Gilles Duverlie

Université de Picardie Jules Verne, Amiens, Picardie, France

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Publications (102)484.75 Total impact

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    ABSTRACT: The pre-therapeutic presence of protease inhibitor (PI) resistance-associated variants (RAVs) has not been shown to be predictive of triple-therapy outcome in treatment-naïve patients. However, they may influence the outcome in patients with less effective Pegylated Interferon (IFN)-ribavirin (RBV) backbones. Using HCV population sequence analysis, we retrospectively investigated the prevalence of baseline NS3 RAVs in a multicenter cohort of poor IFN-RBV responders (i.e. prior null-responders or patients with a viral load decrease of <1 logUI/ml during the pegIFN/RBV lead-in phase). The impact of the presence of these RAVs on triple-therapy outcome was studied. Among 282 patients, the prevalence of baseline RAVs ranged from 5.7% [3.3%-9.0%] to 22.0% [17.3%-27.3%] according to the algorithm used. Among mutations conferring a >3-fold shift in IC50 for telaprevir or boceprevir, T54S was the most frequently detected mutation (3.9%), followed by A156T, R155K (0.7%), V36M and V55A (0.35%). Mutations were more frequently found in patients infected with genotype 1a (7.5-23.6%) than 1b (3.3-19.8%) (p=0.03). No other socio-demographic or viro-clinical characteristic was significantly associated with a higher prevalence of RAVs. No obvious effect of baseline RAVs was observed on viral load. In this cohort of poor responders to IFN-RBV, no link was found with the sustained virological response to triple-therapy, whatever the algorithm used for the detection of mutations. Based on cross-study comparison, baseline RAVs are not more frequent in poor IFN-RBV responders than in treatment-naïve patients and, even in these difficult-to-treat patients, this study demonstrates no impact on treatment outcome, arguing against resistance analysis prior to treatment. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Journal of clinical microbiology 04/2015; DOI:10.1128/JCM.03633-14 · 4.23 Impact Factor
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    ABSTRACT: Hepatitis C virus (HCV) chronic infection is a major cause of hepatocellular carcinoma. Sorafenib is the only medical treatment that has been approved for the treatment of this cancer. It is a multikinase inhibitor with anti-tumor activity against a wide variety of cancers. Sorafenib blocks angiogenesis and tumor cell proliferation through inhibition of kinases, such as VEGFR2, PDGFR, or the serine/threonine kinases RAF. Previous studies have reported an anti-HCV effect of sorafenib in vitro, but various mechanisms of action have been described. The aim of this study was to clarify the action of sorafenib on the complete HCV infectious cycle. In order to examine the action of sorafenib on all steps of the HCV infectious cycle, we used a combination of validated cell culture models, based on the HuH-7 reference cell line and primary human hepatocytes. We found that sorafenib blocks HCV infection by altering the viral entry step and the production of viral particles. Moreover, we observed that treatment with sorafenib lead to a modification of Claudin-1 expression and localization, which could partly be responsible for the anti-HCV effect. Collectively, our findings confirm the anti-HCV effect of sorafenib in vitro, while highlighting the complexity of the action of sorafenib on the HCV infectious cycle. Copyright © 2015. Published by Elsevier B.V.
    Antiviral research 03/2015; 24. DOI:10.1016/j.antiviral.2015.03.012 · 3.43 Impact Factor
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    ABSTRACT: It is generally accepted that thyroid follicle cells are at least semi-permissive for erythrovirus B19 (EVB19). Thus, various laboratory techniques have been successfully used to detect EVB19 in the thyroid gland, including polymerase chain reaction (PCR), immunohistochemistry, and in situ hybridization. However, the detection of EVB19 within the thyroid gland is problematic, and none of the detection protocols in the literature have been unequivocally validated. This multidisciplinary study in which 32 thyroidectomy subjects undergoing thyroidectomy in a French University hospital were prospectively recruited was performed over a period of 3 years. Prior to surgery, all the subjects were assayed for blood levels of anti-EVB19 antibodies and (using a quantitative PCR [qPCR] assay) EVB19 itself. A qPCR assay for EVB19 and an immunohistochemical assay (based on polyclonal anti-VP2 antibodies) were performed on the thyroidectomy samples. None of the subjects had an acute EVB19 infection. A viral load was detected in two serum samples and six thyroid biopsies. Three subjects had both a positive immunohistochemical assay and a positive qPCR assay for the thyroid tissue. It is noteworthy that the thyroid immunohistochemical and qPCR assays were negative in the two patients with detectable serum loads of EVB19. In conclusion, EVB19 can be detected in thyroid follicle cells by using immunohistochemical and qPCR assays. Ideally, patients should be tested with both PCR and immunohistochemical assays, in order to unequivocally confirm or rule out the presence of EVB19 in the thyroid gland. The present protocol must now be validated in larger series - notably with respect to its reliability and in order to determine qPCR positivity thresholds for application in future large-scale studies. J. Med. Virol. 00: 1-6, 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Journal of Medical Virology 03/2015; 87(6). DOI:10.1002/jmv.24147 · 2.22 Impact Factor
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    ABSTRACT: Multilayered blood safety programs reduce the risk of transfusion-transmitted diseases; however, there remains a risk of window period transmission of screened viruses and transmission of unscreened and emerging viruses from asymptomatic donors. To reduce this risk, a riboflavin-and-UV-light-based pathogen reduction process was evaluated against eight viral agents. Riboflavin and UV light was evaluated against the following eight viral agents: encephalomyocarditis virus (EMC), hepatitis A virus (HAV), hepatitis C virus (HCV), influenza A (FLUAV), La Crosse virus (LACV), pseudorabies virus (PRV), sindbis virus (SINV), and vesicular stomatitis virus (VSV). Before treatment, a sample was removed to determine the product's initial viral load. After treatment the product's viral load was reevaluated and the log reduction was calculated. Virus reduction after treatment with riboflavin and UV light is equivalent in platelet (PLT) and plasma units, as demonstrated by a 3.2-log reduction of EMC in plasma, PLTs, and PLT additive solution containing 35% plasma. Additionally, the following viral reductions values were observed: HAV 1.8 log, HCV at least 4.1 log, FLUAV at least 5.0 log, LACV at least 3.5 log, PRV 2.5 log, SINV 3.2 log, and VSV at least 6.3 log. The results observed in this study suggest that treating PLT and plasma products with a riboflavin-and-UV-light-based pathogen reduction process could potentially eliminate window period transmission of screened viruses and greatly reduce the risk of transfusion transmission of unscreened viruses. © 2015 AABB.
    Transfusion 03/2015; DOI:10.1111/trf.13030 · 3.57 Impact Factor
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    IRBM 02/2015; DOI:10.1016/j.irbm.2015.01.010 · 0.38 Impact Factor
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    ABSTRACT: Erythrovirus B19 (EVB19) has been incriminated, over recent years, in the onset and/or pathogenesis of many diseases, especially autoimmune thyroid diseases. This review of the literature (published over the last 40 years using Pubmed and Science Direct search engines) was designed to define the role of EVB19, particularly in autoimmune thyroid diseases.Two cases of subacute thyroiditis, one case of Graves' disease (associated with type 1 diabetes and rheumatoid arthritis), and one case of Hashimoto's thyroiditis following acute EVB19 infection were reported. A retrospective case–control study in a pediatric population demonstrated the role of EVB19 in Hashimoto's thyroiditis. Four retrospective studies of pathology slides (including PCR, immunohistochemistry or in situ hybridization) and a prospective case–control study on pathology slides demonstrated the presence of EVB19 in thyroid tissue of patients with benign multinodular goiter, Graves' disease, autoimmune thyroiditis (including Hashimoto's thyroiditis), and thyroid cancer. EVB19 can be demonstrated in the thyroid gland in a wide range of diseases. Although acute EVB19 infection could theoretically trigger autoimmune thyroid disease, there is currently no evidence that EVB19 plays a specific role in the pathophysiology of autoimmune thyroid diseases. J. Med. Virol. © 2014 Wiley Periodicals, Inc.
    Journal of Medical Virology 01/2015; 87(1). DOI:10.1002/jmv.23963 · 2.22 Impact Factor
  • Etienne Brochot, Sandra Bodeau, Gilles Duverlie
    Therapeutic Drug Monitoring 12/2014; DOI:10.1097/FTD.0000000000000161 · 1.93 Impact Factor
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    ABSTRACT: Anemia is a well-known RBV-related event in HCV therapy which is exacerbated by the addition of telaprevir and boceprevir. This retrospective study evaluated and compared ribavirin exposure and parameters able to influence hemoglobin decrease in a large population of patients treated with dual or triple therapy. Patients on triple therapy had higher ribavirin concentrations at week 12 of treatment (3460 ng/mL vs 1843 ng/mL; p< 0.0001). An association was also observed between week 12 eGFR and ribavirin concentration only for patients on triple therapy (p= 0.002).The proportion of patients with a > 20 ml/min/1.73m2 decrease in eGFR at week 12 was higher among patients on triple therapy: 32%, 14% and 5% for boceprevir, telaprevir and dual therapy, respectively (p= 0.025 and 0.026). No correlation was observed between boceprevir and telaprevir concentrations and hemoglobin or eGFR decrease. Exacerbation of anemia in patients on triple therapy is related to higher ribavirin concentrations. We provide an explanation for this increase in plasma RBV concentration. Triple therapy with PEG-IFN, RBV and telaprevir or boceprevir will remain the only HCV treatment option for many patients. Our data show that the RBV dose can be decreased while maintaining adequate plasma concentrations and reducing anemia. This article is protected by copyright. All rights reserved
    The Journal of Clinical Pharmacology 12/2014; 55(5). DOI:10.1002/jcph.454 · 2.47 Impact Factor
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    ABSTRACT: Objective. Sofosbuvir and simeprevir in combination with standard therapy are now available for the treatment of patients chronically infected with hepatitis C virus (HCV) genotype 1. With boceprevir and telaprevir, four treatment options are, therefore, now available to clinicians. Phase 3 studies conducted with simeprevir and sofosbuvir compared sustained virological response (SVR) data with those obtained with standard combination therapy and did not include a control arm. It is important to quantify the contribution of these molecules compared to the first direct antiviral agents available. Material and methods. For HCV genotype 1 patients, we performed a literature review and compared all SVR data from phase 3 randomized placebo-controlled trials conducted with these four molecules according to virological characteristics (genotype, viral load) and patient characteristics (IL28B polymorphism, stage of fibrosis). Results. Simeprevir and sofosbuvir provide a net gain in terms of SVR compared to boceprevir and telaprevir except in the case of telaprevir for treatment-naïve HCV genotype 1b patients. Sofosbuvir achieves higher SVR rates than simeprevir except for treatment-naïve IL28B CC patients and naïve HCV genotype 1b patient. Further, simeprevir moderately improve SVR rates compared to telaprevir in treatment-naïve patients with F3–F4 fibrosis and with HCV genotype 1a infection. Conclusion. Sofosbuvir and simeprevir greatly improve the virological response rate compared to first-generation protease inhibitors. All of these data may help in guiding the physician’s treatment decisions, based on financial constraints and patient characteristics. These data can be easily updated with future treatment and demonstrate the contribution of new treatment regimens to achieve optimal SVR rates.
    Scandinavian Journal of Gastroenterology 11/2014; DOI:10.3109/00365521.2014.978364 · 2.33 Impact Factor
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    ABSTRACT: Core plays a critical role during HCV assembly, not only as a structural component of the virion, but also as a regulator of the formation of assembly sites. In this study, we observed that core is expressed later than other HCV proteins in a single viral cycle assay, resulting in a relative increase of core expression during a late step of the viral life cycle. This delayed core expression results from an increase of core half-life, indicating that core is initially degraded and is stabilized at a late step of the HCV life cycle. A stabilization-mediated delayed kinetics of core expression was also observed using heterologous expression systems. Core stabilization did not depend on its interaction with non-structural proteins or lipid droplets but was correlated to its expression levels and its oligomerization status. Therefore in the course of a HCV infection, core stabilization likely occurs when the prior amplification of the viral genome during an initial replication step allows core to be synthesized at higher levels as a stable protein during the assembly step of the viral life cycle.
    Journal of General Virology 10/2014; DOI:10.1099/vir.0.070433-0 · 3.53 Impact Factor
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    ABSTRACT: Cell microencapsulation in alginate hydrogel has shown interesting applications in regenerative medicine and the biomedical field through implantation of encapsulated tissue or for bioartificial organ development. Although alginate solution is known to have low antiviral activity, the same property regarding alginate gel has not yet been studied. The aim of this work is to investigate the potential protective effect of alginate encapsulation against hepatitis C virus (HCV) infection for a hepatic cell line (HuH-7) normally permissive to the virus. Our results showed that alginate hydrogel protects HuH-7 cells against HCV when the supernatant was loaded with HCV. In addition, alginate hydrogel blocked HCV particle release out of the beads when the HuH-7 cells were previously infected and encapsulated. There was evidence of interaction between the molecules of alginate hydrogel and HCV, which was dose- and incubation time-dependent. The protective efficiency of alginate hydrogel towards HCV infection was confirmed against a variety of viruses, whether or not they were enveloped. This promising interaction between an alginate matrix and viruses, whose chemical mechanisms are discussed, is of great interest for further medical therapeutic applications based on tissue engineering.
    PLoS ONE 10/2014; 9(10):e109969. DOI:10.1371/journal.pone.0109969 · 3.53 Impact Factor
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    ABSTRACT: http://www.sciencedirect.com/science/article/pii/S1878786X14701561 Le taux d’échec de la culture d’hépatocytes primaires humains (HPH) par absence d’adhésion cellulaire après dissociation reste encore élevé. Ceci pourrait s’expliquer par le contexte pathologique (foie d’hépatopathie chronique) et thérapeutique (embolisation portale, chimiothérapie d’induction, radiofréquence) du donneur, altérant la qualité du parenchyme et favorisant la survenue de complications postopératoires. Entre décembre 2011 et mars 2014, nous avons étudié pour 51 patients, la relation entre l’adhésion (plating) des cellules isolées à partir des pièces d’hépatectomies à J1 et les suites postopératoires. Nos résultats montrents qu'il existe une corrélation entre l’échec de la culture d’HPH (absence de plating) et la survenue de complications majeures Clavien III à V (OR = 4,9 IC95 % [0,045–0,88] p = 0,024). Ces complications (27 %) sont dominées par la fistule biliaire (18 %), l’insuffisance hépatocellulaire (6 %) et le décès (4 %). Il n’y a pas de corrélation entre le plating et la chimiothérapie d’induction, la stéatose ou la fibrose hépatique (p = 0,98 ; p = 0,4 et p = 0,19). Une viabilité cellulaire ≥ 50 % après dissociation à J0 semble être un facteur de bon pronostic de plating (p = 0,08). Cette donnée permettrait au chirurgien de disposer d’un nouveau moyen d’appréhender le foie non tumoral et de prédire les suites postopératoires dès J1. Ces résultats préliminaires devront être confirmés sur une cohorte plus importante de patients.
    116e Congrès Françaisde Chirurgie, Paris; 10/2014
  • Virginie Morel, Gilles Duverlie, Etienne Brochot
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    ABSTRACT: Background Simeprevir (Olysio®), a second-wave protease inhibitor recently approved for the treatment of chronic hepatitis C, is not indicated in patients with genotype 1a strain harboring the Q80K protease mutation. Phase 2 and 3 studies on this molecule mainly focused on North American patients and the prevalence of Q80K is particularly high in the USA (around 50%). The prevalence of this mutation in other parts of the world is currently unknown. Objectives The purpose of our study was to perform a detection of this mutation in a single PCR technique and to study the prevalence of this Q80K mutation in a non-U.S. population. We can thus estimate the proportion of HCV positive patients who can be treated with simeprevir. Study design We conducted a meta-analysis of response rates in the presence or absence of this mutation in randomized trials and then describe a simple and reliable method to detect this mutation. We also examined bilirubin levels in our cohort of 95 HCV genotype 1a patients. Results Ten patients (10.5%) had a Q80K mutation and 12 patients exhibited bilirubin levels above the upper limit of normal at baseline. In our cohort, 21 patients (22%) were therefore ineligible for treatment with simeprevir. The prevalence of this mutation seems to be much lower in European patients. Conclusion In conclusion, before considering treatment with simeprevir, physicians must be able to screen for the Q80K mutation.
    Journal of Clinical Virology 09/2014; 61(1). DOI:10.1016/j.jcv.2014.06.023 · 3.47 Impact Factor
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    ABSTRACT: Simeprevir (TMC435, Olysio™), a second-generation hepatitis C virus (HCV) protease inhibitor, has been recently approved for the treatment of genotype 1 chronic hepatitis C in combination with pegylated interferon and ribavirin. This molecule has very different characteristics from first-generation protease inhibitors. Results from trials show that simeprevir is highly effective and safe, with few adverse events. We discuss the specific features of this new treatment option for HCV infection, in terms of in vitro data, pharmacological data, and clinical trials. We also discuss the impact of Q80K polymorphism at baseline. Studies evaluating interferon-free regimens with simeprevir are ongoing. Future combinations of two or more direct-acting antiviral agents, targeting different viral enzymes and with synergistic antiviral effects, will be approved, allowing treatment of pan-genotypic HCV with optimized sustained virologic responses. Simeprevir will undoubtedly be part of future treatment strategies.
    Pharmacogenomics and Personalized Medicine 08/2014; 7:241-9. DOI:10.2147/PGPM.S52715
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    ABSTRACT: In spite of the high variability of its sequence, Hepatitis C virus (HCV) envelope glycoprotein E2 contains several conserved regions. In this study, we explored the structural and functional features of the highly conserved E2 aa502-520 segment that had been proposed as a fusion peptide and that has been shown to strongly overlap with a potential conserved neutralizing epitope. For this purpose, we used reverse genetics to introduce point mutations within this region, and we characterized the phenotype of these mutants in the light of the recently published structure of E2. The functional analyses showed that their phenotype is in agreement with the position of the corresponding residues in E2 crystal structure. In contrast, our data ruled out the involvement of this region in membrane fusion and they indicate that alternative conformations would be necessary to expose the potential neutralizing epitope present in this segment. Of particular interest, we identified three specific mutations (Y507L, V514A and V515A) located within this neutralizing epitope, which only mildly reduced infectivity and showed no assembly defect. These mutations modulated HCV dependence on the viral receptor SRB1 and/or they also modulated virion sensitivity to neutralizing antibodies. Importantly, their characterization also showed that amino acids Y507, V514 and V515 contribute to E2 interaction with HCV receptor CD81. In conclusion, our data show that the highly conserved E2 aa502-520 segment plays a key role in cell entry by influencing the association of the viral particle with co-receptors and neutralizing antibodies.
    Journal of Virology 07/2014; 88(18). DOI:10.1128/JVI.01402-14 · 4.65 Impact Factor
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    ABSTRACT: To the Editor: Kamar et al. (March 20 issue)(1) describe the successful use of ribavirin for the treatment of chronic hepatitis E virus (HEV) infection in 59 immunosuppressed recipients of solid-organ transplants. One wonders whether the results depended on the type of immunosuppressive therapy that the patients were receiving. The use of immunosuppressive medications has been proposed as a key factor in the development of chronic HEV infection among organ transplant recipients.(2),(3) Clinical evidence, however, suggests that various immunosuppressive regimens may differentially affect the infection course of HEV.(2),(3) The authors of a recent study(2) suggested that glucocorticoids did . . .
    New England Journal of Medicine 06/2014; 370(25):2446-2448. DOI:10.1056/NEJMc1405191#SA2 · 54.42 Impact Factor
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    Journal of Hepatology 01/2014; DOI:10.1016/j.jhep.2013.11.036 · 10.40 Impact Factor
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    ABSTRACT: Serine is encoded by two divergent codon types, UCN and AGY, which are not interchangeable by a single nucleotide substitution. Switching between codon types therefore occurs via intermediates (threonine or cysteine) or via simultaneous tandem substitutions. Hepatitis C Virus (HCV) chronically infects 2-3% of the global population. The highly variable glycoproteins E1 and E2 decorate the surface of the viral envelope, facilitate cellular entry and are targets for host immunity. Comparative sequence analysis of globally sampled E1E2 genes, coupled with phylogenetic analysis, reveals the signatures of multiple archaic codon switching events at seven highly conserved serine residues. Limited detection of intermediate phenotypes indicates associated fitness costs restrict their fixation in divergent HCV lineages. Mutational pathways underlying codon switching were probed via reverse genetics, assessing glycoprotein functionality using multiple in vitro systems. These data demonstrate selection against intermediate phenotypes can act at the structural/functional level, with some intermediates displaying impaired virion assembly and/or decreased capacity for target cell entry. These effects act in residue/isolate-specific manner. Selection against intermediates is also provided by humoral targeting, with some intermediates exhibiting increased epitope exposure and enhanced neutralization sensitivity, despite maintaining capacity for target cell entry. Thus, purifying selection against intermediates limits their frequencies in globally sampled strains, with divergent functional constraints at the protein level restricting the fixation of deleterious mutations. Overall our study provides an experimental framework for identification of barriers limiting viral substitutional evolution, and indicates serine codon-switching represents a genomic 'fossil record' of historical purifying selection against E1E2 intermediate phenotypes.
    Journal of Virology 10/2013; 88(1). DOI:10.1128/JVI.01745-13 · 4.65 Impact Factor
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    ABSTRACT: Background/Case Studies: A number of pathogens (viruses, bacteria, and parasites) can be transmitted through blood or blood products. Hepatitis C virus (HCV) is now mandatorily tested on blood donors worldwide due to the potential serious chronic clinical sequelae (fibrosis and hepatic-carcinoma) associated with its transmission. Despite testing, there remains a window period during which infectious units may test negative. Pathogen reduction technologies could offer a new strategy for dealing with window period viruses. In this study the efficacy of the Mirasol® PRT System for Platelets treated in PAS on the reduction of HCV was evaluated. Study Design/Methods: The virus used in this study is the JFH1 strain of HCV and it was produced in the Huh-7 cell culture model. This study used platelet depleted plasma (PDD) from five different donors in place of platelet units; previous work has shown PDD to yield comparable viral reduction results to treatment performed with platelets. Due to the difficulty of obtaining large quantities of virus, all treatments were performed using a 250 μL volume in a 48-well plate. Each 48-well plate was treated with a scaled dose that was verified to be equivalent to the standard Mirasol PRT process. Additionally, bag material cut from a Mirasol PRT Illumination/Storage bag was placed on top of the 48-well plate during illumination so the that light was properly attenuated, thus mimicking the standard Mirasol PRT process. Each of the five donors was split into three treated units and one untreated unit. After treatment, the infectivity of treated and non-treated samples was measured by immunofluorescence 48hours after inoculation of Huh-7 cells with the samples using a monoclonal antibody directed against the glycoprotein E2 of HCV. Infectious titers before and after treatment were determined by counting the number of foci. Results/Findings: All three treated replicates for each of the five different donors contained no detectable foci and were at the limit of detection for the assay. The average pre-treatment titer for the five donor samples was 4.2 log FFU (foci forming units)/mL and the limit of detection for the assay was ≤ 0.1 log FFU/mL. The calculated reduction observed in this study was ≥ 4.1 log. Conclusion: The Mirasol PRT System for Platelets effectively reduced the infectivity of HCV to the limits of detection using an in vitro cell model. The ≥ 4.1 log reduction observed in this study could potentially eliminate window period transmission of HCV. Log Reduction Replicate #1 4,2 Replicate #2 4,1 Replicate #3 4,0 Replicate #4 4,2 Replicate #5 4,1 Replicate #6 4,0 Average Log reduction 4,1
    AABB Annual Meeting October 12-15, 2013, Denver, CO,; 10/2013
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    ABSTRACT: Chronic infection by hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. At present, the most commonly used in vitro model of HCV infection is based on hepatoma cell lines. However, they were obtained from different patients and different cancers and/or differ in their characteristics and permissiveness to HCV. HCV infection can be modulated by several host factors, so we compared six different hepatoma cell lines that are used as in vitro models for HCV for some of these host factors: the seven known HCV entry factors, the six best-characterized HCV-associated microRNAs, and the two single-nucleotide polymorphisms near the IL28B gene associated with response to pegylated alpha interferon and ribavirin combination therapy, all assessed by quantitative PCR. We showed that the cell lines, including Huh-7 and Huh-7-derived cells, have different microRNA and HCV entry factor expression profiles as well as different IL28B genotypes. In conclusion, some of the observed differences might explain the differences in permissiveness of the cell lines, but, above all, they raise questions about the reliability of in vitro HCV research data gathered to date.
    Archives of Virology 10/2013; 159(3). DOI:10.1007/s00705-013-1862-9 · 2.28 Impact Factor

Publication Stats

2k Citations
484.75 Total Impact Points

Institutions

  • 2007–2015
    • Université de Picardie Jules Verne
      • LG - Laboratoire des glucides
      Amiens, Picardie, France
    • University of Birmingham
      • Institute for Biomedical Research
      Birmingham, England, United Kingdom
    • Institut National de la Transfusion Sanguine, Paris
      Lutetia Parisorum, Île-de-France, France
  • 2011
    • Université Libre de Bruxelles
      • Faculty of Medicine
      Bruxelles, Brussels Capital, Belgium
  • 2005–2011
    • Centre Hospitalier Universitaire d'Amiens
      • Laboratoire de Virologie
      Amiens, Picardie, France
    • Centre Hospitalier Universitaire de Tours
      Tours, Centre, France
  • 2003–2011
    • Institut Pasteur de Lille
      Lille, Nord-Pas-de-Calais, France
  • 2010
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 2002–2007
    • Institut de Biologie de Lille
      Lille, Nord-Pas-de-Calais, France
  • 2006
    • Centre Hospitalier Universitaire de Limoges
      Limages, Limousin, France
  • 1998–2004
    • Institut Universitaire de France
      Lutetia Parisorum, Île-de-France, France
  • 2001
    • CUNY Graduate Center
      New York, New York, United States
  • 2000
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 1997
    • University of Angers
      Angers, Pays de la Loire, France