Increased Inflammasome and Caspase-1 Activation in Visceral adipose tissue from Metabolically Unhealthy Obese compared to Metabolically Healthy Obese subjects
Esser, Nathalie ; L'Homme, Laurent ; DE ROOVER, Arnaud et al
in Diabetes (2013, July), (62/suppl.1), 555Detailed reference viewed: 50 (13 ULg)
Dual-specificity phosphatase 3 knockout female mice are resistant to LPS and to polymicrobial induced septic shock in TNF dependent manner.
Rahmouni, Souad ; ; et al
in Journal of Immunology (2013, May)
We report the generation of dual-specificity phosphatase 3 (DUSP3) deficient mice. These mice develop normally and do not exhibit any spontaneous phenotype. However, VHR-/- females, but not males, are ... [more ▼]
We report the generation of dual-specificity phosphatase 3 (DUSP3) deficient mice. These mice develop normally and do not exhibit any spontaneous phenotype. However, VHR-/- females, but not males, are resistant to LPS- and to polymicrobial infection-induced septic shock. After LPS injection, while VHR-/- males and VHR+/+ mice of both genders, displayed an increased serum levels of TNF-α and IFN, the levels of these cytokines remained significantly low in the VHR-/- females. In vitro experiments using peritoneal macrophages showed the same results suggesting that the systemic cytokines profiles observed are macrophages-dependent. Adoptive transfer of VHR-/- females bone marrow to irradiated VHR+/+ female mice, but not to VHR-/- or VHR+/+ males, protected them from death after administration of LPS. Interestingly, VHR-/- females were sensitive to TNF-α- induced lethality. We also report that the decrease of TNF-α production observed in VHR-/- female’s macrophages after LPS activation was associated with a decreased ERK1/2, but not MEK1/2, activation. Interestingly, pervanadate (PTP pan inhibitor) treatment prior to LPS activation restored ERK1/2 activation in the VHR-deficient macrophages, suggesting that VHR is targeting one of the ERK1/2 PTPs or DUSPs. These results, together with our observation that DUSP3 is the most highly expressed phosphatase in macrophages, suggest a key non-redundant role of VHR as positive regulator of TNF-α in innate immune response in females. [less ▲]Detailed reference viewed: 11 (1 ULg)
Différences d’activité de l’inflammasome NLRP3 entre sujets obèses avec et sans anomalies métaboliques
Esser, Nathalie ; L'Homme, Laurent ; DE ROOVER, Arnaud et al
in Diabètes & Métabolism (2013, March), 39(suppl 1), 102Detailed reference viewed: 55 (16 ULg)
Differences in inflammasome activation between metabolically healthy and unhealthy obese individuals
Esser, Nathalie ; L'Homme, Laurent ; SCHEEN, André et al
Poster (2013, January)Detailed reference viewed: 33 (5 ULg)
Rôle de la vitamine D dans l'infection par le VIH: revue des connaissances actuelles
Pirotte, Benoît ; Rassenfosse, Marie ; Collin, Romain et al
in Revue Médicale de Liège (2013), 68(1), 25-31
La vitamine D possède des propriétés sur le métabolisme phosphocalcique mais aussi dans diverses pathologies telles que les maladies auto-immunes, les cancers, les maladies cardio-vasculaires, l’excès de ... [more ▼]
La vitamine D possède des propriétés sur le métabolisme phosphocalcique mais aussi dans diverses pathologies telles que les maladies auto-immunes, les cancers, les maladies cardio-vasculaires, l’excès de poids ou encore certaines infections. Nous nous intéressons ici aux relations frappantes qui existent entre la vitamine D et le VIH. Cette hormone joue assurément un rôle important dans l’infection par le VIH, tant au niveau squelettique qu’au niveau de l’évolution de la maladie elle-même. Nous remarquons en effet qu’un déficit en vitamine D est très souvent associé à l’infection par le VIH. De plus, un taux indétectable de cette hormone chez les patients séropositifs est associé à une infection cliniquement plus avancée et à une mortalité accrue. Ainsi, le déficit en vitamine D doit être considéré comme un cofacteur important de la progression de l’infection par le VIH. En effet, la vitamine D augmente l’activité des macrophages, entre autres via le processus d’autophagie, ce qui permet d’inhiber l’infection par le VIH-1. Nous parlerons ensuite de l’impact de certains traitements antirétroviraux sur l’altération du métabolisme de la vitamine D. Nous évaluerons enfin le bénéfice d’une supplémentation en vitamine D chez ces patients. [less ▲]Detailed reference viewed: 67 (9 ULg)
Perceptions de la pratique des essais cliniques sur le VIH/sida par les médecins prescripteurs des antirétroviraux agréés de Kinshasa (RD Congo)
; MOUTSCHEN, Michel
in Bulletin de la Société de Pathologie Exotique (2012)
Le but de cette étude, réalisée entre novembre 2005 et janvier 2006 auprès des prescripteurs d’antirétroviraux (ARV), était de cerner leurs perceptions sur les enjeux contextuels liés à la pratique des ... [more ▼]
Le but de cette étude, réalisée entre novembre 2005 et janvier 2006 auprès des prescripteurs d’antirétroviraux (ARV), était de cerner leurs perceptions sur les enjeux contextuels liés à la pratique des essais sur le VIH/sida à Kinshasa. Pour effectuer le repérage de ces enjeux, un ques- tionnaire a été élaboré et finalisé à la suite de la phase explo- ratoire de notre enquête afin d’apprécier les points de vue des médecins agréés par le Programme national de lutte contre le sida du Congo (PNLS) et qui jouent le premier rôle dans le contexte de leur pratique professionnelle. Sur 50 médecins sollicités pour participer à notre enquête, 35 ont retourné le questionnaire, dix n’étaient pas disponibles au moment de l’enquête et cinq n’ont pas retourné le questionnaire à l’adresse et dans le délai que nous avions indiqués. Les résul- tats obtenus témoignent de la nécessité de renforcer les capa- cités des acteurs locaux. Un des objectifs visés par la conduite locale de ces essais étant le transfert des connais- sances, il est nécessaire, au vu des résultats, d’affirmer le rôle pédagogique du comité d’éthique local. Cela devra permettre de relever le défi de la contextualisation et de réduire les tensions susceptibles de compromettre le bon déroulement des essais cliniques. [less ▲]Detailed reference viewed: 45 (8 ULg)
An improved protocol for efficient engraftment in NOD/LTSZ-SCIDIL-2Rgammanull mice allows HIV replication and development of anti-HIV immune responses.
; ; et al
in PLoS ONE (2012), 7(6), 38491
Cord blood hematopoietic progenitor cells (CB-HPCs) transplanted immunodeficient NOD/LtsZ-scidIL2Rgamma(null) (NSG) and NOD/SCID/IL2Rgamma(null) (NOG) mice need efficient human cell engraftment for long ... [more ▼]
Cord blood hematopoietic progenitor cells (CB-HPCs) transplanted immunodeficient NOD/LtsZ-scidIL2Rgamma(null) (NSG) and NOD/SCID/IL2Rgamma(null) (NOG) mice need efficient human cell engraftment for long-term HIV-1 replication studies. Total body irradiation (TBI) is a classical myeloablation regimen used to improve engraftment levels of human cells in these humanized mice. Some recent reports suggest the use of busulfan as a myeloablation regimen to transplant HPCs in neonatal and adult NSG mice. In the present study, we further ameliorated the busulfan myeloablation regimen with fresh CB-CD34+cell transplantation in 3-4 week old NSG mice. In this CB-CD34+transplanted NSG mice engraftment efficiency of human CD45+cell is over 90% in peripheral blood. Optimal engraftment promoted early and increased CD3+T cell levels, with better lymphoid tissue development and prolonged human cell chimerism over 300 days. These humanized NSG mice have shown long-lasting viremia after HIV-1JRCSF and HIV-1Bal inoculation through intravenous and rectal routes. We also saw a gradual decline of the CD4+T cell count, widespread immune activation, up-regulation of inflammation marker and microbial translocation after HIV-1 infection. Humanized NSG mice reconstituted according to our new protocol produced, moderate cellular and humoral immune responses to HIV-1 postinfection. We believe that NSG mice reconstituted according to our easy to use protocol will provide a better in vivo model for HIV-1 replication and anti-HIV-1 therapy trials. [less ▲]Detailed reference viewed: 76 (24 ULg)
Treatment-associated polymorphisms in protease are significantly associated with higher viral load and lower CD4 count in newly diagnosed drug-naive HIV-1 infected patients.
; ; et al
in Retrovirology (2012), 9
BACKGROUND: The effect of drug resistance transmission on disease progression in the newly infected patient is not well understood. Major drug resistance mutations severely impair viral fitness in a drug ... [more ▼]
BACKGROUND: The effect of drug resistance transmission on disease progression in the newly infected patient is not well understood. Major drug resistance mutations severely impair viral fitness in a drug free environment, and therefore are expected to revert quickly. Compensatory mutations, often already polymorphic in wild-type viruses, do not tend to revert after transmission. While compensatory mutations increase fitness during treatment, their presence may also modulate viral fitness and virulence in absence of therapy and major resistance mutations. We previously designed a modeling technique that quantifies genotypic footprints of in vivo treatment selective pressure, including both drug resistance mutations and polymorphic compensatory mutations, through the quantitative description of a fitness landscape from virus genetic sequences. RESULTS: Genotypic correlates of viral load and CD4 cell count were evaluated in subtype B sequences from recently diagnosed treatment-naive patients enrolled in the SPREAD programme. The association of surveillance drug resistance mutations, reported compensatory mutations and fitness estimated from drug selective pressure fitness landscapes with baseline viral load and CD4 cell count was evaluated using regression techniques. Protease genotypic variability estimated to increase fitness during treatment was associated with higher viral load and lower CD4 cell counts also in treatment-naive patients, which could primarily be attributed to well-known compensatory mutations at highly polymorphic positions. By contrast, treatment-related mutations in reverse transcriptase could not explain viral load or CD4 cell count variability. CONCLUSIONS: These results suggest that polymorphic compensatory mutations in protease, reported to be selected during treatment, may improve the replicative capacity of HIV-1 even in absence of drug selective pressure or major resistance mutations. The presence of this polymorphic variation may either reflect a history of drug selective pressure, i.e. transmission from a treated patient, or merely be a result of diversity in wild-type virus. Our findings suggest that transmitted drug resistance has the potential to contribute to faster disease progression in the newly infected host and to shape the HIV-1 epidemic at a population level. [less ▲]Detailed reference viewed: 6 (0 ULg)
Fidaxomicin versus vancomycin for Clostridium difficile infection: meta-analysis of pivotal randomized controlled trials.
; ; et al
in Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America (2012), 55 Suppl 2
Two recently completed phase 3 trials (003 and 004) showed fidaxomicin to be noninferior to vancomycin for curing Clostridium difficile infection (CDI) and superior for reducing CDI recurrences. In both ... [more ▼]
Two recently completed phase 3 trials (003 and 004) showed fidaxomicin to be noninferior to vancomycin for curing Clostridium difficile infection (CDI) and superior for reducing CDI recurrences. In both studies, adults with active CDI were randomized to receive blinded fidaxomicin 200 mg twice daily or vancomycin 125 mg 4 times a day for 10 days. Post hoc exploratory intent-to-treat (ITT) time-to-event analyses were undertaken on the combined study 003 and 004 data, using fixed-effects meta-analysis and Cox regression models. ITT analysis of the combined 003/004 data for 1164 patients showed that fidaxomicin reduced persistent diarrhea, recurrence, or death by 40% (95% confidence interval [CI], 26%-51%; P < .0001) compared with vancomycin through day 40. A 37% (95% CI, 2%-60%; P = .037) reduction in persistent diarrhea or death was evident through day 12 (heterogeneity P = .50 vs 13-40 days), driven by 7 (1.2%) fidaxomicin versus 17 (2.9%) vancomycin deaths at <12 days. Low albumin level, low eosinophil count, and CDI treatment preenrollment were risk factors for persistent diarrhea or death at 12 days, and CDI in the previous 3 months was a risk factor for recurrence (all P < .01). Fidaxomicin has the potential to substantially improve outcomes from CDI. [less ▲]Detailed reference viewed: 9 (0 ULg)
Deleterious mutations in LRBA are associated with a syndrome of immune deficiency and autoimmunity.
; ; et al
in American Journal of Human Genetics (2012), 90(6), 986-1001
Most autosomal genetic causes of childhood-onset hypogammaglobulinemia are currently not well understood. Most affected individuals are simplex cases, but both autosomal-dominant and autosomal-recessive ... [more ▼]
Most autosomal genetic causes of childhood-onset hypogammaglobulinemia are currently not well understood. Most affected individuals are simplex cases, but both autosomal-dominant and autosomal-recessive inheritance have been described. We performed genetic linkage analysis in consanguineous families affected by hypogammaglobulinemia. Four consanguineous families with childhood-onset humoral immune deficiency and features of autoimmunity shared genotype evidence for a linkage interval on chromosome 4q. Sequencing of positional candidate genes revealed that in each family, affected individuals had a distinct homozygous mutation in LRBA (lipopolysaccharide responsive beige-like anchor protein). All LRBA mutations segregated with the disease because homozygous individuals showed hypogammaglobulinemia and autoimmunity, whereas heterozygous individuals were healthy. These mutations were absent in healthy controls. Individuals with homozygous LRBA mutations had no LRBA, had disturbed B cell development, defective in vitro B cell activation, plasmablast formation, and immunoglobulin secretion, and had low proliferative responses. We conclude that mutations in LRBA cause an immune deficiency characterized by defects in B cell activation and autophagy and by susceptibility to apoptosis, all of which are associated with a clinical phenotype of hypogammaglobulinemia and autoimmunity. [less ▲]Detailed reference viewed: 98 (5 ULg)
A national cohort of HIV-infected patients in Belgium: design and main characteristics.
; ; et al
in Acta Clinica Belgica (2012), 67(5), 333-7
In Belgium, individual laboratory and treatment data of all HIV-infected patients seen in the 9 AIDS Reference Centres and 7 AIDS Reference Laboratories are collected prospectively since 2006. We present ... [more ▼]
In Belgium, individual laboratory and treatment data of all HIV-infected patients seen in the 9 AIDS Reference Centres and 7 AIDS Reference Laboratories are collected prospectively since 2006. We present here an analysis of patients recorded in the cohort database between 1st of January 2006 and 31st of December 2008. During that period, 11982 patients were under medical follow-up in Belgium. Sixty-one percent of the patients were male and the median age was 39.8 at the time of first recorded viral load. Among the patients whose nationality or probable mode of transmission was recorded, nearly half (48.0%) were Belgian and 38.3% originated from Sub-Saharan Africa; heterosexual contacts were reported in the majority of cases (56.0%) followed by homosexual contacts (35.3%). A total of 145 deaths were reported. Around three quarters of the patients were on ART. The median CD4 cell count rose from 470 cells/mm3 in 2006 to 501 cells/mm3 in 2008. This cohort enabled us to obtain comprehensive information on the numbers and characteristics of HIV-infected patients currently being followed up in Belgium, and on trends in antiretroviral therapy and biological results. This will serve for planning purposes, evaluation of access to care and as a source of information for further studies. [less ▲]Detailed reference viewed: 54 (21 ULg)
Gentetics, environment and determinants of autoimmune diseases
in Revue Médicale de Liège (2012), 67
We initiate this review article by a brief description of a few monogenic autoimmune diseases such as the APECED and the IPEX syndrome because they allow understand the fundamental mechanisms of self ... [more ▼]
We initiate this review article by a brief description of a few monogenic autoimmune diseases such as the APECED and the IPEX syndrome because they allow understand the fundamental mechanisms of self tolerance. Next we describe with more details the complex autoimmune diseases and discuss the recent data regarding the associated genetic and environmental factors and their modes of interaction. The conclusion of the article deals with the practical implications of this inherent complexity for the researcher and the clinician. [less ▲]Detailed reference viewed: 27 (5 ULg)
Humanized mice as a useful model to study HIV-1 induced immune activation, its mechanisms and potential therapeutic approaches
; ; VAIRA, Dolorès et al
in Retrovirology (2011, October 03), 8
Recent understanding of HIV-1 pathogenesis mechanism has changed our views about possible mechanisms of CD4T-cell depletion during infection. Apart from HIV-1-mediated killing a more comprehensive ... [more ▼]
Recent understanding of HIV-1 pathogenesis mechanism has changed our views about possible mechanisms of CD4T-cell depletion during infection. Apart from HIV-1-mediated killing a more comprehensive explanation has appeared that includes T cell exhaustion and chronic immune activation as a central feature in HIV-1 pathogenesis. While highly active antiretroviral therapy (HAART) markedly reduces viral load, T cell activation levels and soluble markers of inflammation remain abnormally high. Markers of chronic activation, such as CD38, PD-1 or HLA-DR on T cells, appear to be better predictors for clinical progression during HIV infection than HIV RNA levels and CD4Tcell counts alone. Therefore, a better understanding of HIV-índuced immune activation and the design of new immunomodulatory approches in combination with HAART are needed. We have generated an efficient model of human stem cells (HSCs) engraftment in NOD/LtsZ-scidlL-2Rnull (NSG) mice that supports chronic HIV infection with high plasma viral loads. HIV-1 infection in these humanized mice is characterized by widespread immune activation with increased expression of PD-1, HLA-DR, CD38, CD69, CD25 and other immune activation markers. These humanized mice provide an effective in vivo system for the assessing novel approaches for their potential in suppressing chronic immune activation during HIV-1 infection, in absence of interference of antiretroviral therapy. In this study, we evaluated in vivo the benefits of two novel approaches aimed at reducing HIV-induced immune activation. Minocycline is an antibiotic of the tetracycline family with anti-inflammatory and immunomodulatory properties affecting CD4 T cells activation by a mechanism involving the inhibition of the NF-AT1 transcription factor activity. We hypothesized that this antibiotic could suppress the HIV-1-induced chronic immune activation and thus, limit the HIV pathogenesis when combined to HAART. Therefore, we treated HIV-1 (JRCSF) infected-humanized NSG mice with minocycline (100mg/kg/day) for 60 days. We next evaluated the expression, by flow cytometry, of several T cells activation markers together with CD4+T cells counts. Our data suggest that minocycline is effective in suppressing HIV-1 induced immune activation in peripheral blood and lymphoid organs (spleen, lymph nodes and bone marrow). Levels of cellular immune activation markers such as PD-1, HLA-DR, CD38, CD69, CD25, CD28 and CTLA-4 were significantly lower in minocycline treated group. These immunological benefits of minocycline were correlated with higher CD4+T cell counts in the treated group. The immune activation which is associated with retroviral infection is also associated with increased levels of intracytoplasmic cyclic AMP which could act as a positive feedback loop in the infection since several reports have suggested that cAMP and downstream signaling pathways play an important role in the permissivity of susceptible cells to HIV infection and replication. We have used a peptide which prevents the binding of the catalytic subunit of PKA type I to its anchoring protein and therefore blocks most effects of cyclic AMP within lymphocytes and monocytes (RIAD peptide). Mice were treated with 3.5 mg/kg of RIAD peptide weekly. Treatment of humanized mice with RIAD peptide limited viral replication after high dose of HIV intraperitoneal challenge and reduced the intracytoplasmic levels of cyclic AMP. Further experiments are needed to better appreciate the therapeutic potential of these novel therapies in the suppression of HIV-induced chronic immune activation. [less ▲]Detailed reference viewed: 15 (1 ULg)
Mucosal junctions: open doors to HPV and HIV infections?
Herfs, Michael ; Hubert, Pascale ; Moutschen, Michel et al
in Trends in microbiology (2011), 19(3), 114-120
Throughout adult life, new developmental commitment of adult stem cells causes reversible epithelial replacements in various mucosal surfaces, including the uterine cervix and the anal canal. Located at ... [more ▼]
Throughout adult life, new developmental commitment of adult stem cells causes reversible epithelial replacements in various mucosal surfaces, including the uterine cervix and the anal canal. Located at the squamocolumnar junctions, these metaplastic conversions are associated with chronic inflammation and deregulated expression of soluble and cell-membrane factors important for antiviral immune response. In this paper, we propose that these histological and immunological features increase the susceptibility of these metaplastic microenvironments to human papillomavirus and human immunodeficiency virus infections. Identification of the anatomical sites and cell populations within the anogenital tract, which is the site primary infected by these viruses, is crucial for the understanding of the pathogenesis of viral disease and development of antiviral strategies. [less ▲]Detailed reference viewed: 32 (10 ULg)
A pauci-symptomatic case of documented Hantavirus (Puumala) infection in a patient under anti-TNF treatment.
; Bourhaba, Maryam ; FRIPPIAT, Frédéric et al
in Journal of Clinical Virology (2011), 50(3), 247-8
We describe the case of an 18-yr-old male under anti-TNF treatment for Crohn's disease for more than 8 months. He developed fever and biological inflammatory syndrome without absolutely no accompanying ... [more ▼]
We describe the case of an 18-yr-old male under anti-TNF treatment for Crohn's disease for more than 8 months. He developed fever and biological inflammatory syndrome without absolutely no accompanying sign or symptom or paraclinical abnormality despite extensive work-up performed in the context of his immunocompromised state. Symptoms disappeared after 10 days and a diagnosis of Puumala infection was made retrospectively on a serological basis. The case illustrates that anti-TNF treatment does not worsen the course of Puumala infection and could even be associated with a milder clinical picture. [less ▲]Detailed reference viewed: 50 (7 ULg)
Mice with Disrupted Type I Protein Kinase A Anchoring in T Cells Resist Retrovirus-Induced Immunodeficiency
; ; et al
in Journal of Immunology (2011), 186(9), 5119-30
Type I protein kinase A (PKA) is targeted to the TCR-proximal signaling machinery by the A-kinase anchoring protein ezrin and negatively regulates T cell immune function through activation of the C ... [more ▼]
Type I protein kinase A (PKA) is targeted to the TCR-proximal signaling machinery by the A-kinase anchoring protein ezrin and negatively regulates T cell immune function through activation of the C-terminal Src kinase. RI anchoring disruptor (RIAD) is a high-affinity competitor peptide that specifically displaces type I PKA from A-kinase anchoring proteins. In this study, we disrupted type I PKA anchoring in peripheral T cells by expressing a soluble ezrin fragment with RIAD inserted in place of the endogenous A-kinase binding domain under the lck distal promoter in mice. Peripheral T cells from mice expressing the RIAD fusion protein (RIAD-transgenic mice) displayed augmented basal and TCR-activated signaling, enhanced T cell responsiveness assessed as IL-2 secretion, and reduced sensitivity to PGE2- and cAMP-mediated inhibition of T cell function. Hyperactivation of the cAMP–type I PKA pathway is involved in the T cell dysfunction of HIV infection, as well as murine AIDS, a disease model induced by infection of C57BL/6 mice with LP-BM5, a mixture of attenuated murine leukemia viruses. LP-BM5–infected RIADtransgenic mice resist progression of murine AIDS and have improved viral control. This underscores the cAMP–type I PKA pathway in T cells as a putative target for therapeutic intervention in immunodeficiency diseases. [less ▲]Detailed reference viewed: 33 (6 ULg)
Syphilis treatment in the human immunodeficiency virus-infected patient: follow the guidelines.
FRIPPIAT, Frédéric ; Moutschen, Michel
in Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America (2011), 53(8), 845Detailed reference viewed: 31 (3 ULg)
Comparison of phenotypic and genotypic tropism determination in triple-class-experienced HIV patients eligible for maraviroc treatment.
; ; et al
in Journal of Antimicrobial Chemotherapy (2011), 66(2), 265-72
BACKGROUND: Determination of HIV-1 tropism is a pre-requisite to the use of CCR5 antagonists. This study evaluated the potential of population genotypic tropism tests (GTTs) in clinical practice, and the ... [more ▼]
BACKGROUND: Determination of HIV-1 tropism is a pre-requisite to the use of CCR5 antagonists. This study evaluated the potential of population genotypic tropism tests (GTTs) in clinical practice, and the correlation with phenotypic tropism tests (PTTs) in patients accessing routine HIV care. METHODS: Forty-nine consecutive plasma samples for which an original Trofile(TM) assay was performed were obtained from triple-class-experienced patients in need of a therapy change. Viral tropism was defined as the consensus of three or more tropism calls obtained from the combination of two independent population PTT assays (Trofile Biosciences, San Francisco, CA, USA, and Virco, Beerse, Belgium), population GTTs and GTTs based on ultra-deep sequencing. If no consensus was reached, a clonal PTT was performed in order to finalize the tropism call. This two-step approach allowed the definition of a reference tropism call. RESULTS: According to the reference tropism result, 35/49 samples were CCR5 tropic (R5) (patients eligible for maraviroc treatment) and 14/49 were assigned as non-R5 tropic. The non-R5 samples [patients not eligible for maraviroc treatment according to the FDA/European Medicines Agency (EMEA) label] group included both the CXCR4 (X4) samples and the dual and mixed CCR5/CXCR4 (R5/X4) samples. Compared with Trofile(TM) population PTTs, population GTTs showed a higher sensitivity (97%) and a higher negative predictive value (91%), but almost equal specificity and an equal positive predictive value. CONCLUSIONS: In line with recent reports from clinical trial data, our data support the use of population genotypic tropism testing as a tool for tropism determination before the start of maraviroc. [less ▲]Detailed reference viewed: 45 (6 ULg)