Eric S Daar

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

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Publications (183)1098.02 Total impact

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    ABSTRACT: Sexually transmitted infections (STI) are common among HIV-infected men who have sex with men (MSM). While behavioral factors are important in STI acquisition, other biological factors such as immune modulation due to chronic viral infection may further predispose to STI acquisition. Post Hoc analysis including data collected over 12 months of follow-up from 131 HIV-infected MSM receiving antiretroviral therapy and screened for incident bacterial STI every 3 months. Genital secretions collected at baseline were used to measure herpesvirus replication and inflammatory cytokines. Baseline predictors of STI were determined using survival analysis of time to incident STI. All participants were seropositive for cytomegalovirus (CMV), and 52% had detectable genital CMV at baseline. Thirty-five individuals acquired STI during follow-up, sometimes with multiple pathogen (17 syphilis, 21 gonorrhea, 14 chlamydia). Syphilis acquisition was associated with genital CMV replication at baseline (19.1% CMV-shedders versus 4.8% non-shedders, p=0.03) and younger age (p=0.02). Lower seminal MCP-1 was associated with higher seminal CMV levels and with syphilis acquisition (p<0.01). For syphilis acquisition, in multivariable Cox-Proportional Hazard model adjusted hazard rates were 3.56 (95%CI:1.00-12.73) for baseline CMV replication and 2.50 (0.92-6.77) for younger age. This post hoc analysis suggest that CMV-associated decrease in seminal MCP-1 levels might predispose HIV-infected MSM to syphilis acquisition, but not other STI. Future studies should determine underlying mechanisms and if a causal association exists.
    PLoS ONE 06/2015; 10(6):e0130410. DOI:10.1371/journal.pone.0130410 · 3.53 Impact Factor
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    ABSTRACT: Among patients with HIV infection, changes in the kidney filtration marker cystatin C after initiation of antiretroviral therapy (ART) may be related to changes in body composition or biomarkers of inflammation. ACTG A5224s was a substudy of A5202, which randomly assigned ART-naive HIV-infected subjects to blinded abacavir/lamivudine (ABC/3TC) or tenofovir/emtricitabine (TDF/FTC) with open-label efavirenz (EFV) or ritonavir-boosted atazanavir. This analysis explored changes in cystatin C from 0 to 96 weeks. Of the 269 subjects, 85% were male and 66% white non-Hispanics; baseline mean CD4 count was 236 cells per cubic millimeter and cystatin C was 0.89 mg/L. Cystatin C decreased significantly within each arm; however, ritonavir-boosted atazanavir attenuated the beneficial effects of ART on cystatin C compared to EFV. Compared to ABC/3TC, TDF/FTC led to a marginally significant attenuation for percent change analyses only. Higher baseline body mass index and HIV RNA were associated with larger reductions in cystatin C in multivariable models. At baseline, cystatin C was positively correlated with high-sensitivity C-reactive protein (Spearman r = 0.25), interleukin 6 (r = 0.34), soluble intercellular adhesion molecule (r = 0.36), soluble vascular cell adhesion molecule (r = 0.54), tumor necrosis factor α (r = 0.57), and soluble TNF-α receptor I (r = 0.70, all P < 0.001). Reductions in cystatin C from 0 to 96 weeks correlated with reductions in all inflammatory biomarkers (r = 0.39-0.58, P < 0.001) except for high-sensitivity C-reactive protein (r = 0.01, P = 0.89) and IL-6 (r = 0.08, P = 0.24). The beneficial effect of ART on cystatin C concentrations is attenuated by boosted ATV when compared to EFV. Reductions in cystatin C after ART are associated with reductions in systemic inflammation.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 06/2015; 69(2). DOI:10.1097/QAI.0000000000000557 · 4.39 Impact Factor
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    ABSTRACT: Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with ≥3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR ≤ 60 ml/min/1.73 m2. Poisson regression was used to develop a risk score, externally validated on two independent cohorts. In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1:393 chance of developing CKD in the next 5 y in the low risk group (risk score < 0, 33 events), rising to 1:47 and 1:6 in the medium (risk score 0-4, 103 events) and high risk groups (risk score ≥ 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.
    PLoS Medicine 03/2015; 12(3):e1001809. DOI:10.1371/journal.pmed.1001809 · 14.00 Impact Factor
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    ABSTRACT: Many hepatitis C virus regimens are unlikely to be compared head to head. In more difficult to treat populations where there is no standard of care, trials are single arm. We describe a flexible meta-analysis platform in this setting. Our meta-analysis is literature based. We illustrate our methodology and show how inference can be extended to single-arm trials. As an example, in the single arm setting, a regimen with response rates of 84, 72 and 54% in genotype 1a across treatment naive, previous partial responders and previous null responders, respectively, would have 95% probability of superiority to IFN-α + RBV + TPV. This is a rigorous approach to comparative effectiveness that accounts for varying patient populations and plans for the incorporation of emerging treatments.
    03/2015; 4(2):101-114. DOI:10.2217/cer.14.69
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    ABSTRACT: Substance using HIV patients are at risk for non-adherence, and most prior interventions in this population have had only modest effects on adherence. Contingency management (CM) is a promising intervention. The Centralized Off-site Adherence Enhancement (CARE) program involved 12 telephone-delivered substance and adherence-targeted cognitive behavior therapy sessions coupled with CM for adherence to antiretroviral therapy (ART) and counseling participation. CM involved 6 weeks of escalating reinforcement for taking prescribed doses followed by 6 weeks of tapering variable rate reinforcement, and separate reinforcement for counseling ($806 possible). Participants’ adherence was measured by devices which wirelessly provided real-time notification of device-opening. HIV infected patients on ART (N = 10) with recent stimulant or alcohol use completed 10.2 of 12 possible telephone sessions, spent 42.8 min/call, and rated the counseling 6.2 on a 1–7 scale. Medication adherence improved from 81 to 93 % (p = 0.04). CARE appears to be acceptable and engaging.
    AIDS and Behavior 02/2015; DOI:10.1007/s10461-014-0990-x · 3.49 Impact Factor
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    ABSTRACT: HIV-associated brain injury persists despite antiretroviral therapy (cART), but contributing factors remain poorly understood. We postulated that inflammation-associated biomarkers will be associated with cerebral injury on proton magnetic resonance spectroscopy (MRS) in chronically HIV-infected subjects. Five biomarkers were measured in 197 HIV-infected subjects: soluble CD14, MCP-1, IP-10, MIP-1β, and fractalkine. Levels of N-acetyl aspartate (NAA), Choline (Cho), Myoinositol (MI), Glutamate+Glutamine (Glx), and Creatine (Cr) were acquired in the midfrontal cortex (MFC), frontal white matter (FWM), and basal ganglia (BG). Predictive models were built via linear regression and the best models were chosen using the Akaike Information Criterion. Increases in plasma or CSF MCP-1 were associated with lower NAA/Cr in the MFC and BG while metabolite changes in the FWM for NAA/Cr, GlxCr and Cho/Cr were explained almost exclusively by a single factor, sCD14. Plasma and CSF levels of this factor were also significantly associated with Glx/Cr in MFC and BG. Higher CSF FKN was associated with higher NAA/Cr in BG. Best predictors for higher Cho/Cr in BG and MFC were CSF sCD14 and CSF MIP-1β. Plasma and CSF IP-10 were only associated with Cho/Cr in MFC. Of the three models that simultaneously accounted for both plasma and CSF, there were more associations between CSF biomarkers and MRS metabolites. Markers of inflammation and immune activation, in particular MCP-1 and sCD14, predominantly reflecting CNS sources, contribute to the persistence of brain injury in a metabolite and region dependent manner in chronically HIV-infected patients on stable cART.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 01/2015; 69(1). DOI:10.1097/QAI.0000000000000532 · 4.39 Impact Factor
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    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. DOI:10.1016/j.annepidem.2014.09.012 · 2.15 Impact Factor
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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; 25(2). DOI:10.1097/FPC.0000000000000106 · 3.45 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 09/2014; 28(3). DOI:10.1016/j.idc.2014.06.005 · 2.31 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.
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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; · 5.44 Impact Factor
  • Annals of internal medicine 08/2014; 161(4):308-308. · 16.10 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. DOI:10.7326/M14-0293 · 16.10 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; 88(17). DOI:10.1128/JVI.01334-14 · 4.65 Impact Factor
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    ABSTRACT: It is challenge to model medication taking behavior and eventually to predict the change of be-havior, especially for those vulnerable patients (e.g. substance abusers). With the help of modern technology (e.g. Wisepill device), we are able to monitor the medication taking behavior in real time. In the meanwhile, after a few minutes delay of detecting the events and analyzing the events, a real time intervention can be generated to communicate with patients directly by the packages of Python, such as text messages to the mobile phone of the patients. The statistical methods that can be used to model the complexity of the medication taking events and to predict the future missed dosage are important for designing the personalized module of the device and therefore personalized intervention. This intervention not only will improve the medication adherence, but the personal-ized intervention will help to build up the correct medication behavior in the future. In this talk, we use Non-Homogeneous Poisson Process (NHPP) to model the sequence of medication taking during the day. The six hour window (3 hours before and after the dose schedule time) is considered as valid medication taking event. The daily real time medication events were monitored for more than 16 week by Wisepill device. We will model the extreme event of medication taking (outside the designed medication event window). Eventually, we use the model to predict the non-adherence events (missing medication event of the day). Therefore a customized intervention for adherence of medication could be performed on patients in the real-time.
    Joint Research Conference 2014, Seattle, WA; 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; DOI:10.1089/AID.2014.0097 · 2.46 Impact Factor
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    ABSTRACT: Background. Virologic failure (VF) on a first-line ritonavir-boosted protease inhibitor (PI/r) regimen is associated with low rates of resistance, but optimal management after failure is unknown. Methods. The analysis included participants in randomized trials who experienced VF on a first-line regimen of PI/r plus 2 nucleoside reverse transcriptase inhibitors (NRTIs) and had at least 24 weeks of follow-up after VF. Antiretroviral management and virologic suppression (human immunodeficiency virus type 1 [HIV-1] RNA <400 copies/mL) after VF were assessed. Results. Of 209 participants, only 1 participant had major PI-associated treatment-emergent mutations at first-line VF. The most common treatment approach after VF (66%) was to continue the same regimen. The virologic suppression rate 24 weeks after VF was 64% for these participants, compared with 72% for those who changed regimens (P = .19). Participants remaining on the same regimen had lower NRTI resistance rates (11% vs 30%; P = .003) and higher CD4(+) cell counts (median, 275 vs 213 cells/mu L; P = .005) at VF than those who changed. Among participants remaining on their first-line regimen, factors at or before VF significantly associated with subsequent virologic suppression were achieving HIV-1 RNA <400 copies/mL before VF (odds ratio [OR], 3.39 [95% confidence interval {CI}, 1.32-8.73]) and lower HIV-1 RNA at VF (OR for <10 000 vs >= 10 000 copies/mL, 3.35 [95% CI, 1.40-8.01]). Better adherence after VF was also associated with subsequent suppression (OR for <100% vs 100%, 0.38 [95% CI, .15-.97]). For participants who changed regimens, achieving HIV-1 RNA <400 copies/mL before VF also predicted subsequent suppression. Conclusions. For participants failing first-line PI/r with no or limited drug resistance, remaining on the same regimen is a reasonable approach. Improving adherence is important to subsequent treatment success.
    Clinical Infectious Diseases 05/2014; 59(6). DOI:10.1093/cid/ciu367 · 9.42 Impact Factor
  • Value in Health 05/2014; 17(3):A2. DOI:10.1016/j.jval.2014.03.011 · 2.89 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; 88(14). DOI:10.1128/JVI.00831-14 · 4.65 Impact Factor
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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; 88(14). DOI:10.1128/JVI.00482-14 · 4.65 Impact Factor

Publication Stats

8k Citations
1,098.02 Total Impact Points

Institutions

  • 2002–2015
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      • Department of Medicine
      Torrance, California, United States
  • 1991–2015
    • University of California, Los Angeles
      • • Department of Medicine
      • • Division of Infectious Diseases
      Los Ángeles, California, United States
  • 2014
    • George Washington University
      Washington, Washington, D.C., United States
  • 2005–2014
    • Harbor-UCLA Medical Center
      Torrance, California, United States
    • The Chinese University of Hong Kong
      Hong Kong, Hong Kong
  • 2002–2013
    • University of California, San Diego
      • Department of Medicine
      San Diego, California, United States
  • 2011
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2010
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
  • 2009
    • University of Pittsburgh
      • Division of Infectious Diseases
      Pittsburgh, Pennsylvania, United States
  • 2006–2007
    • San Diego State University
      • Department of Psychology
      San Diego, California, United States
  • 2004
    • The University of Edinburgh
      Edinburgh, Scotland, United Kingdom
  • 2001
    • Cornell University
      Итак, New York, United States
  • 1989–2000
    • Cedars-Sinai Medical Center
      • • Division of Infectious Diseases
      • • Department of Medicine
      • • Cedars Sinai Medical Center
      Los Angeles, California, United States