role in this phenomenon.
    Journal of virology. 06/2014;
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    ABSTRACT: Acute HIV-1 infection is characterized by the rapid generation of highly diverse genetic variants to adapt to the new host environment. Understanding the dynamics of viral genetic variation at this stage of infection is critical for vaccine design efforts and early drug treatment. Here, using a high-resolution deep sequencing approach targeting the HIV-1 gag region, we reveal very early immune pressure with dramatic subpopulation shifts in a single acutely infected participant providing further insight into the genetic dynamics of acute HIV-1 infection.
    AIDS Research and Human Retroviruses 06/2014; · 2.71 Impact Factor
  • Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 05/2014;
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    ABSTRACT: The Human Immunodeficiency Virus 1 (HIV-1) accessory protein Nef is heavily targeted by CD8+ T lymphocytes (CTLs) during acute infection and therefore is included in many candidate vaccines. We investigated whether CTL targeting of Nef during acute infection contributes to immune control by disrupting its function. Nef sequence and function in parallel with CTL responses were assessed longitudinally from peak viremia until viremia set point in a cohort of six subjects with acute infection. All but one individual had a single founder strain. Nef-specific CTL responses were detected in all subjects and declined in magnitude over time. These responses were associated with mutations but none were detected in important functional motifs. Nef-mediated CD4 and MHC-Class I downregulation were better preserved in acute infection compared to chronic infection. Finally, Nef-specific CTL responses were not associated with reduction in viremia from its acute peak. Our results indicate that CTLs targeting Nef epitopes outside of critical functional domains have little effect on its pathogenic functions, rendering these responses ineffective in acute infection. These data indicate that using the whole Nef protein as a vaccine immunogen likely allows immunodominance that leads to targeting of CTL responses that are rapidly escaped with little effect on Nef -mediated pathogenic functions. Pursuing vaccination approaches that can more precisely direct responses to vulnerable areas would maximize efficacy. Until vaccine-induced targeting can be optimized, other approaches such as use of Nef function inhibitors or pursuing immuno-therapies such as T cell receptor gene therapy or adoptive transfer may be more likely to result in successful control of viremia.
    Journal of Virology 04/2014; · 5.08 Impact Factor
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    ABSTRACT: Asymptomatic cytomegalovirus (CMV) replication occurs frequently in the genital tract of untreated HIV-infected men and is associated with increased immune activation and HIV disease progression. To determine the connections between CMV-associated immune activation and the size of the viral reservoir, we evaluated the interactions between (i) asymptomatic seminal CMV replication, (ii) levels of T cell activation and proliferation in blood, and (iii) the size and the transcriptional activity of the HIV DNA reservoir in blood from 53 HIV-infected men on long-term antiretroviral therapy (ART) with suppressed HIV RNA in blood plasma. We found that asymptomatic CMV shedding in semen was associated with significantly higher levels of proliferating and activated CD4(+) T-cells in blood (P<0.01). Subjects with detectable CMV in semen had approximately five times higher average levels of HIV DNA in blood CD4+ T cells compared to subjects with no CMV. There was also a trend for CMV shedders to have increased cellular (multiply spliced) HIV RNA transcription (p=0.068) compared to participants without CMV, but it is unclear if this transcription pattern is associated with residual HIV replication. In multivariate analysis, the presence of seminal plasma CMV (P=0.04), detectable 2-LTR and lower nadir CD4+ (P<0.01) were independent predictors of higher levels of proviral HIV DNA. Interventions aimed at reducing seminal CMV and associated immune activation may be important for HIV curative strategies. Future studies of anti-CMV therapeutics will help to establish causality and determine the mechanisms underlying these described associations. Almost all individuals infected with HIV are also infected with cytomegalovirus (CMV), and replication dynamics of those two viruses likely influence each other. This study investigated interactions between asymptomatic CMV replication within the male genital tract, levels of inflammation in blood, and the size of the HIV DNA reservoir in 53 HIV infected men on long-term antiretroviral therapy (ART) with suppressed HIV RNA in blood plasma. In support of our primary hypothesis, shedding of CMV DNA in semen was associated with increased activation and proliferation of T-cells in blood and also significantly higher levels HIV DNA in blood cells. These results suggest that CMV reactivation might play a role in the maintenance of the HIV DNA reservoir during suppressive ART and could be a target of pharmacologic intervention in future studies.
    Journal of Virology 04/2014; · 5.08 Impact Factor
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    ABSTRACT: The reasons for persistent brain dysfunction in chronically HIV-infected persons on stable combined antiretroviral therapies (CART) remain unclear. Host and viral factors along with their interactions were examined in 260 HIV-infected subjects who underwent magnetic resonance spectroscopy (MRS). Metabolite concentrations (NAA/Cr, Cho/Cr, MI/Cr, and Glx/Cr) were measured in the basal ganglia, the frontal white matter, and gray matter, and the best predictive models were selected using a bootstrap-enhanced Akaike information criterion (AIC). Depending on the metabolite and brain region, age, race, HIV RNA concentration, ADC stage, duration of HIV infection, nadir CD4, and/or their interactions were predictive of metabolite concentrations, particularly the basal ganglia NAA/Cr and the mid-frontal NAA/Cr and Glx/Cr, whereas current CD4 and the CPE index rarely or did not predict these changes. These results show for the first time that host and viral factors related to both current and past HIV status contribute to persisting cerebral metabolite abnormalities and provide a framework for further understanding neurological injury in the setting of chronic and stable disease.
    Journal of NeuroVirology 04/2014; · 2.85 Impact Factor
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    ABSTRACT: Prior studies have found that early HIV protease inhibitors contribute to glucose dysregulation. Few randomized trials have evaluated glucose indices in antiretroviral-naive individuals on newer antiretroviral therapy (ART). A5224s was a substudy of A5202, a prospective trial of 1857 ART-naive participants randomized to blinded abacavir-lamivudine (ABC/3TC) or tenofovir DF-emtricitabine (TDF/FTC) with open-label efavirenz (EFV) or atazanavir-ritonavir (ATV/r). Analyses used two-sample t-tests, Spearman correlation coefficients and linear regression. A5224s included 269 nondiabetic individuals: 85% men, 47% white non-Hispanic, baseline median age 38 years, HIV-1 RNA 4.6 log10 copies/ml and CD4 cell count 233 cells/μl. Overall, significant 96-week increases occurred in fasting glucose, insulin and the homeostatic model assessment of insulin resistance (HOMA-IR), P ≤ 0.004. Assignment to EFV (versus ATV/r) resulted in significantly greater glucose increase [mean difference 4.4; 95% confidence interval (CI) 1.3, 7.5 mg/dl; P = 0.006] but not insulin or HOMA-IR (P ≥ 0.72). Glucose indices were not significantly different between ABC/3TC and TDF/FTC arms, P ≥ 0.18. Significant correlations were detected between changes in glucose indices and changes in BMI; all r ≥ 0.23, P ≤ 0.001. In multivariable analyses, in addition to the EFV effect, higher baseline HIV-1 RNA and greater BMI change were significant independent factors associated with greater glucose increase. Changes in glucose metabolism were not significantly different between TDF/FTC and ABC/3TC-based regimens. A small but significantly greater increase in glucose was observed in those assigned to EFV. As glucose dysregulation may increase with time on ART, longer term studies will be needed to further clarify the clinical significance of these findings.
    AIDS (London, England) 03/2014; · 4.91 Impact Factor
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    ABSTRACT: Atazanavir-associated hyperbilirubinemia can cause premature discontinuation of atazanavir and avoidance of its initial prescription. We used genomewide genotyping and clinical data to characterize determinants of atazanavir pharmacokinetics and hyperbilirubinemia in AIDS Clinical Trials Group protocol A5202. Plasma atazanavir pharmacokinetics and indirect bilirubin concentrations were characterized in HIV-1-infected patients randomized to atazanavir/ritonavir-containing regimens. A subset had genomewide genotype data available. Genomewide assay data were available from 542 participants, of whom 475 also had data on estimated atazanavir clearance and relevant covariates available. Peak bilirubin concentration and relevant covariates were available for 443 participants. By multivariate analysis, higher peak on-treatment bilirubin levels were found to be associated with the UGT1A1 rs887829 T allele (P=6.4×10), higher baseline hemoglobin levels (P=4.9×10), higher baseline bilirubin levels (P=6.7×10), and slower plasma atazanavir clearance (P=8.6×10). For peak bilirubin levels greater than 3.0 mg/dl, the positive predictive value of a baseline bilirubin level of 0.5 mg/dl or higher with hemoglobin concentrations of 14 g/dl or higher was 0.51, which increased to 0.85 with rs887829 TT homozygosity. For peak bilirubin levels of 3.0 mg/dl or lower, the positive predictive value of a baseline bilirubin level less than 0.5 mg/dl with a hemoglobin concentration less than 14 g/dl was 0.91, which increased to 0.96 with rs887829 CC homozygosity. No polymorphism predicted atazanavir pharmacokinetics at genomewide significance. Atazanavir-associated hyperbilirubinemia is best predicted by considering UGT1A1 genotype, baseline bilirubin level, and baseline hemoglobin level in combination. Use of ritonavir as a pharmacokinetic enhancer may have abrogated genetic associations with atazanavir pharmacokinetics.
    Pharmacogenetics and Genomics 02/2014; · 3.61 Impact Factor
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    ABSTRACT: HIV transmission risk is increased during antiretroviral therapy (ART) use if individuals are not virologically suppressed and engage in high risk transmission behavior. Baseline data of HIV-infected men who have sex with men (MSM) with recent history of risky behavior on ART for ≥3 months (n = 139) were evaluated to assess predictors of detectable viremia and HIV transmission risk-taking behavior. Twenty-four subjects had viral load (VL) >75 copies/mL and 12 had VL >1000 copies/mL. In multivariable regression analyses, subjects with VL >75 copies/mL were more likely to be Black (OR = 4.48, p = 0.007), have lower CD4 cells (OR = 0.727, p = 0.005) and have used methamphetamines in the last month (OR = 6.64, p = 0.019). Subjects with VL >1000 copies/mL were more likely to have lower CD4 cells (OR = 0.494, p = 0.004), report <90% adherence (OR = 7.94; p = 0.046) and have used methamphetamines in the last month (OR = 10.01, p = 0.034). Subjects with VL >75 copies/mL with the greatest transmission risk behavior (n = 14) were more likely to be Black (OR = 8.00, p = 0.006), have lower CD4 cells (OR = 0.657, p = 0.009) and have used methamphetamines in the last month (OR = 5.20, p = 0.042). High risk HIV transmission behavior with viremia occurred in 10% of the cohort. Future efforts to reduce HIV transmission among MSM on ART will require combined interventions that target risk-taking behaviors and substance use.
    International Journal of STD & AIDS 01/2014; · 1.00 Impact Factor
  • Katya R. Calvo, Eric S. Daar
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    ABSTRACT: Antiretroviral therapy (ART)-experienced individuals may choose to modify their regimens because of suboptimal virologic response, poor tolerability, convenience, or to minimize interactions with other medications or food. Constructing a new regimen for any of these reasons requires a thorough review of prior antiretroviral drug use and available drug resistance results. This article summarizes the strategies used in managing the ART-experienced individual who is considering a modification in therapy at the time of suboptimal virologic response or while virologically suppressed on a stable regimen.
    Infectious Disease Clinics of North America. 01/2014;
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    ABSTRACT: Background. To evaluate treatment responses to atazanavir plus ritonavir or efavirenz in initial antiretroviral regimens among women and men, and determine if treatment outcomes differ by sex. Methods. Randomized trial of open label atazanavir plus ritonavir or efavirenz combined with abacavir/lamivudine or tenofovir/emtricitabine in 1857 HIV-1-infected, treatment-naive persons enrolled between September 2005 and November 2007 at 59 sites in the United States and Puerto Rico.Associations of sex with 3 primary study endpoints of time-to virologic failure, safety and tolerability events were analyzed using Cox proportional hazards models. Model-based population pharmacokinetic analysis was performed using non-linear mixed effects modeling (NONMEM version VII). Results. Of 1857 participants 322 were women. Women assigned to atazanavir/ritonavir had higher risk virologic failure with either nucleoside reverse transcriptase inhibitor backbone than women assigned to efavirenz, or men assigned to atazanavir/ritonavir. The effects of ATV/r and EFV upon safety and tolerability risk did not differ significantly by sex. With ABC/3TC, women had a significant 32% higher safety risk compared to men; with TDF/FTC, the safety risk was 20% larger for women compared to men, but not statistically significant. Women had slower atazanavir clearance and higher pre-dose levels of atazanavir compared to men. Self-reported adherence did not differ significantly by sex. Conclusions. This is the first randomized clinical trial to identify a significantly earlier time to virologic failure in women randomized to atazanavir/ritonavir compared to women randomized to efavirenz. This finding has important clinical implications given that boosted protease inhibitors are often favored over efavirenz in women of childbearing potential.
    Clinical Infectious Diseases 11/2013; · 9.37 Impact Factor
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    ABSTRACT: Our objective here is to demonstrate the population-level effects of individual-level post-diagnosis behavior change (PDBC) in Southern Californian men who have sex with men (MSM), recently diagnosed with HIV. While PDBC has been empirically documented, the population-level effects of such behavior change are largely unknown. To examine these effects, we develop network models derived from the exponential random graph model family. We parameterize our models using behavioral data from the Southern California Acute Infection and Early Disease Research Program, and biological data from a number of published sources. Our models incorporate vital demographic processes, biology, treatment and behavior. We find that without PDBC, HIV prevalence among MSM would be significantly higher at any reasonable frequency of testing. We also demonstrate that higher levels of HIV risk behavior among HIV-positive men relative to HIV-negative men observed in some cross-sectional studies are consistent with individual-level PDBC.
    AIDS and Behavior 10/2013; · 3.49 Impact Factor
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    ABSTRACT: The association of inflammatory biomarkers with clinical events after antiretroviral therapy (ART) initiation is unclear. A5202 randomized 1857 treatment-naive subjects to abacavir/lamivudine or tenofovir-DF/emtricitabine with efavirenz or atazanavir/ritonavir. Substudy A5224s measured inflammatory biomarkers on subjects with available plasma from baseline and weeks 24 or 96. An exploratory analysis of the association of hsCRP, IL-6, sTNF-RI, sTNF-RII, TNF-α, sVCAM-1, and sICAM-1 with times to AIDS and to non-AIDS events used Cox proportional hazards models. Analysis included 244 subjects; 85% male, 48% white non-Hispanic, with median age 39 years, HIV-1 RNA 4.6 log10 copies/mL, and CD4 240 cells/µL. Overall, 13 AIDS events (9 opportunistic infections; 3 AIDS-cancers, 1 recurrent bacterial pneumonia) and 18 non-AIDS events (6 diabetes, 4 cancers, 3 cardiovascular, 5 pneumonias) occurred. Higher baseline IL-6, sTNF-RI, sTNF-RII, and sICAM-1 were significantly associated with increased risk of AIDS-defining events. Adjustment for baseline HIV-1 RNA did not change results, while adjusting for baseline CD4 count left only sTNF-RI and sICAM-1 significantly associated with increased risk. Time-updated values of IL-6, sTNFR-I and II, and sICAM-1 were also associated with an increased risk. For non-AIDS events, only higher baseline hsCRP was significantly associated with increased risk, while higher IL-6 was marginally associated with higher risk. Analyses of time-updated biomarker values showed TNF-α to be significantly associated with increased risk, even after adjustment for ART, and CD4 count or HIV-1 RNA. Higher levels of several inflammatory biomarkers were independently associated with increased risk of AIDS and non-AIDS events.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 10/2013; · 4.65 Impact Factor
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    ABSTRACT: Background: Efavirenz (EFV) is widely used for the treatment of HIV, but there is some uncertainty regarding its relationship to suicidality. Here we examine the effect of initial treatment with an EFV-containing versus EFV-free regimen on the risk of suicidality. Methods: Data from four ACTG studies (A5095, A5142, A5175, A5202) of antiretroviral-nave participants enrolled from 2001-2007 were included. Participants in each trial were randomized to EFV-containing or EFV-free (protease inhibitor or 3-nucleoside) regimens; assignment to EFV was open label in 3 of the 4 trials. Suicidality was defined as suicidal ideation, attempted or completed suicide and was derived from signs, symptoms, diagnoses and death data. The primary analysis included follow-up from randomization through last study contact or data safety and monitoring board (DSMB) recommendations to stop an EFV-free arm for virologic inferiority (A5095 and A5175). As-treated analyses censored follow-up at the earlier of DSMB recommendations, EFV-strategy cross-over or treatment discontinuation plus 28 days. EFV versus EFV-free groups were compared with a cause-specific hazard ratio (HR) with a 95% confidence interval (CI) estimated from a Cox model stratified by study. Results: 5332 participants (EFV: 3241, EFV-free: 2091) had median follow-up of 150 weeks. A majority (74%) enrolled in the United States, 73% were men, median age was 37 years, and 32% had a pre-study psychiatric event or were taking psychoactive medication in the 30 days prior to entry. Baseline characteristics were balanced by randomization. Suicidality incidence per 1000 person-years was 8.08 (47 events) in the EFV group and 3.66 (15 events) in the EFV-free group, HR: 2.28 (95% CI: 1.27, 4.10, p=0.006), with no evidence of a differential effect by clinical trial (p>0.9). Incidence of attempted/completed suicide was 2.90 (17 events) and 1.22 (5 events) in the EFV and EFV-free groups, respectively, HR: 2.58 (95% CI: 0.94, 7.06, p=0.065). Conclusion: Initial treatment with an EFV-containing regimen was associated with a two-fold increase in the hazard of suicidality compared to a regimen without EFV. HIV-infected patients treated with EFV should be carefully monitored for suicide risk.
    IDWeek 2013 Meeting of the Infectious Diseases Society of America; 10/2013
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    ABSTRACT: To compare the effect that initiating different antiretroviral therapy (ART) regimens has on weight, BMI, and lean body mass (LBM) and explore how changes in body composition are associated with bone mineral density (BMD). A5224s was a sub-study of A5202, a prospective trial of 1857 ART-naive participants randomized to blinded abacavir-lamivudine (ABC/3TC) or tenofovir DF-emtricitabine (TDF/FTC) with open-label efavirenz (EFV) or atazanavir-ritonavir (ATV/r). All participants underwent dual-energy absorptiometry (DXA) and abdominal computed tomography for body composition. Analyses used two-sample t-tests and linear regression. A5224s included 269 participants: 85% men, 47% white non-Hispanic, median age 38 years, HIV-1 RNA 4.6 log10 copies/ml, and CD4 cell count 233 cells/μl. Overall, significant gains occurred in weight, BMI, and LBM at 96 weeks postrandomization (all P < 0.001). Assignment to ATV/r (vs. EFV) resulted in significantly greater weight (mean difference 3.35 kg) and BMI gain (0.88 kg/m; both P = 0.02), but not LBM (0.67 kg; P = 0.15), whereas ABC/3TC and TDF/FTC were not significantly different (P ≥ 0.10). In multivariable analysis, only lower baseline CD4 cell count and higher HIV-1 RNA were associated with greater increase in weight, BMI, or LBM. In multivariable analyses, increased LBM was associated with an increased hip BMD. ABC/3TC vs. TDF/FTC did not differ in change in weight, BMI, or LBM; ATV/r vs. EFV resulted in greater weight and BMI gain but not LBM. A positive association between increased LBM and increased hip BMD should be further investigated through prospective interventional studies to verify the impact of increased LBM on hip BMD.
    AIDS (London, England) 08/2013; 27(13):2069-79. · 4.91 Impact Factor

Publication Stats

6k Citations
979.20 Total Impact Points


  • 2005–2014
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      • Department of Medicine
      Torrance, California, United States
  • 1993–2014
    • University of California, Los Angeles
      • • Department of Epidemiology
      • • Department of Medicine
      Los Angeles, California, United States
  • 2013
    • University of Washington Seattle
      • Department of Global Health
      Seattle, Washington, United States
  • 2002–2013
    • University of California, San Diego
      • • Department of Medicine
      • • Department of Pathology
      San Diego, California, United States
  • 2012
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 2011
    • Indiana University-Purdue University Indianapolis
      Indianapolis, Indiana, United States
  • 2009–2011
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, MA, United States
    • University of Pittsburgh
      • Division of Infectious Diseases
      Pittsburgh, Pennsylvania, United States
  • 2005–2011
    • Harbor-UCLA Medical Center
      Torrance, California, United States
  • 2010
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
    • Alpert Medical School - Brown University
      Providence, Rhode Island, United States
  • 2004
    • The University of Edinburgh
      Edinburgh, Scotland, United Kingdom
  • 2001
    • University of California, Irvine
      • Division of Infectious Diseases
      Irvine, California, United States
  • 1989–2000
    • Cedars-Sinai Medical Center
      • • Division of Infectious Diseases
      • • Department of Medicine
      • • Cedars Sinai Medical Center
      Los Angeles, California, United States
  • 1996
    • University of Southern California
      • Department of Medicine
      Los Angeles, CA, United States