Jonathan B Angel

University of Ottawa, Ottawa, Ontario, Canada

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Publications (171)783.03 Total impact

  • JAIDS Journal of Acquired Immune Deficiency Syndromes 06/2015; DOI:10.1097/QAI.0000000000000734 · 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
  • Sandra Côté · Julie Matte · Subash Sad · Jonathan B Angel · Angela M Crawley
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    ABSTRACT: Many soluble cytokine receptors inhibit cytokine bioactivity, while others prolong ligand activity. The biological role of an endogenous soluble form of IL-7Rα, or its therapeutic effects on CD8(+) T-cells are unknown. We demonstrate that recombinant IL-7Rα-Fc, when pre-incubated with IL-7, enhances IL-7-induced CD8(+) T-cell proliferation and viability of human or murine CD8(+) T-cells. Receptor blocking experiments confirmed IL-7-specific activity. These data demonstrate that exogenous soluble IL-7Rα significantly enhances CD8(+) T-cell responses to IL-7 in vitro and paves the way for future research to determine its therapeutic potential to restore impaired CD8(+) T-cell function in disease. Copyright © 2015 Elsevier Inc. All rights reserved.
    Cellular Immunology 01/2015; 293(2):122-125. DOI:10.1016/j.cellimm.2015.01.001 · 1.87 Impact Factor
  • Aurelia Busca · Mansi Saxena · Salma Iqbal · Jonathan Angel · Ashok Kumar
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    ABSTRACT: Resistance to apoptosis is an important characteristic that human macrophages acquire during differentiation from monocytes. However, the intracellular mechanisms that mediate the development of resistance are not well understood. We have used M-CSF-stimulated primary human monocytes and PMA-treated THP1 cells to study apoptosis resistance during differentiation of human macrophages. Our results indicate that PI3K/Akt distinctively regulates survival of macrophages during and after differentiation. More specifically, a signaling pathway consisting of PI3K/Akt-NF-κB-Bcl-xL regulates cell survival during the differentiation process. PI3K/Akt-mediated activation of NF-κB plays a key role in survival of differentiating macrophages by specifically sustaining antiapoptotic Bcl-xL expression. With the use of pharmacological inhibitors and siRNA for Akt and Bcl-xL, we show that in the absence of Akt-dependent Bcl-xL expression during differentiation, cells undergo caspase-mediated apoptosis. In contrast, in differentiated macrophages, Bcl-xL expression is independent of PI3K/Akt activation. Taken together, these results suggest that survival of macrophages is distinctly regulated during and after differentiation. Our results also suggest new, potential therapeutic targets to modulate differentiation and survival of this cell type.
    Journal of Leukocyte Biology 09/2014; 96(6). DOI:10.1189/jlb.1A0414-212R · 4.30 Impact Factor
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    ABSTRACT: Objectives Chloroquine (CQ), an anti-inflammatory drug, inhibits Toll-like receptor (TLR) signalling in plasmacytoid dendritic cells (pDCs) and may be beneficial for HIV-infected patients in whom immune activation persists despite effective antiretroviral therapy (ART). The effect of CQ on CD4 T-cell recovery and immune activation in immune nonresponding patients receiving successful ART was therefore studied.Methods Nineteen adults on ART with CD4 counts ≤350 cells/μL and undetectable viral load (VL) orally received CQ at 250 mg/day for 24 weeks. Side effects, CD4 and CD8 T-cell counts, VL, T-cell activation, pDC proportion and plasma inflammatory markers were assessed at baseline, at 24 weeks, and at 12 weeks after CQ discontinuation (clinicaltrial.org registration #NCT02004314).ResultsCQ was well tolerated and all patients maintained an undetectable VL. The absolute CD4 and CD8 T-cell counts and their percentages, the pDC proportion, T-cell activation, D-dimer and C-reactive protein (CRP) plasma levels and the kynurenine/tryptophan ratio did not change with CQ treatment. Among nine cytokines/chemokines measured, only levels of interferon (IFN)-α2 were significantly increased by CQ treatment.ConclusionsCQ was well tolerated in patients with low CD4 T-cell counts despite long-term effective ART; however, 24 weeks of CQ treatment did not improved CD4 T-cell recovery, lymphoid and myeloid immune activation or inflammatory markers.
    HIV Medicine 06/2014; 16(1). DOI:10.1111/hiv.12171 · 3.45 Impact Factor
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    ABSTRACT: Motherhood is personally, culturally, and historically rooted. Recent publications have focused on medical issues related to pregnancy and HIV, with attention on fetal well-being. There is limited literature on the importance of motherhood for HIV-positive women. Our study's purpose was to investigate the importance of motherhood among HIV-positive women of reproductive age in Ontario, Canada and to analyze the correlates thereof. We present our findings using a secondary analysis of cross-sectionally collected data from a study assessing fertility desires and intentions of HIV-positive women. The sub-analysis's outcome of interest was based on the question: "Being a mother is important to me" with a 5-point Likert scale that was dichotomized into strongly agree/agree vs. neutral/disagree/strongly disagree. Logistic regression models were fit to calculate unadjusted and adjusted odds ratios (ORs) for significant correlates. Of the 497 respondents, median age was 38 (interquartile range [IQR] 32-43), 46% were African, 74% had given birth, and 57% intended to give birth. A total of 452 (91%) agreed (N = 75) or strongly agreed (N = 377) that being a mother was important to them. Age less than 40 years (OR 3.0; 95% confidence interval [CI] 1.6-5.7, African ethnicity (OR 9.2; 95% CI 3.2-26.3), immigration within 10 years (OR 19.6, 95% CI 4.6-83.1), and partner or family desire for a pregnancy (OR 3.3; 95% CI 1.5-7.3) were significant correlates of the importance of motherhood in a univariate analysis. Importance of motherhood was associated with desire (OR 6.2, 95% CI 3.1-12.3) and intention to give birth (OR 6.9, 95% CI 3.1-15.2), and previous birth (OR 8.5, 95% CI 4.2-16.8). In the multivariable model, the significant correlates were of age less than 40 years (OR 3.9; 95% CI 1.8-8.4), immigration within 10 years (OR 14.1; 95% CI 3.2-61.5), and having previously given birth (OR 11.2; 95% CI 5.1-24.4). The majority of women felt strongly that motherhood was important to them particularly among younger women, recent immigrants, and women who were mothers.
    AIDS Care 11/2013; 26(6). DOI:10.1080/09540121.2013.855295 · 1.60 Impact Factor
  • Conference on AIDS Vaccine; 11/2013
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    ABSTRACT: HIV transmitted drug resistance (TDR) surveillance is usually conducted by sampling from a large population. However, overall TDR prevalence results may be inaccurate for many individual clinical setting. We analyzed HIV genotypes at a tertiary care setting in Ottawa, Ontario in order to evaluate local TDR patterns among sub-populations. Genotyping reports were digitized from ART naive patients followed at the Immunodeficiency Clinic at the Ottawa Hospital, between 2008 and 2010. Quality controlled, digitized sequence data were assessed for TDR using the Stanford HIV Database. Patient characteristics were analyzed according to TDR patterns. Finally, a phylogenetic tree was constructed to elucidate the observed pattern of HIV TDR. Among the 155 clinic patients there was no statistically significantly difference in demographics as compared to the Ontario provincial HIV population. The clinic prevalence of TDR was 12.3%; however, in contrast to the data from Ontario, TDR patterns were inverted with a 21% prevalence among MSM and 5.5% among IDU. Furthermore, nearly 80% of the observed TDR was a D67N/K219Q pattern with 87% of these infections arising from a distinct phylogenetic cluster. Local patterns of TDR were distinct to what had been observed provincially. Phylogenetic analysis uncovered a cluster of related infections among MSM that appeared more likely to be recent infections. Results support a paradigm of routine local TDR surveillance to identify the sub-populations under care. Furthermore, the routine application of phylogenetic analysis in the TDR surveillance context provides insights into how best to target prevention strategies; and how to correctly measure outcomes.
    BMC Infectious Diseases 10/2013; 13(1):509. DOI:10.1186/1471-2334-13-509 · 2.61 Impact Factor
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    ABSTRACT: IL-7 plays an important role in T cell survival, function, and memory cell development, yet the role of cytokine signaling pathways in these processes has not been fully elucidated. Moreover, the underlying mechanisms for the observed impairment of IL-7 activity in diseases, such as HIV infection, breast cancer, and autoimmunity, are not well understood. It was therefore hypothesized that IL-7-induced signaling molecules could be linked with distinct IL-7-associated activities. To address this, the activation and functional associations of IL-7-induced signaling pathways, specifically antigen-independent activities that are relevant to T cell homeostasis, were examined. Low concentrations of IL-7 (100 pg/ml) are capable of activating the Jak-STAT and PI3K signaling pathways, whereas higher concentrations (500-1000 pg/ml) were required to induce Bcl-2 production and glucose uptake. Even higher concentrations of IL-7 (10,000 pg/ml) were needed to induce cell proliferation and intracellular accumulation of perforin. Inhibition of Jak activation reduced IL-7-induced Bcl-2 and perforin production, whereas inhibition of Jak/STAT or PI3K pathways reduced glucose uptake and proliferation. This study suggests a complex control of IL-7-associated activities in the absence of antigen stimulation. These data may provide insights into mechanisms of impaired IL-7 signaling and function in disease and could be relevant for the study of IL-7-based immunotherapeutics. Specifically, this study has linked STAT5 and PI3K activation to shared and distinct IL-7-associated activities in human CD8(+) T cells.
    Journal of leukocyte biology 09/2013; 95(1). DOI:10.1189/jlb.0313122 · 4.99 Impact Factor
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    ABSTRACT: Objectives: We determined the proportion and correlates of self-reported pregnancy planning discussions (that is preconception counseling) that HIV-positive women reported to their family physicians (FPs), HIV specialists, and obstetrician/gynecologists (OB/Gyns).
    09/2013; 13(5):424-433. DOI:10.1177/2325957413494238
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    ABSTRACT: IL-27, a member of the IL-12 cytokine family, is a key immunoregulatory cytokine produced predominantly by monocytic cells and mediates innate and adaptive immune responses. IL-27 has been shown to be produced by human monocytic cells primed with IFN-γ and in response to a second stimulus such as LPS. In this study, we show for the first time that IFN-γ alone without any second stimulus can induce IL-27p28 gene expression and IL-27 protein production by human monocytic cells. The signaling pathways that govern IL-27 production in general, and particularly following stimulation of monocytic cells with IFN-γ are not known. We investigated the signaling pathways governing the regulation of IL-27 protein and its subunit IL-27p28 following stimulation with IFN-γ in primary human monocytic cells. Our results suggest that IFN-γ-mediated IL-27 protein but not IL-27p28 gene expression is positively regulated by the C-Jun N-terminal kinases (JNK), mitogen-activated protein kinases (MAPKs) and the phosphoinositide 3-kinase (PI3K), independent of the Janus kinase (Jak)/signal transducers and activators of transcription (STAT) signaling in primary human monocytes.
    Immunobiology 06/2013; 219(1). DOI:10.1016/j.imbio.2013.06.001 · 3.18 Impact Factor
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    ABSTRACT: BACKGROUND: Although some studies show higher antiretroviral concentrations in women compared to men, data are limited. We conducted a cross-sectional study of HIV-positive women to determine if protease inhibitor (PI) and non-nucleoside reverse transcriptase inhibitor (NNRTI) Cmin and Cmax values were significantly different than historical general population (predominantly male) averages and to evaluate correlates of higher concentrations. METHODS: HIV-positive women with virologic suppression (viral load < 50copies/mL) on their first antiretroviral regimen were enrolled. Timed blood samples for Cmin and Cmax were drawn weekly for 3 weeks. The ratio of each individual's median Cmin and Cmax to the published population mean values for their PI or NNRTI was calculated and assessed using Wilcoxon sign-rank. Intra- and inter-patient variability of antiretroviral drug levels was assessed using coefficient of variation and intra-class correlation. Linear regression was used to identify correlates of the square root-transformed Cmin and Cmax ratios. RESULTS: Data from 82 women were analyzed. Their median age was 41 years (IQR=36-48) and duration of antiretrovirals was 20 months (IQR=9-45). Median antiretroviral Cmin and Cmax ratios were 1.21 (IQR=0.72-1.89, p=0.003) (highest ratios for nevirapine and lopinavir) and 0.82 (IQR=0.59-1.14, p=0.004), respectively. Nevirapine and efavirenz showed the least and unboosted atazanavir showed the most intra- and inter-patient variability. Higher CD4+ count correlated with higher Cmin. No significant correlates for Cmax were found. CONCLUSIONS: Compared to historical control data, Cmin in the women enrolled was significantly higher whereas Cmax was significantly lower. Antiretroviral Cmin ratios were highly variable within and between participants. There were no clinically relevant correlates of drug concentrations.Trial registration: http://clinicaltrials.gov/show/NCT00433979.
    BMC Infectious Diseases 06/2013; 13(1):256. DOI:10.1186/1471-2334-13-256 · 2.61 Impact Factor
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    ABSTRACT: Interferon (IFN)-γ is a potent stimulator of the IL-12 family Th1 cytokines, including IL-12/23p40 and IL-23, responsible for coordinating the innate and adaptive immune responses. Our results show that IFN-γ induced the production of IL-12/23p40 and IL-23p19 mRNA as well as IL-12p40 and IL-23 proteins in primary human monocytes isolated by positive selection through anti-CD14 microbeads. These results were confirmed by IFN-γ stimulation of CD14-activated monocytes resulting in IL-12/23p40 and IL-23 production. We investigated the signaling pathways governing the regulation of IL-23 and its subunits IL-23p40 and IL-23p19 following IFN-γ stimulation. We observed a differential regulation of IL-23p19, IL-12/23p40, and IL-23 following IFN-γ stimulation. IFN-γ-induced IL-23 and IL-12/23p40 expression was positively regulated by the p38 mitogen-activated protein kinases (MAPKs), independent of the Janus kinase (Jak)/signal transducers and activators of transcription (STAT) signaling. In contrast, IL-12 and IL-23 were negatively regulated by the Jak/STAT, phosphatidylinositol 3-kinase (PI3K), and the c-Jun-N-terminal kinase (JNK) MAPKs in IFN-γ-stimulated monocytes. Overall, our results suggest for the first time a differential positive regulation of IL-12p40 and IL-23 by p38 MAPKs independent of the Jak/STAT pathways and negative regulation by the Jak/STAT, JNK, and PI3K pathways in CD14-activated primary human monocytes stimulated with IFN-γ.
    Journal of interferon & cytokine research: the official journal of the International Society for Interferon and Cytokine Research 05/2013; DOI:10.1089/jir.2012.0058 · 3.90 Impact Factor
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    ABSTRACT: Human Immunodeficiency Virus (HIV)-infected individuals have a cardiovascular disease risk that is almost thrice than that of their HIV-uninfected counterparts. Given the critical role of endothelial progenitor cells (EPCs) in vascular homeostasis and arterial repair postinjury, coupled with their strength as biomarkers predictive of cardiovascular events, interest has arisen in characterizing EPCs in the context of HIV infection. We conducted a systematic review of the literature to determine the current state of knowledge on EPCs in the context of HIV infection. Herein, we summarize the pertinent findings of these studies and discuss important differences in the subpopulations of EPCs examined and the methodologies used for their enumeration which likely contributed to the heterogeneity observed across studies.
    Trends in cardiovascular medicine 02/2013; 23(6). DOI:10.1016/j.tcm.2012.12.002 · 2.07 Impact Factor
  • AIDS PATIENT CARE and STDs 11/2012; 26(11):645-646. DOI:10.1089/apc.2012.0190 · 3.58 Impact Factor
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    ABSTRACT: Background: HIV reservoirs represent the major obstacles for eradication and are defined as a cell type that allows persistence of replication-competent HIV in patients on optimal long-term antiretroviral therapy (HAART). Several pilot clinical trials have been implemented to assess the value of experimental therapy to reduce reservoir size or eradicate HIV. In order to eradicate HIV, valproic acid was used as a new strategy to increase viral gene expression in the nucleus of infected cells with the expectation of generating a direct cell death or destruction by nearby cytotoxic cells. Previous pilot studies using VPA have showed conflicting results on the ability of VPA to reduce the size of HIV reservoirs. Purpose: As the role of VPA on HIV reservoirs remains unclear, we conducted a multicenter clinical trial with a specific study design to obtain optimal information on reservoir changes while exposing the smallest number of individuals to the experimental medication. Method: To this aim, a randomized, crossover design with 2 different treatment durations was implemented. By doubling the therapeutic period in one study arm, we were in a position to assess the impact of an extended duration of VPA on the size of the HIV reservoir and to evaluate the duration of treatment effects upon VPA withdrawal in the other arm. However, limitations for this type of study design included the logistical complexity of 2 uneven study arms and longer study duration. Conclusion: Despite the absence of demonstrable impact of VPA on reservoir size, such crossover study design should be considered in the early stage testing of novel HIV therapeutics targeted to reduce reservoir size or eradicate HIV.
    HIV Clinical Trials 11/2012; 13(6):301-307. DOI:10.1310/hct1306-301 · 2.14 Impact Factor
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    P Fairman · J B Angel
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    ABSTRACT: Dendritic cells (DC) are mediators of the adaptive immune response responsible for antigen presentation to naive T cells in secondary lymph organs. Human immunodeficiency virus (HIV-1) has been reported to inhibit the maturation of DC, but a clear link between maturation and function has not been elucidated. To understand further the effects of HIV-1 on DC maturation and function, we expanded upon previous investigations and assessed the effects of HIV-1 infection on the expression of surface molecules, carbohydrate endocytosis, antigen presentation and lipopolysaccharide (LPS) responsiveness over the course of maturation. In vitro infection with HIV-1 resulted in an increase in the expression of DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) as well as decreases in maturation-induced CCR7 and major histocompatibility complex (MHC)-II expression. Retention of endocytosis that normally occurs with DC maturation as well as inhibition of antigen presentation to CD8(+) T cells was also observed. Mitogen-activated protein kinase (MAPK) responsiveness to LPS as measured by phosphorylation of p38, c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK)1/2 was not affected by HIV-1 infection. In summary, in-vitro HIV-1 impairs DC maturation, as defined by cell surface protein expression, with selective alterations in mature DC function. Understanding the mechanisms of DC dysfunction in HIV infection will provide further insight into HIV immune pathogenesis.
    Clinical & Experimental Immunology 10/2012; 170(1):101-13. DOI:10.1111/j.1365-2249.2012.04628.x · 3.28 Impact Factor
  • C T Costiniuk · J B Angel
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    ABSTRACT: While only partial immune reconstitution in gut-associated lymphoid tissue typically occurs following initiation of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV) infection, near-complete immune reconstitution has occasionally been described. This review highlights findings from studies examining the effects of HAART and the timing of its initiation on gastrointestinal (GI) CD4+ T-cell recovery. Its effects on specific CD4+ T-cell subtypes, CD8+ T cells, natural killer cells, and immunoglobulins are also described. Finally, the ability of HAART to restore the intestinal epithelial barrier and lymphatic tissue architecture and reduce microbial translocation is addressed. Determining whether HAART has the ability to prevent permanent GI immune damage when commenced in acute HIV infection has implications for the optimal timing of HAART initiation.
    Mucosal Immunology 08/2012; 5(6):596-604. DOI:10.1038/mi.2012.82 · 7.54 Impact Factor
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    The Journal of Infectious Diseases 08/2012; 206(9):1480-1. DOI:10.1093/infdis/jis519 · 5.78 Impact Factor
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    ABSTRACT: Abstract Although there is discordance between human immunodeficiency virus (HIV) blood plasma and seminal plasma viral loads (VL), little is known about the dynamics of VL rebound in these compartments upon discontinuation of highly active antiretroviral therapy (HAART). Therefore, we sought to examine the relationship between blood and semen VL rebound after discontinuation of HAART. Participants in this substudy were men enrolled from two centers of a multicenter, placebo-controlled randomized trial of HIV therapeutic vaccination using ALVAC with or without Remune. With at least 2 years of sustained virologic suppression and following a 20-week vaccination course, subjects underwent structured HAART interruption. Fourteen men provided semen samples. Seven to 12 weeks after HAART interruption, all 14 men had detectable blood VLs whereas 8 of 14 had detectable seminal VLs. There was a significant correlation between blood and seminal VLs (Spearman r=0.58, p=0.03) at the time of semen collection. An earlier time to detectable blood VL after HAART interruption was associated with higher seminal VL (Spearman r=-0.64, p=0.02). These findings support the compartmentalization of HIV and underscore the importance of understanding the genital tract as an HIV reservoir in the quest to minimize HIV transmission.
    AIDS research and human retroviruses 08/2012; 29(2). DOI:10.1089/AID.2011.0343 · 2.46 Impact Factor

Publication Stats

3k Citations
783.03 Total Impact Points

Institutions

  • 1998–2015
    • University of Ottawa
      • • Department of Biochemistry, Microbiology and Immunology
      • • Division of Infectious Diseases
      Ottawa, Ontario, Canada
  • 2002–2014
    • Ottawa Hospital Research Institute
      Ottawa, Ontario, Canada
    • University of Toronto
      • Department of Medicine
      Toronto, Ontario, Canada
  • 2013
    • Children's Hospital of Eastern Ontario
      Ottawa, Ontario, Canada
  • 1997–2013
    • The Ottawa Hospital
      • Department of Medicine
      Ottawa, Ontario, Canada
  • 1988–2009
    • University Hospital Vall d'Hebron
      • Department of Cardiology
      Barcino, Catalonia, Spain
  • 2008
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States
  • 2006
    • Carleton University
      Ottawa, Ontario, Canada
  • 2005
    • Vall d’Hebron Institute of Oncology
      Barcino, Catalonia, Spain
  • 1998–1999
    • New England Baptist Hospital
      Boston, Massachusetts, United States
  • 1995
    • Tufts University
      • Department of Medicine
      Бостон, Georgia, United States