Gilles Duverlie

Université de Picardie Jules Verne, Amiens, Picardie, France

Are you Gilles Duverlie?

Claim your profile

Publications (103)442.64 Total impact

  • [Show abstract] [Hide abstract]
    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;
  • [Show abstract] [Hide abstract]
    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; · 3.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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;
  • [Show abstract] [Hide abstract]
    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. · 54.42 Impact Factor
  • [Show abstract] [Hide abstract]
    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 04/2014; · 2.37 Impact Factor
  • Source
    Journal of Hepatology 01/2014; · 9.86 Impact Factor
  • Virginie Morel, Gilles Duverlie, Etienne Brochot
    [Show abstract] [Hide abstract]
    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. 01/2014;
  • Source
    [Show abstract] [Hide abstract]
    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 01/2014; 7:241-9.
  • Source
    [Show abstract] [Hide abstract]
    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 01/2014; 9(10):e109969. · 3.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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; · 5.08 Impact Factor
  • [Show abstract] [Hide abstract]
    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; · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The optimization of combination therapy with ribavirin (RBV) and pegylated interferon alpha has substantially improved sustained virologic response (SVR) rates and lowered virologic relapse rates in patients infected with hepatitis C virus (HCV). In this study, we performed an analysis of the relationship between the end-of-treatment plasma RBV concentration and virologic relapse. Thirty-four patients with HCV treated with pegylated interferon/RBV and with an end-of-treatment response were assayed for plasma RBV concentration using liquid chromatography assay coupled to tandem mass-spectrometric detection on the last day of the treatment. Clinical data and the concentration of RBV were compared between patients classified as either relapsers or nonrelapsers. Eleven patients (32.4%) relapsed and 23 patients (67.6%) achieved an SVR. The mean plasma RBV concentration on the last day of treatment was 1380 ± 312 ng/mL for relapsers and 2278 ± 569 ng/mL for SVR patients (P < 0.0001). A receiver operating characteristic analysis showed that a threshold of 1960 ng/mL was associated with the greatest sensitivity and specificity (100% and 83%, respectively, with an area under the curve of 0.94; P < 0.0001) for discriminating between patients who relapsed and those who did not. A univariate logistic regression analysis indicated that a plasma RBV concentration of <1960 ng/mL at the end of the treatment was strongly associated with relapse (odds ratio, 55; 95% confidence interval, 7.24-∞; P = 0.0001) independently of age, body weight, RBV dose, baseline viral load, the interleukin-28B genotype, and response to previous courses of treatment. Our study results highlight the relevance of measuring plasma RBV concentrations during and at the end of HCV treatment, with a view to avoiding virologic relapse.
    Therapeutic drug monitoring 08/2013; · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Environmental factors, such as viruses, are thought to contribute to the development of thyroid autoimmunity. Erythrovirus B19 (EVB19) is suspected to be involved in Hashimoto's thyroiditis, but no direct evidence is available concerning the role of EVB19 infection in Graves' disease. The objective of this study was to investigate whether the presence of EVB19 is more frequent in thyroidectomy specimens of patients undergoing thyroidectomy for Graves' disease (cases) than for multinodular thyroid (controls). Serum and thyroidectomy specimens were prospectively collected from 64 patients referred for total thyroidectomy over a 5-year period (2007-2011) and were investigated retrospectively and blindly for circulating EVB19 DNA by q-PCR (Qiagen), and for EVB19 thyrocyte infection by immunochemistry (VP2-Antibody, Dako). EVB19 serology was also determined. General clinical and laboratory data were collected. Twenty patients were referred for Graves' disease and 44 patients were referred for non-autoimmune multinodular thyroid. Patients with thyroid cancer were excluded. Ten percent of Graves' disease patients and 27.7% of control patients had positive staining of thyrocytes for EVB19 antibodies (ns). EVB19-positive and EVB19-negative cases did not differ. EVB19-positive controls were older than EVB19-negative controls (mean age: 57.5 [35-74] vs. 45 [28-80] years, P = 0.03) No case of acute EVB19 infection was identified. EVB19-positive serology was more frequent in controls than in Graves' disease patients (88% vs. 45%, P < 0.0001). EVB19 was detected in thyrocytes, but not more frequently in Graves' disease patients than in controls. Further studies are needed to determine the role of EVB19 infection in thyroid diseases. J. Med. Virol. 85:1414-1419, 2013. © 2013 Wiley Periodicals, Inc.
    Journal of Medical Virology 08/2013; 85(8):1414-9. · 2.37 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To optimize standard treatment of chronic hepatitis C in responder patients who have achieved undetectable viral load, a prospective study was conducted to determine the factors and kinetics of virologic relapse. Responder patients were monitored 2, 4, 8, 12, 16, and 24 weeks after the end of treatment with pegylated interferon and ribavirin. Forty-seven of the 154 patients (30.5%) relapsed. Relapse was significantly associated with absence of rapid virologic response (RVR), retreatment, higher baseline viral load, older age, and lower weight-based dose of pegylated interferon. Relapse was more frequent in patients failing to achieve a RVR after receiving pegylated interferon alpha 2a < 2.5 µg/week or alpha 2b < 1.5 µg/week (P = 0.002). Among patients infected with hepatitis C virus (HCV) genotype 1 with non-CC IL-28B polymorphism (rs12979860), viral decay during treatment was lower in relapsers (P = 0.003 at week 4). Relapse was detected at weeks 2, 4, 8, and 12 after the end of treatment for 5, 8, 10, and 6 patients infected with HCV genotype 1, respectively. Positive predictive values for sustained virologic response were 70.9%, 80.2%, 91.9%, and 98.8% at weeks 2, 4, 8, and 12, respectively. Only one patient relapsed beyond 24 weeks. Closer follow-up and treatment adaptation in patients failing to achieve RVR may decrease the relapse rate in slower responders and heavier patients. Monitoring viral load as early as 1 month after the end of treatment could be useful to assess virologic response. J. Med. Virol. 85:1191-1198, 2013. © 2013 Wiley Periodicals, Inc.
    Journal of Medical Virology 07/2013; 85(7):1191-8. · 2.37 Impact Factor
  • Source
    C Fournier, G Duverlie, S Castelain
    [Show abstract] [Hide abstract]
    ABSTRACT: Complementation is a naturally occurring genetic mechanism that has been studied for a number of plus-strand RNA viruses. Although trans-complementation is well documented for Flaviviridae family viruses, the first such system for hepatitis C virus (HCV) was only described in 2005. Since then, the development of a number of HCV trans-complementation models has improved our knowledge of HCV protein functions and interactions, genome replication and viral particle assembly. These models have also been used to produce defective viruses and so improvements are necessary for vaccine assays. This review provides an update on HCV trans-complementation systems, the viral mechanisms studied therewith and the production and characterization of trans-encapsidated particles.
    Journal of Viral Hepatitis 04/2013; 20(4):225-233. · 3.08 Impact Factor
  • Etienne Brochot, Eric Nguyen-Khac, Gilles Duverlie
    [Show abstract] [Hide abstract]
    ABSTRACT: Two types of peginterferon alfa (2a and 2b) are available for the treatment of chronic hepatitis C genotype 1 or non-1. Comparative studies of bitherapy suggest equivalent results in terms of sustained virologic response for the two types of interferon possibly with a slight advantage in favor of type 2a. However, these studies report only limited data concerning relapse. We analyzed studies comparing the two types of peginterferon with data concerning relapse. In the 6 studies examined (8538 patients), peginterferon 2a was clearly associated with a much higher rate of end of treatment response but also a higher relapse rate than type 2b (29.3% vs 21.1%; relative risk of relapse with peginterferon 2a:1.54 [1.35-1.76], p=0.0024). These data are highlighted in overweight patients. We tried to explain these differences between these two types of interferon by discussing in terms of pharmacokinetics. Peginterferon remains the cornerstone of HCV treatment and must be carefully chosen on the basis of the patient's history and cofactors. These data are important and must be considered in the era of DAA.
    Antiviral research 02/2013; 98(1):1-3. · 3.61 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Correction to Hoffmann et al., Virology Journal 2012 9:109.
    Virology Journal 02/2013; 10(1):59. · 2.09 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Hepatitis C virus (HCV) is a major cause of chronic liver disease. Despite recent success in improving anti-HCV therapy, additional progress is still needed to develop cheaper and interferon-free treatments. Here, we report that Ferroquine (FQ), an antimalarial ferrocenic analogue of chloroquine, is a novel inhibitor of HCV. FQ potently inhibited HCV infection of hepatoma cell lines by affecting an early step of the viral life cycle. The antiviral activity of FQ on HCV entry was confirmed with pseudoparticles expressing HCV envelope glycoproteins E1 and E2 from six different genotypes. In addition to its effect on HCV entry, FQ also inhibited HCV RNA replication, albeit at a higher concentration. We also showed that FQ has no effect on viral assembly and virion secretion. Using a binding assay at 4°C, we showed that FQ does not prevent attachment of the virus to the cell surface. Furthermore, virus internalization was not affected by FQ, whereas the fusion process was impaired in the presence of FQ as shown in a cell-cell fusion assay. Finally, virus with resistance to FQ was selected by sequential passage in the presence of the drug, and resistance was shown to be conferred by a single mutation in E1 glycoprotein (S327A). By inhibiting cell-free virus transmission using a neutralizing antibody, we also showed that FQ inhibits HCV cell-to-cell spread between neighboring cells. Combinations of FQ with interferon, or an inhibitor of HCV NS3/4A protease also resulted in additive to synergistic activity. CONCLUSION: FQ is a novel interesting anti-HCV molecule that could be used in combination with other direct acting antivirals. (HEPATOLOGY 2013.).
    Hepatology 01/2013; · 12.00 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A trans-packaging system for hepatitis C virus (HCV) replicons lacking envelope glycoproteins was developed. The replicons were efficiently encapsidated into infectious particles after expression in trans of homologous HCV envelope proteins under the control of an adenoviral vector. Interestingly, expression in trans of core or core, p7 and NS2 with envelope proteins did not enhance trans-encapsidation. Expression of heterologous envelope proteins, in the presence or absence of heterologous core, p7 and NS2, did not rescue single-round infectious particle production. To increase the titre of homologous, single-round infectious particles in our system, successive cycles of trans-encapsidation and infection were performed. Four cycles resulted in a hundred-fold increase in the yield of particles. Sequence analysis revealed a total of 16 potential adaptive mutations in two independent experiments. Except for a core mutation in one experiment, all the mutations were located in non-structural regions mainly in NS5A (four in domain III and two near the junction with the NS5B gene). Reverse genetics studies suggested that D2437A and S2443T adaptive mutations, which are located into the NS5A-B cleavage site did not affect viral replication but enhanced the single-round infectious particles assembly only in trans-encapsidation model. In conclusion, our trans-encapsidation system enables the production of HCV single-round infectious particles. This system is adaptable and can positively select variants. The adapted variants promote trans-encapsidation and should constitute a valuable tool in the development of replicon-based HCV vaccines.
    Journal of General Virology 01/2013; · 3.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Significant progress has been made in Hepatitis C virus (HCV) culture since the JFH1 strain cloning. However, developing efficient and physiologically relevant culture systems for all viral genotypes remains an important goal. In this work, we aimed at producing a high titer JFH1 derived virus to test different hepatic cells' permissivity. To this end, we performed successive infections and obtained a JFH1 derived virus reaching high titers. Six potential adaptive mutations were identified (I599V in E2, R1373Q and M1611T in NS3, S2364P and C2441S in NS5A and R2523K in NS5B) and the effect of these mutations on HCV replication and infectious particle production was investigated. This cell culture adapted virus enabled us to efficiently infect primary human hepatocytes, as demonstrated using the RFP-NLS-IPS reporter protein and intracellular HCV RNA quantification. However, the induction of a strong type III interferon response in these cells was responsible for HCV inhibition. The disruption of this innate immune response led to a strong infection enhancement and permitted the detection of viral protein expression by western blotting as well as progeny virus production. This cell culture adapted virus also enabled us to easily compare the permissivity of seven hepatoma cell lines. In particular, we demonstrated that HuH-7, HepG2-CD81, PLC/PRF/5 and Hep3B cells were permissive to HCV entry, replication and secretion even if the efficiency was very low in PLC/PRF/5 and Hep3B cells. In contrast, we did not observe any infection of SNU-182, SNU-398 and SNU-449 hepatoma cells. Using iodixanol density gradients, we also demonstrated that the density profiles of HCV particles produced by PLC/PRF/5 and Hep3B cells were different from that of HuH-7 and HepG2-CD81 derived virions. These results will help the development of a physiologically relevant culture system for HCV patient isolates.
    PLoS ONE 01/2013; 8(8):e70809. · 3.53 Impact Factor

Publication Stats

2k Citations
442.64 Total Impact Points

Institutions

  • 2002–2014
    • Université de Picardie Jules Verne
      Amiens, Picardie, France
  • 2011–2013
    • University of Lille Nord de France
      Lille, Nord-Pas-de-Calais, France
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital Region, Belgium
    • Université de Rennes 1
      Roazhon, Brittany, France
  • 2005–2011
    • Institut National de la Transfusion Sanguine, Paris
      Lutetia Parisorum, Île-de-France, France
    • Centre Hospitalier Universitaire de Tours
      Tours, Centre, France
  • 2003–2011
    • Institut Pasteur de Lille
      Lille, Nord-Pas-de-Calais, France
  • 1988–2011
    • Centre Hospitalier Universitaire d'Amiens
      • Laboratoire de Virologie
      Amiens, Picardie, France
  • 2007–2010
    • Institut de Biologie de Lille
      Lille, Nord-Pas-de-Calais, France
    • University of Birmingham
      Birmingham, England, United Kingdom
  • 1987–2007
    • Institut Universitaire de France
      Lutetia Parisorum, Île-de-France, France
  • 2006
    • Centre Hospitalier Universitaire de Limoges
      Limages, Limousin, France
  • 2000
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany