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18. Nicotinic acid effects on insulin sensitivity and hepatic lipid metabolism: an in vivo to in vitro study

Author

Blond, E., Rieusset, J., Alligier, M., Lambert-Porcheron, S., Bendridi, N., Gabert, L., Chetiveaux, M., Debard, C., Chauvin, M. A., Normand, S., Roth, H., Gouville, A. C., Krempf, M., Vidal, Hubert, Goudable, Joëlle, Laville, M., Niacin\\' Study, Group, Centre de Recherche en Nutrition Humaine Rhône-Alpes (CRNH-RA), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Recherche Agronomique (INRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Jean Monnet [Saint-Étienne] (UJM)-CHU Saint-Etienne-Hospices Civils de Lyon (HCL)-CHU Grenoble, Hospices Civils de Lyon (HCL), Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon, GlaxoSmithKline, Les Ulis, France, Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), and Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL)

Subjects
Male, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, [SDV]Life Sciences [q-bio], Clinical Biochemistry, 030204 cardiovascular system & hematology, Lipoproteins, VLDL, Biochemistry, Insulin/*pharmacology, chemistry.chemical_compound, Mice, 0302 clinical medicine, Endocrinology, Signal Transduction/drug effects, Triglycerides/metabolism, Insulin, Protein Kinase C, 0303 health sciences, Tumor, biology, medicine.diagnostic_test, Protein Kinase C/antagonists & inhibitors/metabolism, General Medicine, Middle Aged, Hepatocytes/drug effects/metabolism, 3. Good health, Liver, Diglycerides/metabolism, Signal Transduction, Niacin/administration & dosage/*pharmacology, medicine.medical_specialty, Lipid Metabolism/*drug effects, Lipoproteins, Niacin, Cell Line, Diglycerides, 03 medical and health sciences, Insulin resistance, Internal medicine, Cell Line, Tumor, medicine, Humans, Animals, Protein Kinase Inhibitors, Triglycerides, 030304 developmental biology, Diacylglycerol kinase, Liver/*metabolism, Triglyceride, Biochemistry (medical), VLDL/metabolism, Metabolism, medicine.disease, Lipid Metabolism, Insulin receptor, Kinetics, chemistry, Protein Kinase Inhibitors/pharmacology, biology.protein, Hepatocytes, Metabolic syndrome, Lipid profile
Abstract

International audience; Our aim was to characterize the effects and the underlying mechanisms of the lipid-regulating agent Niaspan((R)) on both insulin action and triglyceride decrease in 20 nondiabetic, dyslipidemic men with metabolic syndrome receiving Niaspan((R)) (2 g/day) or placebo for 8 weeks in a randomized, cross-over study. The effects on plasma lipid profile were characterized at the beginning and the end of each treatment period; insulin sensitivity was assessed using the 2-step euglycemic hyperinsulinemic clamp and VLDL-triglyceride turnover by measuring plasma glycerol enrichment, both at the end of each treatment period. The mechanism of action of nicotinic acid was studied in HuH7 and mouse primary hepatocytes. Lipid profile was improved after Niaspan((R)) treatment with a significant-28% decrease in triglyceride levels, a+17% increase in HDL-C concentration and unchanged levels of fasting nonesterified fatty acid. VLDL-tri-glyceride production rate was markedly reduced after Niaspan((R)) (-68%). However, the treatment induced hepatic insulin resistance, as assessed by reduced inhibition of endogenous glucose production by insulin (0.7+/-0.4 vs. 1.0+/-0.5 mg/kg . min, p\textless0.05) and decrease in fasting hepatic insulin sensitivity index (4.8+/-1.8 vs. 3.2+/-1.6, p\textless0.05) in the Niaspan((R)) condition. Nicotinic acid also reduced insulin action in HuH7 and primary hepatocytes, independently of the activation of hepatic PKCepsilon. This effect was associated with an increase in diacylglycerol and a decrease in tri-glyceride contents that occurred in the absence of modification of DGAT2 expression and activity. Eight weeks of Niaspan((R)) treatment in dyslipidemic patients with metabolic syndrome induce hepatic insulin resistance. The mechanism could involve an accumulation of diacylglycerol and an alteration of insulin signaling in hepatocytes.

Published
2014
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20. Jejunal proteins secreted by db/db mice or insulin-resistant humans impair the insulin signaling and determine insulin resistance

Author

Salinari, S, Debard, C, Bertuzzi, A, Durand, C, Zimmet, P, Vidal, H, Mingrone, Geltrude, Mingrone, Geltrude (ORCID:0000-0003-2021-528X), Salinari, S, Debard, C, Bertuzzi, A, Durand, C, Zimmet, P, Vidal, H, Mingrone, Geltrude, and Mingrone, Geltrude (ORCID:0000-0003-2021-528X)

Abstract

Two recent studies demonstrated that bariatric surgery induced remission of type 2 diabetes very soon after surgery and far too early to be attributed to weight loss. In this study, we sought to explore the mechanism/s of this phenomenon by testing the effects of proteins from the duodenum-jejunum conditioned-medium (CM) of db/db or Swiss mice on glucose uptake in vivo in Swiss mice and in vitro in both Swiss mice soleus and L6 cells. We studied the effect of sera and CM proteins from insulin resistant (IR) and insulin-sensitive subjects on insulin signaling in human myoblasts.

Published
2013

21. Potential for the integration of alternative energies in the process industry

Author

Payet Lucille, Carlu Elieta, Pasquier Léo, and Debard Christophe

Subjects
Engineering (General). Civil engineering (General), TA1-2040
Abstract

In the current context of energy transition, industry has a major role to play. In France, it represents 20% of overall energy consumption, with a predominantly carbon-based energy mix (Fig. 1). To decarbonize French industry, the first lever is therefore to reduce this energy consumption by working on energy efficiency and process optimization. In order to pursue their decarbonization roadmap, manufacturers will have to act on their energy mix. In France, very low-carbon electricity opens up a real opportunity for the electrification of thermal processes. Since electrification cannot concern all uses, carbon-free gases will also play a crucial role in this energy transition. As such, the ALLICE Alliance has investigated these two decarbonization pathways for its members in two in-depth studies on the subject ([1] and [2]). This article highlights the main results of these two studies, each of which is the subject of public summaries [3].

Published
2023
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22. P206 L’huile de palme, mais pas l’huile de colza ni l’huile de tournesol, prévient l’hyperperméabilité intestinale dans un modèle animal de syndrome de l’intestin irritable : mécanismes impliquant les cellules à mucus et la production de MUC2

Author

Benoît, B., primary, Bruno, J., additional, Kayal, F., additional, Estienne, M., additional, Debard, C., additional, Loizon, E., additional, Ducroc, R., additional, and Plaisancie, P., additional

Published
2013
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28. Tpl2 kinase is upregulated in adipose tissue in obesity and may mediate interleukin-1beta and tumor necrosis factor-{alpha} effects on extracellular signal-regulated kinase activation and lipolysis.

Author

Jager J, Grémeaux T, Gonzalez T, Bonnafous S, Debard C, Laville M, Vidal H, Tran A, Gual P, Le Marchand-Brustel Y, Cormont M, Tanti JF, Jager, Jennifer, Grémeaux, Thierry, Gonzalez, Teresa, Bonnafous, Stéphanie, Debard, Cyrille, Laville, Martine, Vidal, Hubert, and Tran, Albert

Abstract

Objective: Activation of extracellular signal-regulated kinase-(ERK)-1/2 by cytokines in adipocytes is involved in the alterations of adipose tissue functions participating in insulin resistance. This study aims at identifying proteins regulating ERK1/2 activity, specifically in response to inflammatory cytokines, to provide new insights into mechanisms leading to abnormal adipose tissue function.Research Design and Methods: Kinase activities were inhibited with pharmacological inhibitors or siRNA. Lipolysis was monitored through glycerol production. Gene expression in adipocytes and adipose tissue of obese mice and subjects was measured by real-time PCR.Results: IkappaB kinase-(IKK)-beta inhibition prevented mitogen-activated protein (MAP) kinase kinase (MEK)/ERK1/2 activation in response to interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha but not insulin in 3T3-L1 and human adipocytes, suggesting that IKKbeta regulated a MAP kinase kinase kinase (MAP3K) involved in ERK1/2 activation induced by inflammatory cytokines. We show that the MAP3K8 called Tpl2 was expressed in adipocytes and that IL-1beta and TNF-alpha activated Tpl2 and regulated its expression through an IKKbeta pathway. Pharmacological inhibition or silencing of Tpl2 prevented MEK/ERK1/2 activation by these cytokines but not by insulin, demonstrating its involvement in ERK1/2 activation specifically in response to inflammatory stimuli. Importantly, Tpl2 was implicated in cytokine-induced lipolysis and in insulin receptor substrate-1 serine phosphorylation. Tpl2 mRNA expression was upregulated in adipose tissue of obese mice and patients and correlated with TNF-alpha expression.Conclusions: Tpl2 is selectively involved in inflammatory cytokine-induced ERK1/2 activation in adipocytes and is implicated in their deleterious effects on adipocyte functions. The deregulated expression of Tpl2 in adipose tissue suggests that Tpl2 may be a new actor in adipose tissue dysfunction in obesity. [ABSTRACT FROM AUTHOR]

Published
2010
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30. WY-14643 and 9-cis-retinoic acid induce IRS-2/PI 3-kinase signalling pathway and increase glucose transport in human skeletal muscle cells: differential effect in myotubes from healthy subjects and Type 2 diabetic patients

Author

Debard, C., Laville, M., Vanessa Euthine, Loizon, E., Guillet, C., Morio-Liondore, B., Yves Boirie, Vidal, H., Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL), Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA), Bioinformatique, phylogénie et génomique évolutive (BPGE), Département PEGASE [LBBE] (PEGASE), Laboratoire de Biométrie et Biologie Evolutive - UMR 5558 (LBBE), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Laboratoire de Biométrie et Biologie Evolutive - UMR 5558 (LBBE), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS), Unité de Nutrition Humaine (UNH), Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université-Institut National de la Recherche Agronomique (INRA), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL), Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université, Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM), and EUTHINE, Vanessa

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

31. n-3 PUFA added to high-fat diets affect differently adiposity and inflammation when carried by phospholipids or triacylglycerols in mice

Author

Awada Manar, Meynier Anne, Soulage Christophe O, Hadji Lilas, Géloën Alain, Viau Michèle, Ribourg Lucie, Benoit Berengère, Debard Cyrille, Guichardant Michel, Lagarde Michel, Genot Claude, and Michalski Marie-Caroline

Subjects
n-3 PUFA, Phospholipid, Triacylglycerol, High-fat diet, Inflammation, Oxidative stress, Adipose tissue, Nutrition. Foods and food supply, TX341-641, Nutritional diseases. Deficiency diseases, RC620-627
Abstract

Abstract Background Dietary intake of n-3 polyunsaturated fatty acids (PUFA) is primarily recognized to protect against cardiovascular diseases, cognitive dysfunctions and the onset of obesity and associated metabolic disorders. However, some of their properties such as bioavailability can depend on their chemical carriers. The objective of our study was to test the hypothesis that the nature of n-3 PUFA carrier results in different metabolic effects related to adiposity, oxidative stress and inflammation. Methods 4 groups of C57BL/6 mice were fed for 8 weeks low fat (LF) diet or high-fat (HF, 20%) diets. Two groups of high-fat diets were supplemented with long-chain n-3 PUFA either incorporated in the form of phospholipids (HF-ω3PL) or triacylglycerols (HF-ω3TG). Results Both HF-ω3PL and HF-ω3TG diets reduced the plasma concentrations of (i) inflammatory markers such as monocyte chemoattractant protein-1 (MCP-1) and interleukin 6 (IL-6), (ii) leptin and (iii) 4-hydroxy-2-nonenal (4-HNE), a marker of n-6 PUFA-derived oxidative stress compared with the control HF diet. Moreover, in both HF-ω3PL and HF-ω3TG groups, MCP-1 and IL-6 gene expressions were decreased in epididymal adipose tissue and the mRNA level of gastrointestinal glutathione peroxidase GPx2, an antioxidant enzyme, was decreased in the jejunum compared with the control HF diet. The type of n-3 PUFA carrier affected other outcomes. The phospholipid form of n-3 PUFA increased the level of tocopherols in epididymal adipose tissue compared with HF-ω3TG and resulted in smaller adipocytes than the two others HF groups. Adipocytes in the HF-ω3PL and LF groups were similar in size distribution. Conclusion Supplementation of mice diet with long-chain n-3 PUFA during long-term consumption of high-fat diets had the same lowering effects on inflammation regardless of triacyglycerol or phospholipid carrier, whereas the location of these fatty acids on a PL carrier had a major effect on decreasing the size of adipocytes that was not observed with the triacyglycerol carrier. Altogether, these results would support the development functional foods containing LC n-3 PUFA in the form of PL in order to prevent some deleterious outcomes associated with the development of obesity.

Published
2013
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32. No increased risk of Kaposi sarcoma relapse in patients with controlled HIV‐1 infection after switching protease inhibitor‐based antiretroviral therapy

Author

Lajaunie, Rébecca, Cuzin, Lise, Palich, Romain, Makinson, Alain, Bani-Sadr, Firouzé, Duvivier, Claudine, Arvieux, Cedric, Rey, David, Poizot-Martin, Isabelle, Delpierre, Cyril, Delobel, Pierre, Martin-Blondel, Guillaume, Chirouze, C., Drobacheff-Thiébaut, C., Foltzer, A., Bouiller, K., Hustache- Mathieu, L., Lepiller, Q., Bozon, F., Babre, O, Brunel, As., Muret, P., Chevalier, E., Jacomet, C., Laurichesse, H., Lesens, O., Vidal, M., Mrozek, N., Aumeran, C., Baud, O., Corbin, V., Goncalvez, E., Mirand, A, Brebion, A, Henquell, C, Lamaury, I., Fabre, I., Curlier, E., Ouissa, R., Herrmann-Storck, C., Tressieres, B., Receveur, Mc., Boulard, F., Daniel, C., Clavel, C., Roger, Pm., Markowicz, S., Chellum Rungen, N., Merrien, D., Perré, P., Guimard, T., Bollangier, O., Leautez, S., Morrier, M., Laine, L., Boucher, D., Point, P., Cotte, L., Ader, F., Becker, A., Boibieux, A., Brochier, C., Brunel-Dalmas, F., Cannesson, O., Chiarello, P., Chidiac, C., Degroodt, S., Ferry, T., Godinot, M., Livrozet, J.M., Makhloufi, D., Miailhes, P., Perpoint, T., Perry, M., Pouderoux, C., Roux, S., Triffault-Fillit, C., Valour, F., Charre, C., Icard, V., Tardy, J.C., Trabaud, M.A., Ravaux, I., Ménard, A., Belkhir, Ay., Colson, P., Dhiver, C., Madrid, A., Martin-Degioanni, M., Meddeb, L., Mokhtari, M., Motte, A., Raoux, A., Toméi, C., Tissot-Dupont, H., Poizot-Martin, I., Brégigeon, S., Zaegel-Faucher, O., Obry-Roguet, V., Laroche, H, Orticoni, M., Soavi, M.J., Ressiot, E., Ducassou, M.J., Jaquet, I., Galie, S., Colson, H., Ritleng, A.S., Ivanova, A., Debreux, C., Lions, C., Rojas-Rojas, T, Cabié, A., Abel, S., Bavay, J., Bigeard, B., Cabras, O., Cuzin, L., Dupin de Majoubert, R., Fagour, L., Guitteaud, K., Marquise, A., Najioullah, F., Pierre-François, S., Pasquier, J., Richard, P., Rome, K., Turmel, Jm, Varache, C., Atoui, N., Bistoquet, M., Delaporte, E, Le Moing, V., Makinson, A., Meftah, N., Merle de Boever, C., Montes, B., Montoya Ferrer, A., Tuaillon, E., Reynes, J., Lefèvre, B., Jeanmaire, E., Hénard, S., Frentiu, E., Charmillon, A., Legoff, A., Tissot, N., André, M., Boyer, L., Bouillon, Mp., Delestan, M., Goehringer, F., Bevilacqua, S., Rabaud, C., May, T., Raffi, F., Allavena, C., Aubry, O., Billaud, E., Biron, C., Bonnet, B., Bouchez, S., Boutoille, D., Brunet-Cartier, C., Deschanvres, C., Gaborit, B.J., Grégoire, A., Grégoire, M., Grossi, O., Guéry, R., Jovelin, T., Lefebvre, M., Le Turnier, P., Lecomte, R., Morineau, P., Reliquet, V., Sécher, S., Cavellec, M., Paredes, E., Soria, A., Ferré, V., André-Garnier, E., Rodallec, A., Pugliese, P., Breaud, S., Ceppi, C., Chirio, D., Cua, E., Dellamonica, P., Demonchy, E., de Monte, A., Durant, J., Etienne, C., Ferrando, S., Garraffo, R., Michelangeli, C., Mondain, V., Naqvi, A., Oran, N., Perbost, I., Carles, M., Klotz, C., Maka, A., Pradier, C., Prouvost-Keller, B., Risso, K., Rio, V., Rosenthal, E., Touitou, I., Wehrlen-Pugliese, S., Zouzou, G., Hocqueloux, L., Prazuck, T., Gubavu, C., Sève, A., Giaché, S., Rzepecki, V., Colin, M., Boulard, C., Thomas, G., Cheret, A., Goujard, C., Quertainmont, Y., Teicher, E., Lerolle, N., Jaureguiberry, S., Colarino, R., Deradji, O., Castro, A., Barrail-Tran, A., Yazdanpanah, Y., Landman, R., Joly, V., Ghosn, J., Rioux, C., Lariven, S., Gervais, A., Lescure, Fx., Matheron, S., Louni, F., Julia, Z., Le Gac, S., Charpentier, C., Descamps, D., Peytavin, G., Duvivier, C., Aguilar, C., Alby-Laurent, F., Amazzough, K., Benabdelmoumen, G., Bossi, P., Cessot, G., Charlier, C., Consigny, P.H., Jidar, K., Lafont, E., Lanternier, F., Leporrier, J., Lortholary, O., Louisin, C., Lourenco, J., Parize, P., Pilmis, B., Rouzaud, C., Touam, F., Valantin, Ma., Tubiana, R., Agher, R., Seang, Sophie, Schneider, L., Palich, R., Blanc, C., Katlama, C., Bani-Sadr, F., Berger, Jl., N’guyen, Y., Lambert, D., Kmiec, I., Hentzien, M., Brunet, A., Romaru, J., Marty, H., Brodard, V., Arvieux, C., Tattevin, P., Revest, M., Souala, F., Baldeyrou, M., Patrat-Delon, S., Chapplain, J.M., Benezit, F., Dupont, M., Poinot, M., Maillard, A., Pronier, C., Lemaitre, F., Morlat, C., Poisson-Vannier, M., Sinteff, Jp., Gagneux-Brunon, A., Botelho-Nevers, E., Frésard, A., Ronat, V., Lucht, F., Rey, D., Fischer, P., Partisani, M., Cheneau, C., Priester, M., Batard, Ml., Mélounou, C, Bernard-Henry, C., de Mautort, E., Fafi-Kremer, S., Delobel, P., Alvarez, M., Biezunski, N., Debard, A., Delpierre, C., Gaube, G., Lansalot, P., Lelièvre, L., Marcel, M., Martin-Blondel, G., Piffaut, M., Porte, L., Saune, K., Robineau, O., Ajana, F., Aïssi, E., Alcaraz, I., Alidjinou, E., Baclet, V., Bocket, L., Boucher, A., Digumber, M., Huleux, T., Lafon-Desmurs, B., Meybeck, A., Pradier, M., Tetart, M., Thill, P., Viget, N., Valette, M., Service Maladies infectieuses et tropicales [CHU Toulouse], Pôle Inflammation, infection, immunologie et loco-moteur [CHU Toulouse] (Pôle I3LM Toulouse), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), CHU de la Martinique [Fort de France], Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Département Maladies Infectieuses et Tropicales, Hôpital Universitaire, Montpellier, France, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre Hospitalier Universitaire de Reims (CHU Reims), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre Médical de l'Institut Pasteur (CMIP), Institut Pasteur [Paris] (IP)-Université Paris Cité (UPCité), CHU Pontchaillou [Rennes], CHU Strasbourg, Sciences Economiques et Sociales de la Santé & Traitement de l'Information Médicale (SESSTIM - U1252 INSERM - Aix Marseille Univ - UMR 259 IRD), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Toulouse III Paul Sabatier - Faculté de médecine Purpan (UTPS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), And The Dat’AIDS study group: C Chirouze, C Drobacheff-Thiébaut, A Foltzer, K Bouiller, L Hustache-Mathieu, Q Lepiller, F Bozon, O Babre, A S Brunel, P Muret, E Chevalier, C Jacomet, H Laurichesse, O Lesens, M Vidal, N Mrozek, C Aumeran, O Baud, V Corbin, E Goncalvez, A Mirand, A Brebion, C Henquell, I Lamaury, I Fabre, E Curlier, R Ouissa, C Herrmann-Storck, B Tressieres, M C Receveur, F Boulard, C Daniel, C Clavel, P M Roger, S Markowicz, N Chellum Rungen, D Merrien, P Perré, T Guimard, O Bollangier, S Leautez, M Morrier, L Laine, D Boucher, P Point, L Cotte, F Ader, A Becker, A Boibieux, C Brochier, F Brunel-Dalmas, O Cannesson, P Chiarello, C Chidiac, S Degroodt, T Ferry, M Godinot, J M Livrozet, D Makhloufi, P Miailhes, T Perpoint, M Perry, C Pouderoux, S Roux, C Triffault-Fillit, F Valour, C Charre, V Icard, J C Tardy, M A Trabaud, I Ravaux, A Ménard, A Y Belkhir, P Colson, C Dhiver, A Madrid, M Martin-Degioanni, L Meddeb, M Mokhtari, A Motte, A Raoux, C Toméi, H Tissot-Dupont, I Poizot-Martin, S Brégigeon, O Zaegel-Faucher, V Obry-Roguet, H Laroche, M Orticoni, M J Soavi, E Ressiot, M J Ducassou, I Jaquet, S Galie, H Colson, A S Ritleng, A Ivanova, C Debreux, C Lions, T Rojas-Rojas, A Cabié, S Abel, J Bavay, B Bigeard, O Cabras, L Cuzin, R Dupin de Majoubert, L Fagour, K Guitteaud, A Marquise, F Najioullah, S Pierre-François, J Pasquier, P Richard, K Rome, J M Turmel, C Varache, N Atoui, M Bistoquet, E Delaporte, V Le Moing, A Makinson, N Meftah, C Merle de Boever, B Montes, A Montoya Ferrer, E Tuaillon, J Reynes, B Lefèvre, E Jeanmaire, S Hénard, E Frentiu, A Charmillon, A Legoff, N Tissot, M André, L Boyer, M P Bouillon, M Delestan, F Goehringer, S Bevilacqua, C Rabaud, T May, F Raffi, C Allavena, O Aubry, E Billaud, C Biron, B Bonnet, S Bouchez, D Boutoille, C Brunet-Cartier, C Deschanvres, B J Gaborit, A Grégoire, M Grégoire, O Grossi, R Guéry, T Jovelin, M Lefebvre, P Le Turnier, R Lecomte, P Morineau, V Reliquet, S Sécher, M Cavellec, E Paredes, A Soria, V Ferré, E André-Garnier, A Rodallec, P Pugliese, S Breaud, C Ceppi, D Chirio, E Cua, P Dellamonica, E Demonchy, A De Monte, J Durant, C Etienne, S Ferrando, R Garraffo, C Michelangeli, V Mondain, A Naqvi, N Oran, I Perbost, M Carles, C Klotz, A Maka, C Pradier, B Prouvost-Keller, K Risso, V Rio, E Rosenthal, I Touitou, S Wehrlen-Pugliese, G Zouzou, L Hocqueloux, T Prazuck, C Gubavu, A Sève, S Giaché, V Rzepecki, M Colin, C Boulard, G Thomas, A Cheret, C Goujard, Y Quertainmont, E Teicher, N Lerolle, S Jaureguiberry, R Colarino, O Deradji, A Castro, A Barrail-Tran, Y Yazdanpanah, R Landman, V Joly, J Ghosn, C Rioux, S Lariven, A Gervais, F X Lescure, S Matheron, F Louni, Z Julia, S Le Gac, C Charpentier, D Descamps, G Peytavin, C Duvivier, C Aguilar, F Alby-Laurent, K Amazzough, G Benabdelmoumen, P Bossi, G Cessot, C Charlier, P H Consigny, K Jidar, E Lafont, F Lanternier, J Leporrier, O Lortholary, C Louisin, J Lourenco, P Parize, B Pilmis, C Rouzaud, F Touam, M A Valantin, R Tubiana, R Agher, S Seang, L Schneider, R Palich, C Blanc, C Katlama, F Bani-Sadr, J L Berger, Y N'Guyen, D Lambert, I Kmiec, M Hentzien, A Brunet, J Romaru, H Marty, V Brodard, C Arvieux, P Tattevin, M Revest, F Souala, M Baldeyrou, S Patrat-Delon, J M Chapplain, F Benezit, M Dupont, M Poinot, A Maillard, C Pronier, F Lemaitre, C Morlat, M Poisson-Vannier, T Jovelin, J P Sinteff, A Gagneux-Brunon, E Botelho-Nevers, A Frésard, V Ronat, F Lucht, D Rey, P Fischer, M Partisani, C Cheneau, M Priester, M L Batard, C Mélounou, C Bernard-Henry, E de Mautort, S Fafi-Kremer, P Delobel, M Alvarez, N Biezunski, A Debard, C Delpierre, G Gaube, P Lansalot, L Lelièvre, M Marcel, G Martin-Blondel, M Piffaut, L Porte, K Saune, O Robineau, F Ajana, E Aïssi, I Alcaraz, E Alidjinou, V Baclet, L Bocket, A Boucher, M Digumber, T Huleux, B Lafon-Desmurs, A Meybeck, M Pradier, M Tetart, P Thill, N Viget, M Valette, Malbec, Odile, Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service de Maladies Infectieuses et Tropicales [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Universitaire de Rennes (CHU Rennes), Laboratoire de Physique des Lasers (LPL), Université Paris 13 (UP13)-Centre National de la Recherche Scientifique (CNRS)-Université Sorbonne Paris Nord, Service d'Immuno-hématologie clinique [Hôpital Sainte Marguerite - APHM], Assistance Publique - Hôpitaux de Marseille (APHM)-Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Institut des sciences de la santé publique [Marseille] (ISSPAM), European Infective Endocarditis Registry (Euro-Endo), EMERGEN consortium, Stratégies thérapeutiques contre l'infection VIH et les maladies virales associées [iPLesp] (THERAVIR), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Laboratoire Microorganismes : Génome et Environnement (LMGE), and Centre National de la Recherche Scientifique (CNRS)-Université Clermont Auvergne (UCA)

Subjects
medicine.medical_specialty, MESH: CD4 Lymphocyte Count, [SDV]Life Sciences [q-bio], antiretroviral therapy, Human immunodeficiency virus (HIV), protease inhibitors, HIV Infections, medicine.disease_cause, MESH: HIV-1, Acquired immunodeficiency syndrome (AIDS), MESH: Neoplasm Recurrence, Local / complications, Internal medicine, medicine, Humans, HHV8, MESH: HIV Infections* / complications, MESH: Protease Inhibitors / adverse effects, Pharmacology (medical), Protease inhibitor (pharmacology), Sarcoma, Kaposi, Retrospective Studies, MESH: Humans, business.industry, Health Policy, Kaposi sarcoma, MESH: Retrospective Studies, Viral Load, MESH: HIV Infections* / drug therapy, medicine.disease, Antiretroviral therapy, switch, CD4 Lymphocyte Count, AIDS, [SDV] Life Sciences [q-bio], Regimen, Infectious Diseases, Increased risk, MESH: Sarcoma, Kaposi* / drug therapy, HIV-1, Sarcoma, Neoplasm Recurrence, Local, business, MESH: Viral Load, Viral load
Abstract

International audience; Objectives: Our aim was to assess if switching from a protease inhibitors (PI)-based regimen to a PI-free one is associated with an increased risk of Kaposi Sarcoma (KS) relapse among patients living with HIV (PLHIV) with history of KS and controlled HIV replication.Methods: In a retrospective analysis of the prospectively collected Dat'AIDS database we selected patients who both had a past KS history and a HIV-1 viral load below 200 copies/mL while being PI-treated. We searched for KS relapses while persistent virological success was maintained for at least 6 months, whether patients kept taking the PI, or switched to PI-free regimen.Results: Among the 216 patients with past KS event and a history of HIV-1 infection efficiently treated by a PI-based regimen, 148 patients (68.5%) later switched to a PI-sparing regimen. Their baseline characteristics were not different from non-switching patients. We described 7 cases of relapse (3.2% of the 216 patients). Five cases of relapse occurred in switching patients (3.4%). The remaining two relapses occurred in PI-treated patients (2.9%). At KS relapse, CD4 cell count was 459 cells/μL (range 225-560) for switching patients, compared with 362 and 136 cells/μL for the other two patients.Conclusions: In this large cohort of PLHIV with a history of KS and ART-controlled HIV replication, KS relapses were described in 3.2% of the patients, and were not more frequent when a PI-containing ART regimen has been switched to a PI-free regimen. Our results do not support a specific effect of PI on KS.

Published
2022
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33. Microelimination or Not? The Changing Epidemiology of Human Immunodeficiency Virus-Hepatitis C Virus Coinfection in France 2012-2018

Author

Pradat, Pierre, Chirouze, C, Drobacheff-Thiébaut, C, Foltzer, A, Bouiller, K, Hustache-Mathieu, L, Lepiller, Q, Bozon, F, Babre, O, Brunel, A, Muret, P, Chevalier, E, Jacomet, C, Laurichesse, H, LESENS, O, Vidal, M, Mrozek, N, Aumeran, C, Baud, O, Corbin, V, Goncalvez, E, Mirand, A, brebion, A, Henquell, C, Lamaury, I, Fabre, I, Curlier, E, Ouissa, R, Herrmann-Storck, C, Tressieres, B, Receveur, M, Boulard, F, Daniel, C, CLAVEL, C, Roger, P, Markowicz, S, Chellum Rungen, N, Merrien, D, Perré, P, Guimard, T, Bollangier, O, Leautez, S, Morrier, M, Laine, L, Boucher, D, Point, P, Cotte, Laurent, Ader, F, Becker, A, Boibieux, A, Brochier, C, Brunel-Dalmas, F, Cannesson, O, Chiarello, P, Chidiac, C, Degroodt, S, FERRY, T, Godinot, M, Livrozet, J, Makhloufi, D, Miailhes, P, Perpoint, T, Perry, M, Pouderoux, C, Roux, Stéphane, Triffault-Fillit, C, Valour, F, Charre, C, Icard, V, Tardy, J, Trabaud, M, Ravaux, I, Ménard, A, Belkhir, A, Colson, P, Dhiver, C, Madrid, A, Martin-Degioanni, M, Meddeb, L, Mokhtari, M, Motte, A, Raoux, A, Toméi, C, Tissot-Dupont, H, Poizot-Martin, Isabelle, Brégigeon, S, Zaegel-Faucher, O, Obry-Roguet, V, Laroche, H, Orticoni, M, Soavi, M, Ressiot, E, Ducassou, M, Jaquet, I, Galie, S, Colson, H, Ritleng, A, Ivanova, A, Debreux, C, Lions, C, Rojas-Rojas, T, Cabié, André, Abel, S, Bavay, J, Bigeard, B, Cabras, O, Cuzin, L, Dupin de Majoubert, R, Fagour, L, Guitteaud, K, Marquise, A, Najioullah, F, Pierre-François, S, Pasquier, J, Richard, P, Rome, K, Turmel, J, Varache, C, Atoui, N, Bistoquet, M, Delaporte, E, Le Moing, V, Makinson, A, Meftah, N, Merle de Boever, C, Montes, B, Montoya Ferrer, A, Tuaillon, E, Reynes, J, Lefèvre, B, Jeanmaire, E, Hénard, S, Frentiu, E, Charmillon, A, Legoff, A, Tissot, N, André, M, Boyer, L, Bouillon, M, Delestan, M, Goehringer, F, Bevilacqua, S, Rabaud, C, May, T, Raffi, F, Allavena, C, Aubry, O, Billaud, E, Biron, C, Bonnet, B, Bouchez, S, Boutoille, D, Brunet-Cartier, C, Deschanvres, C, Gaborit, B, Grégoire, A, Grégoire, M, Grossi, O, Guéry, R, Lefebvre, Maeva, Le Turnier, P, Lecomte, R, Morineau, P, Reliquet, V, Sécher, S, Cavellec, M, Paredes, E, Soria, A, Ferré, V, André-Garnier, E, Rodallec, A, Pugliese, Pascal, Breaud, S, Ceppi, C, Chirio, D, Cua, E, Dellamonica, P, Demonchy, E, De Monte, A, Durant, J, Etienne, C, Ferrando, S, Garraffo, R, Michelangeli, C, Mondain, V, Naqvi, A, Oran, N, Perbost, I, Carles, M, Klotz, C, Maka, A, Pradier, C, Prouvost-Keller, B, Risso, K, Rio, V, Rosenthal, E, Touitou, I, Wehrlen-Pugliese, S, Zouzou, G, Hocqueloux, Laurent, Prazuck, T, Gubavu, C, Sève, A, Giaché, S, Rzepecki, V, Colin, M, Boulard, C, Thomas, G, Cheret, A, Goujard, C, Quertainmont, Y, Teicher, E, Lerolle, N, Jaureguiberry, S, Colarino, R, Deradji, O, Castro, A, Barrail-Tran, A, Yazdanpanah, Y, Landman, R, Joly, V, Ghosn, J, Rioux, C, Lariven, S, gervais, a, Lescure, F, Matheron, S, Louni, F, Julia, Z, Le Gac, S, Charpentier, c, Descamps, D, Peytavin, G, Duvivier, C, Aguilar, C, Alby-Laurent, F, Amazzough, K, Benabdelmoumen, G, Bossi, P, Cessot, G, Charlier, C, Consigny, P, Jidar, K, Lafont, E, Lanternier, F, Leporrier, J, Lortholary, O, Louisin, C, Lourenco, J, Parize, P, Pilmis, B, Rouzaud, C, Touam, F, Valantin, M, Tubiana, R, Agher, R, Seang, S, Schneider, L, PaLich, R, Blanc, C, Katlama, C, Bani-Sadr, Firouze, Berger, J, N’Guyen, Y, Lambert, D, Kmiec, I, Hentzien, M, Brunet, A, Romaru, J, Marty, H, Brodard, V, Arvieux, C, Tattevin, P, Revest, M, Souala, F, Baldeyrou, M, Patrat-Delon, S, Chapplain, J, Benezit, F, Dupont, M, Poinot, M, MAILLARD, A, Pronier, C, Lemaitre, F, Morlat, C, Poisson-Vannier, M, Jovelin, T, Sinteff, J, Gagneux-Brunon, A, Botelho-Nevers, E, Frésard, A, Ronat, V, Lucht, F, Rey, David, Fischer, P, Partisani, M, Cheneau, C, Priester, M, Mélounou, C, Bernard-Henry, C, de Mautort, E, Fafi-Kremer, S, Delobel, P, Alvarez, M, Biezunski, N, Debard, A, Delpierre, C, Gaube, G, Lansalot, P, Lelièvre, L, Marcel, M, Martin-Blondel, G, Piffaut, M, Porte, L, Saune, K, Robineau, O, Ajana, F, Aïssi, E, Alcaraz, I, Alidjinou, E, Baclet, V, Bocket, L, Boucher, A, Digumber, M, Huleux, Thomas, Lafon-Desmurs, B, Meybeck, A, Pradier, M, Tetart, M, Thill, P, Viget, N, Valette, M, Pathogenesis and Control of Chronic and Emerging Infections (PCCEI), Université des Antilles (UA)-Etablissement français du don du sang [Montpellier]-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Centre Hospitalier Régional d'Orléans (CHRO), Centre d’Investigation Clinique de Nantes (CIC Nantes), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre hospitalier universitaire de Nantes (CHU Nantes), Hôpital universitaire Robert Debré [Reims], Centre Hospitalier Gustave Dron [Tourcoing], Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Aix Marseille Université (AMU), Sciences Economiques et Sociales de la Santé & Traitement de l'Information Médicale (SESSTIM - U1252 INSERM - Aix Marseille Univ - UMR 259 IRD), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Nice (CHU Nice), Hôpital l'Archet, Les Hôpitaux Universitaires de Strasbourg (HUS), Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], Université des Antilles (UA), Centre d'Investigation Clinique Antilles-Guyane (CIC - Antilles Guyane), Université des Antilles et de la Guyane (UAG)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Dat’AIDS Study Group Besançon: C. Chirouze, C. Drobacheff-Thiébaut, A. Foltzer, K. Bouiller, L. Hustache- Mathieu, Q. Lepiller, F. Bozon, O. Babre, AS. Brunel, P. Muret, E. Chevalier. Clermont-Ferrand: C. Jacomet, H. Laurichesse, O. Lesens, M. Vidal, N. Mrozek, C. Aumeran, O. Baud, V. Corbin, E. Goncalvez, A Mirand, A brebion, C Henquell. Guadeloupe: I. Lamaury, I. Fabre, E. Curlier, R. Ouissa, C. Herrmann-Storck, B. Tressieres, MC. Receveur, F. Boulard, C. Daniel, C. Clavel, PM. Roger, S. Markowicz, N. Chellum Rungen. La Roche sur Yon: D. Merrien, P. Perré, T. Guimard, O. Bollangier, S. Leautez, M. Morrier, L. Laine, D. Boucher, P. Point. Lyon: L. Cotte, F. Ader, A. Becker, A. Boibieux, C. Brochier F, Brunel-Dalmas, O. Cannesson, P. Chiarello, C. Chidiac, S. Degroodt, T. Ferry, M. Godinot, J.M. Livrozet, D. Makhloufi, P. Miailhes, T. Perpoint, M. Perry, C. Pouderoux, S. Roux, C. Triffault-Fillit, F. Valour, C. Charre, V. Icard, J.C. Tardy, M.A. Trabaud. Marseille IHU Méditerrannée: I. Ravaux, A. Ménard, AY. Belkhir, P. Colson, C. Dhiver, A. Madrid, M. Martin-Degioanni, L. Meddeb, M. Mokhtari, A. Motte, A. Raoux, C. Toméi, H. Tissot-Dupont. Marseille Ste Marguerite: I. Poizot-Martin, S. Brégigeon, O. Zaegel-Faucher, V. Obry-Roguet, H Laroche, M. Orticoni, M.J. Soavi, E. Ressiot, M.J. Ducassou, I. Jaquet, S. Galie, H. Colson, A.S. Ritleng, A. Ivanova, C. Debreux, C. Lions, T Rojas-Rojas. Martinique: A. Cabié, S. Abel, J. Bavay, B. Bigeard, O. Cabras, L. Cuzin, R. Dupin de Majoubert, L. Fagour, K. Guitteaud, A. Marquise, F. Najioullah, S. Pierre-François, J. Pasquier, P. Richard, K. Rome, JM Turmel, C. Varache. Montpellier: N. Atoui, M. Bistoquet, E Delaporte, V. Le Moing, A. Makinson, N. Meftah, C. Merle de Boever, B. Montes, A. Montoya Ferrer, E. Tuaillon, J. Reynes. Nancy: B. Lefèvre, E. Jeanmaire, S. Hénard, E. Frentiu, A. Charmillon, A. Legoff, N. Tissot, M. André, L. Boyer, MP. Bouillon, M. Delestan, F. Goehringer, S. Bevilacqua, C. Rabaud, T. May. Nantes: F. Raffi, C. Allavena, O. Aubry, E. Billaud, C. Biron, B. Bonnet, S. Bouchez, D. Boutoille, C. Brunet-Cartier, C. Deschanvres, B.J. Gaborit, A. Grégoire, M. Grégoire, O. Grossi, R. Guéry, T. Jovelin, M. Lefebvre, P. Le Turnier, R. Lecomte, P. Morineau, V. Reliquet, S. Sécher, M. Cavellec, E. Paredes, A. Soria, V. Ferré, E. André-Garnier, A. Rodallec. Nice: P. Pugliese, S. Breaud, C. Ceppi, D. Chirio, E. Cua, P. Dellamonica, E. Demonchy, A. De Monte, J. Durant, C. Etienne, S. Ferrando, R. Garraffo, C. Michelangeli, V. Mondain, A. Naqvi, N. Oran, I. Perbost, M. Carles, C. Klotz, A. Maka, C. Pradier, B. Prouvost- Keller, K. Risso, V. Rio, E. Rosenthal, I. Touitou, S. Wehrlen-Pugliese, G. Zouzou. Orléans: L. Hocqueloux, T. Prazuck, C. Gubavu, A. Sève, S. Giaché, V. Rzepecki, M. Colin, C. Boulard, G. Thomas. Paris APHP Bicètre: A. Cheret, C. Goujard, Y. Quertainmont, E. Teicher, N. Lerolle, S. Jaureguiberry, R. Colarino, O. Deradji, A. Castro, A. Barrail-Tran. Paris APHP Bichat: Y. Yazdanpanah, R. Landman, V. Joly, J. Ghosn, C. Rioux, S. Lariven, A. Gervais, FX. Lescure, S. Matheron, F. Louni, Z. Julia, S. Le GAC, C. Charpentier, D. Descamps, G. Peytavin. Paris APHP Necker Pasteur: C. Duvivier, C. Aguilar, F. Alby-Laurent, K. Amazzough, G. Benabdelmoumen, P. Bossi, G. Cessot, C. Charlier, P.H. Consigny, K. Jidar, E. Lafont, F. Lanternier, J. Leporrier, O. Lortholary, C. Louisin, J. Lourenco, P. Parize, B. Pilmis, C. Rouzaud, F. Touam. Paris APHP Pitié Salpetrière: MA. Valantin, R. Tubiana, R. Agher, S. Seang, L. Schneider, R. PaLich, C. Blanc, C. Katlama. Reims: F. Bani-Sadr, JL. Berger, Y. N’Guyen, D. Lambert, I. Kmiec, M. Hentzien, A. Brunet, J. Romaru, H. Marty, V. Brodard. Rennes: C. Arvieux, P. Tattevin, M. Revest, F. Souala, M. Baldeyrou, S. Patrat-Delon, J.M. Chapplain, F. Benezit, M. Dupont, M. Poinot, A. Maillard, C. Pronier, F. Lemaitre, C. Morlat, M. Poisson-Vannier, T. Jovelin, JP. Sinteff. St Etienne: A. Gagneux-Brunon, E. Botelho-Nevers, A. Frésard, V. Ronat, F. Lucht. Strasbourg: D. Rey, P. Fischer, M. Partisani, C. Cheneau, M. Priester, C. Mélounou, C. Bernard-Henry, E. de Mautort, S. Fafi-Kremer. Toulouse: P. Delobel, M. Alvarez, N. Biezunski, A. Debard, C. Delpierre, G. Gaube, P. Lansalot, L. Lelièvre, M. Marcel, G. Martin-Blondel, M. Piffaut, L. Porte, K. Saune. Tourcoing: O. Robineau, F. Ajana, E. Aïssi, I. Alcaraz, E. Alidjinou, V. Baclet, L. Bocket, A. Boucher, M. Digumber, T. Huleux, B. Lafon-Desmurs, A. Meybeck, M. Pradier, M. Tetart, P. Thill, N. Viget, M. Valette., CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française]-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Institut National de la Santé et de la Recherche Médicale (INSERM)-Université des Antilles et de la Guyane (UAG), and Malbec, Odile

Subjects
Microbiology (medical), Male, medicine.medical_specialty, Hepatitis C virus, [SDV]Life Sciences [q-bio], Population, men having sex with men, HIV Infections, Hepacivirus, medicine.disease_cause, Antiviral Agents, Men who have sex with men, 03 medical and health sciences, Sexual and Gender Minorities, 0302 clinical medicine, Internal medicine, medicine, Humans, 030212 general & internal medicine, Prospective Studies, Human Immunodeficiency virus, Homosexuality, Male, education, Retrospective Studies, Hepatitis, education.field_of_study, business.industry, Coinfection, Mortality rate, Incidence (epidemiology), microelimination, virus diseases, HIV, Hepatitis C, Chronic, medicine.disease, Hepatitis C, digestive system diseases, 3. Good health, [SDV] Life Sciences [q-bio], Infectious Diseases, Cohort, 030211 gastroenterology & hepatology, epidemiology, France, business
Abstract

Background The arrival of highly effective, well-tolerated, direct-acting antiviral agents (DAA) led to a dramatic decrease in hepatitis C virus (HCV) prevalence. Human immunodeficiency virus (HIV)-HCV–coinfected patients are deemed a priority population for HCV elimination, while a rise in recently acquired HCV infections in men who have sex with men (MSM) has been described. We describe the variations in HIV-HCV epidemiology in the French Dat’AIDS cohort. Methods This was a retrospective analysis of a prospective cohort of persons living with HIV (PLWH) from 2012 to 2018. We determined HCV prevalence, HCV incidence, proportion of viremic patients, treatment uptake, and mortality rate in the full cohort and by HIV risk factors. Results From 2012 to 2018, 50 861 PLWH with a known HCV status were followed up. During the period, HCV prevalence decreased from 15.4% to 13.5%. HCV prevalence among new HIV cases increased from 1.9% to 3.5% in MSM but remained stable in other groups. Recently acquired HCV incidence increased from 0.36/100 person-years to 1.25/100 person-years in MSM. The proportion of viremic patients decreased from 67.0% to 8.9%. MSM became the first group of viremic patients in 2018 (37.9%). Recently acquired hepatitis represented 59.2% of viremic MSM in 2018. DAA treatment uptake increased from 11.4% to 61.5%. More treatments were initiated in MSM in 2018 (41.2%) than in intravenous drug users (35.6%). In MSM, treatment at the acute phase represented 30.0% of treatments in 2018. Conclusions A major shift in HCV epidemiology was observed in PLWH in France from 2012 to 2018, leading to a unique situation in which the major group of HCV transmission in 2018 was MSM. Clinical Trials Registration. NCT02898987.

Published
2020
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34. Post-exposure prophylaxis completion and condom use in the context of potential sexual exposure to HIV

Author

Claudine Duvivier, André Cabié, Sylvie Bregigeon, Alain Makinson, David Rey, C Allavena, Jacques Reynes, Laurent Cotte, Isabelle Ravaux, Pierre Gantner, Les Hôptaux universitaires de Strasbourg (HUS), CHU Strasbourg, Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôtel-Dieu de Nantes, Centre d'infectiologie Necker-Pasteur [CHU Necker], Institut Pasteur [Paris] (IP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Médical de l'Institut Pasteur (CMIP), Institut Pasteur [Paris] (IP), Infection à VIH, réservoirs, diversité génétique et résistance aux antirétroviraux (ARV) (EA 7327), Université Paris Descartes - Paris 5 (UPD5), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre d'Investigation Clinique Antilles-Guyane (CIC - Antilles Guyane), Université des Antilles et de la Guyane (UAG)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Maladies infectieuses et tropicales dans la Caraïbe (MAITC EA 4537), CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de la Martinique [Fort de France]-Université des Antilles (UA), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques et émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Institut Hospitalier Universitaire Méditerranée Infection (IHU Marseille), Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Dat'AIDS Study Group: Besançon: C. Drobacheff-Thiébaut, A. Foltzer, K. Bouiller, L. Hustache-Mathieu, C. Chirouze, F. Bozon, O. Babre, P. Muret, Clermont-Ferrand: H. Laurichesse, O. Lesens, M. Vidal, N. Mrozek, C. Aumeran, O. Baud, V. Corbin, P. Letertre, S. Casanova, C. Jacomet, Guadeloupe: B. Hoen, I. Lamaury, I. Fabre, E. Curlier, R. Ouissa, K. Schepers, C. Herrmann-Storck, N. Dournon, La Roche sur Yon: D. Merrien, P. Perré, T. Guimard, O. Bollangier, S. Leautez, M. Morrier, Lyon: F. Ader, F. Biron, A. Boibieux, L. Cotte, T. Ferry, P. Miailhes, T. Perpoint, S. Roux, S. Degroodt, C. Brochier, F. Valour, C. Chidiac, Marseille (IHU): C. Dhiver, M. Saadia Mokhtari, A. Ménard, H. Tissot Dupont, C. Toméi, L. Meddeb, A.Y. Belkhir, I. Ravaux, Marseille (Ste Marguerite): S. Brégigeon, O. Zaegel-Faucher, V. Obry-Roguet, H. Laroche, M. Orticoni, M.J. Soavi, P. Geneau de Lamarlière, E. Ressiot, M.J. Ducassou, I. Jaquet, S. Galie, A. Galinier, P. Martinet, M. Landon, A.S. Ritleng, A. Ivanova, C. Debreux, C. Lions, I. Poizot-Martin, Martinique: S. Abel, R. Césaire, L. Cuzin, G. Dos Santos, L. Fagour, M. Illiaquer, F. Najioullah, D. Nguyen, M. Ouka, S. Pierre-François, J. Pasquier, M. Pircher, B. Rozé, A. Cabié, Montpellier: N. Atoui, V. Le Moing, A. Makinson, N. Meftah, C. Merle de Boever, B. Montes, A. Montoya Ferrer, J. Reynes, Nancy: M. André, L. Boyer, M.P. Bouillon, M. Delestan, T. May, Nantes: C. Allavena, C. Bernaud, E. Billaud, C. Biron, B. Bonnet, S. Bouchez, D. Boutoille, C. Brunet-Cartier, C. Deschanvres, N. Hall, T. Jovelin, P. Morineau, V. Reliquet, H. Hue, S. Sécher, M. Cavellec, A. Soria, V. Ferré, E. André-Garnier, A. Rodallec, M. Lefebvre, O. Grossi, O. Aubry, F. Raffi, Nice: P. Pugliese, S. Breaud, C. Ceppi, J. Courjon, E. Cua, J. Cottalorda, P. Dellamonica, E. Demonchy, A. De Monte, J. Durant, C. Etienne, S. Ferrando, J.G. Fuzibet, R. Garraffo, A. Joulie, K. Risso, V. Mondain, A. Naqvi, N. Oran, I. Perbost, S. Pillet, B. Prouvost-Keller, C. Pradier, S. Wehrlen-Pugliese, V. Rio, E. Rosenthal, S. Sausse, G. Zouzou, Orléans: L. Hocqueloux, T. Prazuck, C. Gubavu, A. Sève, M. Niang, C. Boulard, Paris (Bicêtre): A. Cheret, C. Goujard, Y. Quertainmont, E. Teicher, N. Lerolle, D. Vittecoq, O. Deradji, F. Fourreau, C. Pallier, A. Barrail-Tran, Paris (Bichat): R. Landman, V. Joly, C. Rioux, S. Lariven, A. Gervais, F.X. Lescure, S. Matheron, F. Louni, C. Godard, Z. Julia, M. Chansombat, D. Rahli, C. Mackoumbou-Nkouka, C. Charpentier, D. Descamps, G. Peytavin, Y. Yazdanpanah, Paris (Pasteur-Necker): P.H. Consigny, G. Cessot, P. Bossi, J. Goesch, J. Benabdelmoumen, F. Lanternier, C. Charlier, K. Amazzough, B. Henry, B. Pilmis, C. Rouzaud, M. Morgand, F. Touam, C. Louisin, C. Duvivier, O. Lortholary, R. Guery, F. Danion, J. Lourenco, P. Parize, M. Launay, V. Avettand-Fenoel, Paris (Pitié): M.A. Valantin, F. Caby, R. Tubiana, R. Agher, S. Seang, L. Schneider, R. Palich, C. Blanc, C. Katlama, Reims: J.L. Berger, Y. N'Guyen, D. Lambert, D. Lebrun, I. Kmiec, M. Hentzien, V. Brodard, F. Bani-Sadr, Saint-Etienne: E. Botelho-Nevers, A. Gagneux-Brunon, A. Frésard, F. Lucht, Strasbourg: P. Fischer, M. Partisani, C. Cheneau, M. Priester, M.L. Batard, C. Bernard-Henry, E. de Mautort, P. Gantner, D. Rey, Toulouse: M. Alvarez, N. Biezunski, A. Debard, C. Delpierre, P. Lansalot, L. Lelièvre, G. Martin-Blondel, M. Piffaut, L. Porte, K. Saune, P. Delobel, and Tourcoing: F. Ajana, I. Alcaraz, V. Baclet, A. Boucher, P. Choisy, T. Huleux, B. Lafon-Desmurs, H. Melliez, A. Meybeck, A. Pasquet, M. Pradier, O. Robineau, N. Viget, M. Valette.

Subjects
0301 basic medicine, Male, HIV Infections, law.invention, Men who have sex with men, Condoms, 0302 clinical medicine, MESH: Tenofovir, law, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Emtricitabine, MESH: Sexual Partners, Emtricitabine, Pharmacology (medical), 030212 general & internal medicine, Condom use, Health Policy, MESH: HIV Infections, Infectious Diseases, Sexual Partners, Cohort, cardiovascular system, Female, France, Post-Exposure Prophylaxis, circulatory and respiratory physiology, medicine.drug, Adult, medicine.medical_specialty, Unprotected Sexual Intercourse, MESH: Unsafe Sex, Treatment discontinuation, education, Context (language use), MESH: Multivariate Analysis, Medication Adherence, MESH: Homosexuality, Male, 03 medical and health sciences, MESH: Condoms, Condom, Internal medicine, medicine, Humans, Homosexuality, Male, Tenofovir, Retrospective Studies, MESH: Humans, Unsafe Sex, business.industry, HIV, MESH: Adult, MESH: Retrospective Studies, Odds ratio, MESH: Medication Adherence, 030112 virology, MESH: Male, Discontinuation, Sexual exposure, MESH: France, Multivariate Analysis, business, MESH: Female, MESH: Post-Exposure Prophylaxis
Abstract

International audience; ObjectivesPost-exposure prophylaxis (PEP) care remains a challenge for individuals with potential sexual exposure to HIV in terms of PEP completion and ongoing risk behaviours.MethodsA retrospective analysis was carried out on data from the French Dat’AIDS prevention cohort (NCT03795376) for individuals evaluated for PEP between 2004 and 2017. A multivariable analysis was performed of predictors of both PEP completion and condom use [odds ratios (ORs)] and their associated probabilities (P, with P > 95% being clinically relevant).ResultsOverall, 29 060 sexual exposures to HIV were evaluated for PEP [36% in men who have sex with men (MSM) and 64% in heterosexuals]. Overall, 12 different PEP regimens were offered in 19 240 cases (46%). Tenofovir disoproxil fumarate (TDF)/emtricitabine (FTC) was the preferred backbone (n = 14 304; 74%). We observed a shift from boosted protease inhibitor-based regimens to nonnucleoside reverse transcriptase inhibitor- or integrase inhibitor-based regimens in recent years. Overall, 20% of PEP prescriptions were prematurely discontinued. Older age, MSM, intercourse with a sex worker, rape and intercourse with a known HIV-infected source patient were factors associated with increased rates of PEP completion (OR > 1; P > 98%). None of the 12 PEP regimens was associated with premature discontinuation. We also found 12 774 cases of unprotected sexual intercourse (48%). Condom use decreased (OR < 1; P > 99%) with the year of exposure, and was lower in MSM and rape victims. Condom use increased (OR > 1, P > 99%) with age, and was higher in those who had intercourse with a sex worker or with a female partner and in those with knowledge of the partner’s HIV status.ConclusionsWe provide new insights into how rates of condom use and PEP completion might be improved in those receiving PEP by targeting certain groups of individuals for interventions. In particular, youth and MSM at risk should be linked in a prevention-to-care continuum.

Published
2020
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35. Kaposi sarcoma among people living with HIV in the French DAT'AIDS cohort between 2010 and 2015

Author

Obry-Roguet, Véronique, Duvivier, Claudine, Lions, Caroline, Huleux, Thomas, Jacomet, Christine, Ferry, Tristan, Cheret, Antoine, Allavena, Clotilde, Bani-Sadr, Firouzé, Palich, Romain, Cabié, André, Pugliese, Pascal, Delobel, Pierre, Lamaury, Isabelle, Hustache-Mathieu, Laurent, Bregigeon, Sylvie, Makinson, Alain, Rey, David, Poizot-Martin, Isabelle, Hustache‐Mathieu, Laurent, Drobacheff‐Thiébaut, C., Foltzer, A., Bouiller, K., Hustache‐ Mathieu, L., Chirouze, C., LEPILLER, Q., Bozon, F., Babre, O, Brunel, A.S., Muret, P., Laurichesse, H., Lesens, O., Vidal, M., Mrozek, N., Aumeran, C., Baud, O., Corbin, V., Letertre‐Gibert, P., Casanova, S., Prouteau, J., Fabre, I., Curlier, E., Ouissa, R., Herrmann‐Storck, C., Tressieres, B., Bonijoly, T., Receveur, M.C., Boulard, F., Daniel, C., Clavel, C., Merrien, D., Perré, P., Guimard, T., Bollangier, O., Leautez, S., Morrier, M., Laine, L., Ader, F., Becker, A., Biron, F., Boibieux, A., Cotte, L., Miailhes, P., Perpoint, T., Roux, S., Triffault‐Fillit, C., Degroodt, S., Brochier, C., Valour, F., Chidiac, C., Ménard, A., Belkhir, A.Y., Colson, P., Dhiver, C., Madrid, A., Martin‐Degioanni, M., Meddeb, L., Mokhtari, M., Motte, A., Raoux, A., Ravaux, I., Tamalet, C., Tomei, C., Tissot Dupont, H., Zaegel‐Faucher, O., Obry‐Roguet, Véronique, Laroche, H, Orticoni, M., Soavi, M.J., Geneau de Lamarlière, P, Ressiot, E, Ducassou, M.J., Jaquet, I., Galie, S., Galinier, A., Martinet, P., Landon, M., Ritleng, A.S., Ivanova, A., Debreux, C., Poizot‐Martin, I., Abel, S., Cabras, O., Cuzin, L., Guitteaud, K., Illiaquer, M., Pierre‐François, S., Osei, L., Pasquier, J., Rome, K., Sidani, E., Turmel, JM, Varache, C., Atoui, N., Bistoquet, M., Delaporte, E., Le Moing, V., Meftah, N., Merle de Boever, C., Montes, B., Montoya Ferrer, A., Tuaillon, E., Reynes, J., André, M., Boyer, L., Bouillon, MP., Delestan, M., Rabaud, C., May, T., Hoen, B., Bernaud, C., Billaud, E., Biron, C., Bonnet, B., Bouchez, S., Boutoille, D., Brunet‐Cartier, C., Deschanvres, C., Hall, N., Morineau, P., Reliquet, V., Sécher, S., Cavellec, M., Soria, A., Paredes, E., Ferre, V., André‐Garnier, E., Rodallec, A., Lefebvre, M., Grossi, O., Aubry, O., Raffi, F., Breaud, S., Ceppi, C., Chirio, D., Cua, E., Dellamonica, P., Demonchy, E., De Monte, A., Durant, J., Etienne, C., Ferrando, S., Garraffo, R., Michelangeli, C., Mondain, V., Naqvi, A., Oran, N., Perbost, I., Pillet, S., Pradier, C., Prouvost‐Keller, B., Risso, K., Rio, V., Roger, PM., Rosenthal, E., Sausse, S., Touitou, I., Wehrlen‐Pugliese, S., Zouzou, G., Hocqueloux, L., Prazuck, T., Gubavu, C., Sève, A., Maka, A., Boulard, C., Thomas, G., Lerolle, N., Landman, R., Joly, V., Ghosn, J., Rioux, C., Lariven, S., Gervais, A., Lescure, F.X., Matheron, S., Louni, F., Julia, Z., Mackoumbou‐Nkouka, C., Le Gac, S., Charpentier, C., Descamps, D., Peytavin, G., Yazdanpanah, Y., Amazzough, K., Benabdelmoumen, G., Bossi, P., Cessot, G., Charlier, C., Consigny, P.H., Danion, F., Dureault, A., Goesch, J., Guery, R., Henry, B., Jidar, K., Lanternier, F., Loubet, P., Lortholary, O., Louisin, C., Lourenco, J., Parize, P., Pilmis, B., Touam, F, Valantin, M.A., Tubiana, R., Agher, R, Seang, S., Schneider, L., Blanc, C., Katlama, C., Berger, J.L., N'guyen, Y., Lambert, D., Kmiec, I., Hentzien, M., Brunet, A., Brodard, V., Bani‐Sadr, Firouze, Tattevin, P., Revest, M., Souala, F., Baldeyrou, M., Patrat‐Delon, S., Chapplain, J.M., Bénézit, F., Dupont, M., Poinot, M., Maillard, A., Pronier, C., Lemaitre, F., Guennoun, C., Poisson‐Vanier, M., Jovelin, T., Sinteff, J.P., Arvieux, C., Botelho‐Nevers, E., Gagneux‐Brunon, A., Frésard, Anne, Ronat, V., Lucht, F., Fischer, P., Partisani, M., Cheneau, C., Priester, M, Batard, ML, Bernard‐Henry, C, de Mautort, E, Fafi‐Kremer, S., Alvarez, M., Biezunski, N., Debard, A., Delpierre, C., Lansalot, P., Lelievre, L., Martin‐Blondel, G., Piffaut, M., Porte, L., Saune, K., Ajana, F., Aïssi, E., Alcaraz, I., Baclet, V., Bocket, L., Boucher, A., Choisy, P., Lafon‐Desmurs, B., Meybeck, A., Pradier, M., Robineau, O., Viget, N., Valette, M., Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Centre d'infectiologie Necker-Pasteur [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Sciences Economiques et Sociales de la Santé & Traitement de l'Information Médicale (SESSTIM - U1252 INSERM - Aix Marseille Univ - UMR 259 IRD), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Tourcoing, Département des Maladies Infectieuses et Tropicales [CHU Gabriel-Montpied, Clermont-Ferrand], CHU Gabriel Montpied [Clermont-Ferrand], Pathogénie des Staphylocoques – Staphylococcal Pathogenesis, Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Services des maladies infectieuses [CH Turcoing], Centre Hospitalier de Tourcoing, Service de maladies infectieuses et tropicales [Nantes], Université de Nantes (UN)-Hôtel-Dieu-Centre hospitalier universitaire de Nantes (CHU Nantes), Centre Hospitalier Universitaire de Reims (CHU Reims), Alliance for International medical Action (ALIMA), Service de Maladies Infectieuses et Tropicales [Fort-de-France, Martinique], CHU de la Martinique [Fort de France]-Hôpital Pierre Zobda-Quitman [CHU de la Martinique], CHU de la Martinique [Fort de France]-Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], Service de Maladies Infectieuses [Nice], Centre de Physiopathologie Toulouse Purpan ex IFR 30 et IFR 150 (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), CHU Pointe-à-Pitre/Abymes [Guadeloupe], service de maladies infectieuses CHU J Minjoz Besancon, Hôpital Jean Minjoz, Service d'Immuno-hématologie clinique [Hôpital Sainte Marguerite - APHM], Assistance Publique - Hôpitaux de Marseille (APHM)-Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Universtié Yaoundé 1 [Cameroun]-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), Laboratoire d'Ingénierie Circulation Transport (LICIT), Institut Français des Sciences et Technologies des Transports, de l'Aménagement et des Réseaux (IFSTTAR)-École Nationale des Travaux Publics de l'État (ENTPE)-Université de Lyon, Laboratoire Chrono-environnement - CNRS - UFC (UMR 6249) (LCE), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre Hospitalier Universitaire de Besançon (CHU Besançon), Université libre de Bruxelles (ULB), Hôpital Gabriel Montpied, Service des Maladies Infectieuses et Tropicales, Centre Hospitalier Universitaire de Clermont-Ferrand, Laboratoire Microorganismes : Génome et Environnement - Clermont Auvergne (LMGE), Université Clermont Auvergne (UCA)-Centre National de la Recherche Scientifique (CNRS), CHU Gabriel Montpied (CHU), CHU Clermont-Ferrand, CCLIN Sud-Est – Centre de Coordination de la Lutte contre les Infections Nosocomiales Sud-Est, Montpellier Research in Management (MRM), Université Montpellier 1 (UM1)-Université Paul-Valéry - Montpellier 3 (UPVM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Perpignan Via Domitia (UPVD)-Groupe Sup de Co Montpellier (GSCM) - Montpellier Business School-Université de Montpellier (UM), Laboratoire Traitement et Communication de l'Information (LTCI), Télécom ParisTech-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS), Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 (P3CELL), Université de Reims Champagne-Ardenne (URCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hosp Civils Lyon, Serv Malad Infect, Lyon, France, Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Equipe 15, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon], Service de Maladies Infectieuses et Tropicales [Hôpital de la Croix-Rousse - HCL], Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Institut Hospitalier Universitaire Méditerranée Infection (IHU AMU), Microbes évolution phylogénie et infections (MEPHI), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Neurobiologie, plasticité tissulaire et métabolisme énergétique (NPTME), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), CECIL, Space Research Institute of the Russian Academy of Sciences (IKI), Russian Academy of Sciences [Moscow] (RAS), Système membranaires, photobiologie, stress et détoxication (SMPSD), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre IRD de Montpellier (IRD), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre d'études et de recherche sur les services de santé et la qualité de vie (CEReSS), Aix Marseille Université (AMU), Service des Maladies Infectieuses et Tropicales [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Bell Labs (BELL), Lucent Technologies, Service des maladies infectieuses et tropicales, Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Hôpital Saint-Jacques, Centre hospitalier universitaire de Nantes (CHU Nantes), Unité de Nutrition Humaine - Clermont Auvergne (UNH), Institut National de la Recherche Agronomique (INRA)-Université Clermont Auvergne (UCA), Service des maladies infectieuses et tropicales [CHU Nantes], Plant Biomechanics Group, Botanischer Garten, Albert-Ludwigs-Universität Freiburg, Service de virologie [CHU Nantes], Centre de recherche en neurosciences de Lyon (CRNL), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service des maladies infectieuses, Centre Hospitalier Universitaire de Nice (CHU Nice)-University Hospital, CHU Nice [Cimiez], Hôpital Cimiez [Nice] (CHU), Centre Hospitalier Universitaire de Nice (CHU Nice), Hopital l'Archet, Centre d'Information et de Soins de I'Immunodéficience Humaine (CISIH). Hôpital l'Archet 1, Hôpital l'Archet, Public Health Department, Hôpital de l'Archet, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse, Infectious Diseases Department, Université Montpellier 1 (UM1), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Centre Régional de recherche et de Formation à la prise en charge Clinique de Fann (CRCF), CHNU Fann, Registre EPIMAD, CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-CHU Amiens-Picardie-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre d'Etudes Lasers Intenses et Applications (CELIA), Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université de Bordeaux (UB), Pharmacie de l'Hôpital Bichat, UMR CNRS 8179, Université de Lille, Sciences et Technologies-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5), Service de rhumatologie [Strasbourg], CHU Strasbourg-Hôpital de Hautepierre [Strasbourg], Pathogénie des infections systémiques (UMR_S 570), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service des maladies infectieuses [CHU Pitié-Salêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université, Service des maladies infectieuses et tropicales [CHU Pitié-Salpêtrière], Laboratoire d'aérologie (LA), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Observatoire Midi-Pyrénées (OMP), Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Université Fédérale Toulouse Midi-Pyrénées-Centre National d'Études Spatiales [Toulouse] (CNES)-Météo France-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Météo France-Centre National de la Recherche Scientifique (CNRS), McGill University = Université McGill [Montréal, Canada], Service des maladies infectieuses et réanimation médicale, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Hôpital Pontchaillou, Centre d'Investigation Clinique [Rennes] (CIC), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Hôpital Pontchaillou-Institut National de la Santé et de la Recherche Médicale (INSERM), Les Hôpitaux Universitaires de Strasbourg (HUS), Service de pneumologie, Hôpital Pontchaillou-CHU Pontchaillou [Rennes], CHU Pontchaillou [Rennes], SEV, Groupe d'Etudes et de Contrôle des Variétés et des Semences (GEVES), Service de virologie [Rennes], Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-CHU Pontchaillou [Rennes], Centre Hospitalier Universitaire de Saint-Etienne (CHU de Saint-Etienne), University Hospital and University Jean Monnet, Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Génomique métabolique (UMR 8030), Genoscope - Centre national de séquençage [Evry] (GENOSCOPE), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Université d'Évry-Val-d'Essonne (UEVE)-Centre National de la Recherche Scientifique (CNRS), Virologie et pathogenèse virale (VPV), Institut Pasteur [Paris] (IP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Institut Pasteur [Paris] (IP), Centre Hospitalier Gustave Dron [Tourcoing], Infection à VIH, réservoirs, diversité génétique et résistance aux antirétroviraux (ARV) (EA 7327), AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Département d'Hématologie Clinique [CHU Nantes] (Hôtel-Dieu), Hôtel-Dieu de Nantes-Centre hospitalier universitaire de Nantes (CHU Nantes), Hôpital Robert Debré, Hôpital Robert Debré-Centre Hospitalier Universitaire de Reims (CHU Reims), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], Maladies infectieuses et tropicales dans la Caraïbe (MAITC EA 4537), CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de la Martinique [Fort de France]-Université des Antilles (UA), Centre d'Investigation Clinique Antilles-Guyane (CIC - Antilles Guyane), Université des Antilles et de la Guyane (UAG)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Centre Hospitalier Universitaire de Saint-Etienne [CHU Saint-Etienne] (CHU ST-E), Centre de Physiopathologie Toulouse Purpan (CPTP), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service Maladies infectieuses et tropicales [CHU Toulouse], Pôle Inflammation, infection, immunologie et loco-moteur [CHU Toulouse] (Pôle I3LM Toulouse), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Dermatologie et Maladies infectieuses [Pointe-à-Pitre], CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Centre de Gestion du Risque Infectieux Nosocomial [Pointe-à-Pitre] (CGRIN), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Infectious and Tropical Diseases Department [Montpellier], Institut de Recherche pour le Développement (IRD)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM), Dat'AIDS study group: C Drobacheff-Thiébaut, A Foltzer, K Bouiller, C Chirouze, Q Lepiller, F Bozon, O Babre, A S Brunel, P Muret, H Laurichesse, O Lesens, M Vidal, N Mrozek, C Aumeran, O Baud, V Corbin, P Letertre-Gibert, S Casanova, J Prouteau, I Fabre, E Curlier, R Ouissa, C Herrmann-Storck, B Tressieres, T Bonijoly, M C Receveur, F Boulard, C Daniel, C Clavel, D Merrien, P Perré, T Guimard, O Bollangier, S Leautez, M Morrier, L Laine, F Ader, A Becker, F Biron, A Boibieux, L Cotte, P Miailhes, T Perpoint, S Roux, C Triffault-Fillit, S Degroodt, C Brochier, F Valour, C Chidiac, A Ménard, A Y Belkhir, P Colson, C Dhiver, A Madrid, M Martin-Degioanni, L Meddeb, M Mokhtari, A Motte, A Raoux, I Ravaux, C Tamalet, C Toméi, H Tissot Dupont, O Zaegel-Faucher, H Laroche, M Orticoni, M J Soavi, P Geneau de Lamarlière, E Ressiot, M J Ducassou, I Jaquet, S Galie, A Galinier, P Martinet, M Landon, A S Ritleng, A Ivanova, C Debreux, S Abel, O Cabras, L Cuzin, K Guitteaud, M Illiaquer, S Pierre-François, L Osei, J Pasquier, K Rome, E Sidani, J M Turmel, C Varache, N Atoui, M Bistoquet, E Delaporte, V Le Moing, N Meftah, C Merle de Boever, B Montes, A Montoya Ferrer, E Tuaillon, J Reynes, M André, L Boyer, M P Bouillon, M Delestan, C Rabaud, T May, B Hoen, C Bernaud, E Billaud, C Biron, B Bonnet, S Bouchez, D Boutoille, C Brunet-Cartier, C Deschanvres, N Hall, T Jovelin, P Morineau, V Reliquet, S Sécher, M Cavellec, A Soria, E Paredes, V Ferré, E André-Garnier, A Rodallec, M Lefebvre, O Grossi, O Aubry, F Raffi, S Breaud, C Ceppi, D Chirio, E Cua, P Dellamonica, E Demonchy, A De Monte, J Durant, C Etienne, S Ferrando, R Garraffo, C Michelangeli, V Mondain, A Naqvi, N Oran, I Perbost, S Pillet, C Pradier, B Prouvost-Keller, K Risso, V Rio, P M Roger, E Rosenthal, S Sausse, I Touitou, S Wehrlen-Pugliese, G Zouzou, L Hocqueloux, T Prazuck, C Gubavu, A Sève, A Maka, C Boulard, G Thomas, C Goujard, Y Quertainmont, E Teicher, N Lerolle, O Deradji, A Barrail-Tran, R Landman, V Joly, J Ghosn, C Rioux, S Lariven, A Gervais, F X Lescure, S Matheron, F Louni, Z Julia, C Mackoumbou-Nkouka, S Le Gac, C Charpentier, D Descamps, G Peytavin, Y Yazdanpanah, K Amazzough, G Benabdelmoumen, P Bossi, G Cessot, C Charlier, P H Consigny, F Danion, A Dureault, J Goesch, R Guery, B Henry, K Jidar, F Lanternier, P Loubet, O Lortholary, C Louisin, J Lourenco, P Parize, B Pilmis, F Touam, M A Valantin, R Tubiana, R Agher, S Seang, L Schneider, C Blanc, C Katlama, J L Berger, Y N'Guyen, D Lambert, I Kmiec, M Hentzien, A Brunet, V Brodard, P Tattevin, M Revest, F Souala, M Baldeyrou, S Patrat-Delon, J M Chapplain, F Benezit, M Dupont, M Poinot, A Maillard, C Pronier, F Lemaitre, C Guennoun, M Poisson-Vanier, T Jovelin, J P Sinteff, C Arvieux, E Botelho-Nevers, A Gagneux-Brunon, A Frésard, V Ronat, F Lucht, P Fischer, M Partisani, C Cheneau, M Priester, M L Batard, C Bernard-Henry, E de Mautort, S Fafi-Kremer, M Alvarez, N Biezunski, A Debard, C Delpierre, P Lansalot, L Lelièvre, G Martin-Blondel, M Piffaut, L Porte, K Saune, F Ajana, E Aïssi, I Alcaraz, V Baclet, L Bocket, A Boucher, P Choisy, B Lafon-Desmurs, A Meybeck, M Pradier, O Robineau, N Viget, M Valette., Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut Pasteur [Paris], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut Pasteur [Paris], Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU), Institut National de la Recherche Agronomique (INRA)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020]), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-CHU Amiens-Picardie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université d'Évry-Val-d'Essonne (UEVE)-Centre National de la Recherche Scientifique (CNRS), Recherches Translationnelles sur le VIH et les maladies infectieuses (TransVIHMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Recherche pour le Développement (IRD)-Université Montpellier 1 (UM1)-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Universtié Yaoundé 1 [Cameroun]-Université de Montpellier (UM), Université Paul-Valéry - Montpellier 3 (UPVM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Perpignan Via Domitia (UPVD)-Université Montpellier 1 (UM1)-Groupe Sup de Co Montpellier (GSCM) - Montpellier Business School-Université de Montpellier (UM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Observatoire Midi-Pyrénées (OMP), Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Université Fédérale Toulouse Midi-Pyrénées-Centre National d'Études Spatiales [Toulouse] (CNES)-Météo France-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Université Fédérale Toulouse Midi-Pyrénées-Centre National d'Études Spatiales [Toulouse] (CNES)-Météo France-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon, and Dupuis, Christine

Subjects
0301 basic medicine, Pediatrics, medicine.medical_specialty, MESH: Sarcoma, Kaposi* / epidemiology, [SDV]Life Sciences [q-bio], 030106 microbiology, HIV Infections, Dermatology, Skin Infectiology, Venereology and Sexual Health, 03 medical and health sciences, 0302 clinical medicine, Acquired immunodeficiency syndrome (AIDS), medicine, Humans, MESH: HIV Infections* / complications, 030212 general & internal medicine, Sarcoma, Kaposi, Retrospective Studies, Response rate (survey), MESH: Acquired Immunodeficiency Syndrome, MESH: Herpesvirus 8, Human, Acquired Immunodeficiency Syndrome, MESH: Humans, business.industry, Kaposi sarcoma, HIV, Retrospective cohort study, MESH: Retrospective Studies, MESH: HIV Infections* / drug therapy, medicine.disease, 3. Good health, [SDV] Life Sciences [q-bio], medical dermatology, Regimen, Infectious Diseases, Clinical research, clinical research, Herpesvirus 8, Human, Cohort, oncology, Original Article, Sarcoma, business, Viral load, MESH: HIV Infections* / epidemiology, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Background - Although antiretroviral therapy (ART) has reduced the risk of Kaposi sarcoma (KS), KS cases still occur in HIV-infected people. Objective - To describe all KS cases observed between 2010 and 2015 in a country with high ART coverage. Methods - Retrospective study using longitudinal data from 44 642 patients in the French Dat'AIDS multicenter cohort. Patients' characteristics were described at KS diagnosis according to ART exposure and to HIV-plasma viral load (HIV-pVL) (≤50 or >50) copies/mL. Results - Among the 209 KS cases diagnosed during the study period, 33.2% occurred in ART naïve patients, 17.3% in ART-experienced patients and 49.5% in patients on ART, of whom 23% for more than 6 months. Among these patients, 24 (11.5%) had HIV-pVL ≤50 cp/mL, and 16 (66%) were treated with a boosted-PI-based regimen. The distribution of KS localization did not differ by ART status nor by year of diagnosis. Limitations - Data on human herpesvirus 8, treatment modalities for KS and response rate were not collected. Conclusion - Half of KS cases observed in the study period occurred in patients not on ART, reflecting the persistence of late HIV diagnosis. Factors associated with KS in patients on ART with HIV-pVL ≤50 cp/mL remain to be explored.

Published
2020
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36. Prostate Cancer Patients' Perceptions Regarding the Relevance of a Digital Rectal Examination During Their Follow-Up After Radiation Therapy.

Author

Klein C, Bosc N, Marty S, Calen L, Debard C, Robert G, and Haaser T

Subjects
Humans, Male, Aged, Middle Aged, Surveys and Questionnaires, Follow-Up Studies, Aged, 80 and over, Perception, Digital Rectal Examination psychology, Prostatic Neoplasms radiotherapy, Prostatic Neoplasms psychology
Abstract

Background: Prostate cancer is an example of the undervaluation of clinical examinations in care of patients. After external radiotherapy, cancer recurrence is primarily determined biologically by measuring prostate-specific antigen concentration. Consequently, there is no systematic requirement for the digital rectal examination (DRE). Nevertheless, research has shown that patients attach both practical and symbolic significance to being examined by their physicians. This study aimed to assess how patients perceive DRE omission after prostate cancer radiation therapy., Materials and Methods: We conducted a survey of 107 men in remission after radiotherapy for prostate cancer in the Radiotherapy Oncology Department of Bordeaux University Hospital, France. The aim of the survey was to assess the significance that patients place on undergoing a DRE as part of their follow-up care, both from a practical perspective (medical relevance) and a symbolic perspective (influence on the perception of the treating radiation oncologist)., Results: Despite receiving information on the lack of relevance of DRE during follow-up, 40 of the 100 respondents still perceived a practical benefit of undergoing DRE (pragmatic dimension). On a symbolic level, many patients associated the performance of DRE by their radiotherapy oncologist with impressions of competence, concern for their health and concern for them personally (61%, 63% and 64%, respectively). Although the correlations between the pragmatic and symbolic dimensions were significant, more than one-third of patients who understood the lack of clinical relevance of DRE still attributed symbolic value to it., Conclusions: A positive perception of DRE persists among patients, mainly at the symbolic level, including a proportion of patients who understand the low clinical utility of DRE. Importantly, the persistence of these perceptions regarding DRE should not be misconstrued as justification for performing pelvic examinations without clear clinical reasons., (© 2025 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.)

Published
2025
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37. Evaluation of Three Devices for the Isolation of the Stromal Vascular Fraction from Adipose Tissue and for ASC Culture: A Comparative Study.

Author

Rodriguez J, Pratta AS, Abbassi N, Fabre H, Rodriguez F, Debard C, Adobati J, Boucher F, Mallein-Gerin F, Auxenfans C, Damour O, and Mojallal A

Abstract

Adipose-derived stem/stromal cells (ASCs) reside in the stromal vascular fraction (SVF) of adipose tissue (AT) and can be easily isolated. However, extraction of the SVF from lipoaspirate is a critical step in generating ASC, and semiautomated devices have been developed to enhance the efficacy and reproducibility of the outcomes and to decrease manipulation and contamination. In this study, we compared the reference method used in our lab for SVF isolation from lipoaspirate, with three medical devices: GID SVF-1™, Puregraft™, and Stem.pras®. Cell yield and their viability were evaluated as well as their phenotype with flow cytometry. Further on, we determined their proliferative potential using population doublings (PD), PD time (PDT), and clonogenicity assay (CFU-F). Finally, we checked their genetic stability using RT-qPCR for TERT mRNA assay and karyotyping as well as their multilineage potential including adipogenic, chondrogenic, and osteogenic differentiation. Our results demonstrate that all the devices allow the production of SVF cells with consistent yield and viability, in less time than the reference method. Expanded cells from the four methods showed no significant differences in terms of phenotype, proliferation capabilities, differentiation abilities, and genetic stability., Competing Interests: The authors declare that they have no competing interests.

Published
2017
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38. Saturated and Unsaturated Fatty Acids Differently Modulate Colonic Goblet Cells In Vitro and in Rat Pups.

Author

Benoit B, Bruno J, Kayal F, Estienne M, Debard C, Ducroc R, and Plaisancié P

Subjects
Animal Feed analysis, Animals, Diet, Dietary Fats administration & dosage, Fatty Acids administration & dosage, Fatty Acids, Unsaturated administration & dosage, Goblet Cells metabolism, HT29 Cells, Humans, Mucin 5AC genetics, Mucin 5AC metabolism, Mucin-2 genetics, Mucin-2 metabolism, Plant Oils administration & dosage, Plant Oils chemistry, Rats, Rats, Wistar, Colon cytology, Dietary Fats pharmacology, Fatty Acids pharmacology, Fatty Acids, Unsaturated pharmacology, Goblet Cells drug effects
Abstract

Background: High-fat diets induce intestinal barrier alterations and promote intestinal diseases. Little is known about the effects of long-chain fatty acids (LCFAs) on mucin 2 (MUC2) production by goblet cells, which are crucial for intestinal protection., Objective: We investigated the effects of LCFAs on the differentiation of colonic goblet cells, MUC2 expression, and colonic barrier function., Methods: Upon reaching confluence, human colonic mucus-secreting HT29-MTX cells were stimulated (21 d) with a saturated LCFA (palmitic or stearic acid), a monounsaturated LCFA (oleic acid), or a polyunsaturated LCFA (linoleic, γ-linolenic, α-linolenic, or eicosapentaenoic acid). In addition, rat pups underwent oral administration of oil (palm, rapeseed, or sunflower oil) or water (10 μL/g body weight, postnatal days 10-15). Subsequently, colon goblet cells were studied by Western blotting, reverse transcriptase-quantitative polymerase chain reaction, and immunohistochemistry and colonic transmucosal electrical resistance was measured by using Ussing chambers., Results: In vitro, palmitic acid enhanced MUC2 production (140% of control) and hepatocyte nuclear factor 4α expression, whereas oleic, linoleic, γ-linolenic, α-linolenic, and eicosapentaenoic acids reduced MUC2 expression (at least -50% of control). All unsaturated LCFAs decreased the expression of human atonal homolog 1, a transcription factor controlling goblet cell differentiation (at least -31% vs. control). In vivo, rats fed palm oil had higher palmitic acid concentrations (3-fold) in their colonic contents and increased mucus granule surfaces in their goblet cells (>2-fold) than did all other groups. Palm oil also increased colonic transmucosal electrical resistance (245% of control), yet had no effect on occludin and zonula occludens-1 expression. In contrast, sunflower and rapeseed oils decreased goblet cell number when compared with control (at least -10%) and palm oil (at least -14%) groups., Conclusions: Palm oil in rat pups and palmitic acid in HT29-MTX cells increase the production of MUC2 and strengthen the intestinal barrier. In contrast, unsaturated LCFAs decrease MUC2 expression. These data should be taken into account in the context of preventive or therapeutic nutritional programs., (© 2015 American Society for Nutrition.)

Published
2015
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39. Human monocyte-derived dendritic cells turn into foamy dendritic cells with IL-17A.

Author

Salvatore G, Bernoud-Hubac N, Bissay N, Debard C, Daira P, Meugnier E, Proamer F, Hanau D, Vidal H, Aricò M, Delprat C, and Mahtouk K

Subjects
Atherosclerosis immunology, Atherosclerosis pathology, Cell Differentiation genetics, Cell Proliferation genetics, Dendritic Cells immunology, Foam Cells metabolism, Gene Expression Regulation, Humans, Interleukin-17 genetics, Interleukin-17 immunology, Lipid Droplets immunology, Lipid Droplets metabolism, Lipid Metabolism immunology, Liver X Receptors, Macrophages immunology, Macrophages metabolism, Monocytes immunology, Monocytes metabolism, Orphan Nuclear Receptors biosynthesis, Orphan Nuclear Receptors metabolism, T-Lymphocytes immunology, T-Lymphocytes metabolism, Atherosclerosis metabolism, Dendritic Cells metabolism, Fatty Acids metabolism, Interleukin-17 metabolism
Abstract

Interleukin 17A (IL-17A) is a proinflammatory cytokine involved in the pathogenesis of chronic inflammatory diseases. In the field of immunometabolism, we have studied the impact of IL-17A on the lipid metabolism of human in vitro-generated monocyte-derived dendritic cells (DCs). Microarrays and lipidomic analysis revealed an intense remodeling of lipid metabolism induced by IL-17A in DCs. IL-17A increased 2-12 times the amounts of phospholipids, cholesterol, triglycerides, and cholesteryl esters in DCs. Palmitic (16:0), stearic (18:0), and oleic (18:ln-9c) acid were the main fatty acid chains present in DCs. They were strongly increased in response to IL-17A while their relative proportion remained unchanged. Capture of extracellular lipids was the major mechanism of lipid droplet accumulation, visualized by electron microscopy and Oil Red O staining. Besides this foamy phenotype, IL-17A induced a mixed macrophage-DC phenotype and expression of the nuclear receptor NR1H3/liver X receptor-α, previously identified in the context of atherosclerosis as the master regulator of cholesterol homeostasis in macrophages. These IL-17A-treated DCs were as competent as untreated DCs to stimulate allogeneic naive T-cell proliferation. Following this first characterization of lipid-rich DCs, we propose to call these IL-17A-dependent cells "foamy DCs" and discuss the possible existence of foamy DCs in atherosclerosis, a metabolic and inflammatory disorder involving IL-17A., (Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc.)

Published
2015
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40. Insulin resistance is associated with MCP1-mediated macrophage accumulation in skeletal muscle in mice and humans.

Author

Patsouris D, Cao JJ, Vial G, Bravard A, Lefai E, Durand A, Durand C, Chauvin MA, Laugerette F, Debard C, Michalski MC, Laville M, Vidal H, and Rieusset J

Subjects
Animals, Cell Line, Cell Movement, Diabetes Mellitus, Type 2 immunology, Diabetes Mellitus, Type 2 metabolism, Humans, Male, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Muscle, Skeletal metabolism, Muscle, Skeletal pathology, Myositis metabolism, Chemokine CCL2 physiology, Insulin Resistance immunology, Macrophages immunology, Muscle, Skeletal immunology, Myositis immunology
Abstract

Inflammation is now recognized as a major factor contributing to type 2 diabetes (T2D). However, while the mechanisms and consequences associated with white adipose tissue inflammation are well described, very little is known concerning the situation in skeletal muscle. The aim of this study was to investigate, in vitro and in vivo, how skeletal muscle inflammation develops and how in turn it modulates local and systemic insulin sensitivity in different mice models of T2D and in humans, focusing on the role of the chemokine MCP1. Here, we found that skeletal muscle inflammation and macrophage markers are increased and associated with insulin resistance in mice models and humans. In addition, we demonstrated that intra-muscular TNFα expression is exclusively restricted to the population of intramuscular leukocytes and that the chemokine MCP1 was associated with skeletal muscle inflammatory markers in these models. Furthermore, we demonstrated that exposure of C2C12 myotubes to palmitate elevated the production of the chemokine MCP1 and that the muscle-specific overexpression of MCP1 in transgenic mice induced the local recruitment of macrophages and altered local insulin sensitivity. Overall our study demonstrates that skeletal muscle inflammation is clearly increased in the context of T2D in each one of the models we investigated, which is likely consecutive to the lipotoxic environment generated by peripheral insulin resistance, further increasing MCP1 expression in muscle. Consequently, our results suggest that MCP1-mediated skeletal muscle macrophages recruitment plays a role in the etiology of T2D.

Published
2014
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41. Pasture v. standard dairy cream in high-fat diet-fed mice: improved metabolic outcomes and stronger intestinal barrier.

Author

Benoit B, Plaisancié P, Géloën A, Estienne M, Debard C, Meugnier E, Loizon E, Daira P, Bodennec J, Cousin O, Vidal H, Laugerette F, and Michalski MC

Subjects
Adipose Tissue, White immunology, Adipose Tissue, White metabolism, Adipose Tissue, White pathology, Animal Husbandry, Animals, Dairy Products adverse effects, Dairy Products analysis, Diet, High-Fat adverse effects, Dietary Fats adverse effects, Dietary Fats analysis, Dietary Fats metabolism, Female, Hypertriglyceridemia etiology, Hypertriglyceridemia prevention & control, Intestinal Mucosa immunology, Intestinal Mucosa metabolism, Intestinal Mucosa pathology, Intestinal Mucosa physiopathology, Lactation, Liver metabolism, Male, Mice, Mice, Inbred C57BL, Obesity immunology, Obesity metabolism, Obesity pathology, Panniculitis etiology, Plant Components, Aerial chemistry, Plant Components, Aerial growth & development, Poaceae chemistry, Poaceae growth & development, Random Allocation, Cattle physiology, Diet veterinary, Dietary Fats therapeutic use, Functional Food analysis, Milk adverse effects, Milk chemistry, Milk metabolism, Obesity physiopathology, Panniculitis prevention & control
Abstract

Dairy products derived from the milk of cows fed in pastures are characterised by higher amounts of conjugated linoleic acid and α-linolenic acid (ALA), and several studies have shown their ability to reduce cardiovascular risk. However, their specific metabolic effects compared with standard dairy in a high-fat diet (HFD) context remain largely unknown; this is what we determined in the present study with a focus on the metabolic and intestinal parameters. The experimental animals were fed for 12 weeks a HFD containing 20 % fat in the form of a pasture dairy cream (PDC) or a standard dairy cream (SDC). Samples of plasma, liver, white adipose tissue, duodenum, jejunum and colon were analysed. The PDC mice, despite a higher food intake, exhibited lower fat mass, plasma and hepatic TAG concentrations, and inflammation in the adipose tissue than the SDC mice. Furthermore, they exhibited a higher expression of hepatic PPARα mRNA and adipose tissue uncoupling protein 2 mRNA, suggesting an enhanced oxidative activity of the tissues. These results might be explained, in part, by the higher amounts of ALA in the PDC diet and in the liver and adipose tissue of the PDC mice. Moreover, the PDC diet was found to increase the proportions of two strategic cell populations involved in the protective function of the intestinal epithelium, namely Paneth and goblet cells in the small intestine and colon, compared with the SDC diet. In conclusion, a PDC HFD leads to improved metabolic outcomes and to a stronger gut barrier compared with a SDC HFD. This may be due, at least in part, to the protective mechanisms induced by specific lipids.

Published
2014
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42. High-fat diet action on adiposity, inflammation, and insulin sensitivity depends on the control low-fat diet.

Author

Benoit B, Plaisancié P, Awada M, Géloën A, Estienne M, Capel F, Malpuech-Brugère C, Debard C, Pesenti S, Morio B, Vidal H, Rieusset J, and Michalski MC

Subjects
Animals, Diet, Fat-Restricted standards, Dietary Fats administration & dosage, Energy Intake, Liver drug effects, Macrophages drug effects, Male, Mice, Mice, Inbred C57BL, Subcutaneous Fat metabolism, Weight Gain, Adipose Tissue metabolism, Adiposity, Biomedical Research methods, Diet, High-Fat adverse effects, Inflammation etiology, Insulin Resistance, Lipid Metabolism drug effects
Abstract

Animal studies using a high-fat diet (HFD) have studied the effects of lipid overconsumption by comparing a defined HFD either with a natural-ingredient chow diet or with a defined low-fat diet (LFD), despite the dramatic differences between these control diets. We hypothesized that these differences in the control diet could modify the conclusions regarding the effects that an increase of fat in the diet has on several metabolic parameters. For 11 weeks, C57bl6/J mice were fed a low-fat chow diet (8% energy from fat), a typical semisynthetic LFD (12%), or a semisynthetic HFD (sy-HF) (40%). Conclusions about the effect of sy-HF on body weight gain, subcutaneous adipose tissue, insulin sensitivity, and adipose tissue inflammation were modified according to the control LFD. Conversely, conclusions about epididymal and retroperitoneal adipose tissue; fat intake effects on liver and muscular lipids, cholesterol, free fatty acids, and markers of low-grade inflammation; and of adipose tissue macrophage infiltration were the same regardless of the use of low-fat chow diet or semisynthetic LFD. For some physiological outcomes, conflicting conclusions were even reached about the effects of increased fat intake according to the chosen low-fat control. Some deleterious effects of sy-HF may not be explained by lipid overconsumption but rather by the overall quality of ingredients in a semisynthetic diet. According to the control LFD chosen, conclusions on the lipid-related effects of HFDs must be formulated with great care because some end points are profoundly affected by the ingredient composition of the diet rather than by fat content., (© 2013.)

Published
2013
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43. Low-dose food contaminants trigger sex-specific, hepatic metabolic changes in the progeny of obese mice.

Author

Naville D, Pinteur C, Vega N, Menade Y, Vigier M, Le Bourdais A, Labaronne E, Debard C, Luquain-Costaz C, Bégeot M, Vidal H, and Le Magueresse-Battistoni B

Subjects
Animals, Benzhydryl Compounds toxicity, Blotting, Western, Body Weight drug effects, Female, Male, Mice, Mice, Inbred C57BL, Mice, Obese, Phenols toxicity, Polychlorinated Biphenyls toxicity, Polychlorinated Dibenzodioxins toxicity, Reverse Transcriptase Polymerase Chain Reaction, Liver drug effects, Liver metabolism
Abstract

Environmental contaminants are suspected to be involved in the epidemic incidence of metabolic disorders, food ingestion being a primarily route of exposure. We hypothesized that life-long consumption of a high-fat diet that contains low doses of pollutants will aggravate metabolic disorders induced by obesity itself. Mice were challenged from preconception throughout life with a high-fat diet containing pollutants commonly present in food (2,3,7,8-tetrachlorodibenzo-p-dioxin, polychlorinated biphenyl 153, diethylhexyl phthalate, and bisphenol A), added at low doses in the tolerable daily intake range. We measured several blood parameters, glucose and insulin tolerance, hepatic lipid accumulation, and gene expression in adult mice. Pollutant-exposed mice exhibited significant sex-dependent metabolic disorders in the absence of toxicity and weight gain. In males, pollutants increased the expression of hepatic genes (from 36 to 88%) encoding proteins related to cholesterol biosynthesis and decreased (40%) hepatic total cholesterol levels. In females, there was a marked deterioration of glucose tolerance, which may be related to the 2-fold induction of estrogen sulfotransferase and reduced expression of estrogen receptor α (25%) and estrogen target genes (>34%). Because of the very low doses of pollutants used in the mixture, these findings may have strong implications in terms of understanding the potential role of environmental contaminants in food in the development of metabolic diseases.

Published
2013
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44. The eicosapentaenoic acid metabolite 15-deoxy-δ(12,14)-prostaglandin J3 increases adiponectin secretion by adipocytes partly via a PPARγ-dependent mechanism.

Author

Lefils-Lacourtablaise J, Socorro M, Géloën A, Daira P, Debard C, Loizon E, Guichardant M, Dominguez Z, Vidal H, Lagarde M, and Bernoud-Hubac N

Subjects
3T3-L1 Cells, Adipocytes metabolism, Adiponectin blood, Adiponectin genetics, Adipose Tissue drug effects, Adipose Tissue metabolism, Anilides pharmacology, Animals, Dietary Fats administration & dosage, Eicosapentaenoic Acid administration & dosage, Eicosapentaenoic Acid metabolism, Eicosapentaenoic Acid pharmacology, Epididymis drug effects, Epididymis metabolism, Gas Chromatography-Mass Spectrometry, Male, Mice, PPAR gamma antagonists & inhibitors, PPAR gamma genetics, Prostaglandin D2 metabolism, Prostaglandin D2 pharmacology, Reverse Transcriptase Polymerase Chain Reaction, Adipocytes drug effects, Adiponectin metabolism, PPAR gamma metabolism, Prostaglandin D2 analogs & derivatives
Abstract

The intake of ω-3 polyunsaturated fatty acids (PUFAs), which are abundant in marine fish meat and oil, has been shown to exert many beneficial effects. The mechanisms behind those effects are numerous, including interference with the arachidonic acid cascade that produces pro-inflammatory eicosanoids, formation of novel bioactive lipid mediators, and change in the pattern of secreted adipocytokines. In our study, we show that eicosapentaenoic acid (EPA) increases secreted adiponectin from 3T3-L1 adipocytes and in plasma of mice as early as 4 days after initiation of an EPA-rich diet. Using 3T3-L1 adipocytes, we report for the first time that 15-deoxy-δ(12,14)-PGJ3 (15d-PGJ3), a product of EPA, also increases the secretion of adiponectin. We demonstrate that the increased adiponectin secretion induced by 15d-PGJ3 is partially peroxisome proliferator-activated receptor-gamma (PPAR-γ)-mediated. Finally, we show that 3T3-L1 adipocytes can synthesize 15d-PGJ3 from EPA. 15d-PGJ3 was also detected in adipose tissue from EPA-fed mice. Thus, these studies provide a novel mechanism(s) for the therapeutic benefits of ω-3 polyunsaturated fatty acids dietary supplementation.

Published
2013
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45. Differential dose effect of fish oil on inflammation and adipose tissue gene expression in chronic kidney disease patients.

Author

Guebre-Egziabher F, Debard C, Drai J, Denis L, Pesenti S, Bienvenu J, Vidal H, Laville M, and Fouque D

Subjects
Adipokines genetics, Adipokines metabolism, Adipose Tissue metabolism, Adult, Antigens, CD genetics, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic genetics, Antigens, Differentiation, Myelomonocytic metabolism, Body Weight drug effects, Dose-Response Relationship, Drug, Energy Intake drug effects, Fatty Acids, Omega-3 administration & dosage, Fatty Acids, Omega-3 pharmacology, Fatty Acids, Omega-3 therapeutic use, Female, Fish Oils pharmacology, Fish Oils therapeutic use, Humans, Inflammation genetics, Inflammation metabolism, Interleukin-5 blood, Male, Matrix Metalloproteinase 9 genetics, Matrix Metalloproteinase 9 metabolism, Middle Aged, Receptors, Adiponectin genetics, Receptors, Adiponectin metabolism, Renal Insufficiency, Chronic genetics, Renal Insufficiency, Chronic metabolism, Subcutaneous Fat drug effects, Subcutaneous Fat metabolism, Up-Regulation, Adipose Tissue drug effects, Fish Oils administration & dosage, Gene Expression drug effects, Inflammation drug therapy, Inflammation Mediators metabolism, Lipids blood, Renal Insufficiency, Chronic drug therapy
Abstract

Objective: The beneficial effects of ω-3 polyunsaturated fatty acids (PUFAs) in cardiovascular disease are partly attributed to their anti-inflammatory properties. Their potential effect on the adipose tissue of chronic kidney disease (CKD) patients has never been explored., Methods: To determine the metabolic effect of supplementation with two different doses of fish oil (FO), 12 non-dialyzed patients with stage IV/V CKD were randomly allocated to receive 1.8 g or 3.6 g/d of ω-3 PUFA for 10 wk. Metabolic parameters, adipose tissue function, and gene expression were evaluated at baseline and 10 wk., Results: Body weight, fat mass, energy intake, fasting glucose, and insulin were unchanged. The daily intake of 3.6 g of ω-3 PUFA resulted in decreased serum triacylglycerol and increased high-density lipoprotein cholesterol, whereas low-density lipoprotein cholesterol increased with 1.8 g of ω-3 PUFA. Serum adiponectin, leptin, C-reactive protein, and tumor necrosis factor-α were not modified in either group. Interleukin-6 levels tended to decrease with 1.8 g of ω-3 PUFA. Additionally, a subset of inflammation-related genes (CD68 and MMP9) was reduced in subcutaneous adipose tissue in this group. Adiponectin, leptin, and adipoR2 gene expression were upregulated with 3.6 g of ω-3 PUFA., Conclusions: A moderate dose of FO alters the gene expression profile of adipose tissue to a more antiinflammatory status. Higher doses of FO have a favorable effect on lipid profile and lead to the upregulation of adipokines gene expression suggesting a different dose response to ω-3 PUFA administration in patients with CKD., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Published
2013
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46. Visceral fat accumulation during lipid overfeeding is related to subcutaneous adipose tissue characteristics in healthy men.

Author

Alligier M, Gabert L, Meugnier E, Lambert-Porcheron S, Chanseaume E, Pilleul F, Debard C, Sauvinet V, Morio B, Vidal-Puig A, Vidal H, and Laville M

Subjects
Adult, Gene Expression, Glucose Clamp Technique, Humans, Insulin Resistance physiology, Male, Obesity metabolism, Intra-Abdominal Fat metabolism, Lipid Metabolism physiology, Overnutrition metabolism, Subcutaneous Fat metabolism
Abstract

Context: The hypothesis of a limited expansion of sc adipose tissue during weight gain provides an attractive explanation for the reorientation of excess lipids toward ectopic sites, contributing to visceral adipose depots and metabolic syndrome., Objective: Our objective was to define whether the characteristics of sc adipose tissue influence the partition of lipids toward abdominal fat depots during weight gain in healthy men., Research Design and Methods: Forty-one healthy nonobese volunteers performed a 56-day overfeeding protocol (+760 kcal/d). Insulin sensitivity was estimated by euglycemic hyperinsulinemic clamp. Changes in abdominal visceral and sc adipose tissue depots were measured by magnetic resonance imaging. The fate of ingested lipids before and after overfeeding was investigated using a [d31]palmitate test meal, and gene expression was measured by real-time PCR in sc fat biopsies., Results: Overfeeding led to a 2.5-kg body weight increase with large interindividual variations in abdominal sc and visceral adipose tissues. There was no relationship between the relative expansions of these 2 depots, but the increase in visceral depot was positively associated with the magnitude of the postprandial exogenous fatty acid release in the circulation during the test meal. The regulation of lipid storage-related genes (DGAT2, SREBP1c, and CIDEA) was defective in the sc fat of the subjects exhibiting the largest accumulation in visceral depot., Conclusions: Characteristics of sc adipose tissue appear therefore to contribute to the development of visceral fat depot, supporting the adipose tissue expandability theory and extending it to early stages of weight gain in nonobese subjects.

Published
2013
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47. Jejunal proteins secreted by db/db mice or insulin-resistant humans impair the insulin signaling and determine insulin resistance.

Author

Salinari S, Debard C, Bertuzzi A, Durand C, Zimmet P, Vidal H, and Mingrone G

Subjects
Adult, Animals, Cell Differentiation drug effects, Culture Media, Conditioned pharmacology, Deoxyglucose metabolism, Diabetes Mellitus, Experimental enzymology, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Humans, Mice, Mice, Inbred C57BL, Muscle Fibers, Skeletal drug effects, Muscle Fibers, Skeletal metabolism, Muscle Fibers, Skeletal pathology, Phosphorylation drug effects, Phosphoserine metabolism, Proto-Oncogene Proteins c-akt metabolism, Ribosomal Protein S6 Kinases, 70-kDa metabolism, Diabetes Mellitus, Experimental pathology, Insulin metabolism, Insulin Resistance, Jejunum metabolism, Proteins metabolism, Signal Transduction
Abstract

Background: Two recent studies demonstrated that bariatric surgery induced remission of type 2 diabetes very soon after surgery and far too early to be attributed to weight loss. In this study, we sought to explore the mechanism/s of this phenomenon by testing the effects of proteins from the duodenum-jejunum conditioned-medium (CM) of db/db or Swiss mice on glucose uptake in vivo in Swiss mice and in vitro in both Swiss mice soleus and L6 cells. We studied the effect of sera and CM proteins from insulin resistant (IR) and insulin-sensitive subjects on insulin signaling in human myoblasts., Methodology/principal Findings: db/db proteins induced massive IR either in vivo or in vitro, while Swiss proteins did not. In L6 cells, only db/db proteins produced a noticeable increase in basal (473)Ser-Akt phosphorylation, lack of GSK3β inhibition and a reduced basal (389)Thr-p70-S6K1 phosphorylation. Human IR serum markedly increased basal (473)Ser-Akt phosphorylation in a dose-dependent manner. Human CM IR proteins increased by about twofold both basal and insulin-stimulated (473)Ser-Akt. Basal (9)Ser-GSK3β phosphorylation was increased by IR subjects serum with a smaller potentiating effect of insulin., Conclusions: These findings show that jejunal proteins either from db/db mice or from insulin resistant subjects impair muscle insulin signaling, thus inducing insulin resistance.

Published
2013
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48. Dietary oxidized n-3 PUFA induce oxidative stress and inflammation: role of intestinal absorption of 4-HHE and reactivity in intestinal cells.

Author

Awada M, Soulage CO, Meynier A, Debard C, Plaisancié P, Benoit B, Picard G, Loizon E, Chauvin MA, Estienne M, Peretti N, Guichardant M, Lagarde M, Genot C, and Michalski MC

Subjects
Aldehydes administration & dosage, Animals, Biomarkers metabolism, Caco-2 Cells, Endoplasmic Reticulum Chaperone BiP, Glutathione Peroxidase metabolism, Heat-Shock Proteins metabolism, Humans, Intestinal Absorption physiology, Lipid Peroxidation, Male, Mice, Mice, Inbred C57BL, Oxidation-Reduction, Aldehydes pharmacokinetics, Diet, High-Fat, Fatty Acids, Omega-3 metabolism, Inflammation metabolism, Intestinal Mucosa metabolism, Oxidative Stress
Abstract

Dietary intake of long-chain n-3 PUFA is now widely advised for public health and in medical practice. However, PUFA are highly prone to oxidation, producing potentially deleterious 4-hydroxy-2-alkenals. Even so, the impact of consuming oxidized n-3 PUFA on metabolic oxidative stress and inflammation is poorly described. We therefore studied such effects and hypothesized the involvement of the intestinal absorption of 4-hydroxy-2-hexenal (4-HHE), an oxidized n-3 PUFA end-product. In vivo, four groups of mice were fed for 8 weeks high-fat diets containing moderately oxidized or unoxidized n-3 PUFA. Other mice were orally administered 4-HHE and euthanized postprandially versus baseline mice. In vitro, human intestinal Caco-2/TC7 cells were incubated with 4-hydroxy-2-alkenals. Oxidized diets increased 4-HHE plasma levels in mice (up to 5-fold, P < 0.01) compared with unoxidized diets. Oxidized diets enhanced plasma inflammatory markers and activation of nuclear factor kappaB (NF-κB) in the small intestine along with decreasing Paneth cell number (up to -19% in the duodenum). Both in vivo and in vitro, intestinal absorption of 4-HHE was associated with formation of 4-HHE-protein adducts and increased expression of glutathione peroxidase 2 (GPx2) and glucose-regulated protein 78 (GRP78). Consumption of oxidized n-3 PUFA results in 4-HHE accumulation in blood after its intestinal absorption and triggers oxidative stress and inflammation in the upper intestine.

Published
2012
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49. Insulin-sensitizing effects on muscle and adipose tissue after dietary fiber intake in men and women with metabolic syndrome.

Author

Robertson MD, Wright JW, Loizon E, Debard C, Vidal H, Shojaee-Moradie F, Russell-Jones D, and Umpleby AM

Subjects
Adult, Aged, Biomarkers analysis, Biomarkers metabolism, Biopsy, Cytokines metabolism, Diet, Female, Gene Expression drug effects, Glucose metabolism, Glucose Clamp Technique, Humans, Lipid Metabolism drug effects, Liver metabolism, Male, Membrane Potentials drug effects, Metabolic Syndrome physiopathology, Middle Aged, RNA, Messenger biosynthesis, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Single-Blind Method, Zea mays chemistry, Adipose Tissue drug effects, Adipose Tissue metabolism, Dietary Fiber pharmacology, Insulin Resistance physiology, Metabolic Syndrome diet therapy, Metabolic Syndrome metabolism, Muscles drug effects, Muscles metabolism
Abstract

Context: Dietary fibers have been associated with a reduced incidence of type 2 diabetes mellitus in epidemiological studies; however, the precise mechanisms are unknown., Objective: The objective of the study was to evaluate the efficacy and site of action of an insoluble dietary fiber derived from maize (HAM-RS2) in improving insulin resistance in subjects at increased risk of type 2 diabetes mellitus., Design: This study was a randomized, controlled crossover, dietary intervention study., Setting: The study was conducted at the Centre for Diabetes, Endocrinology, and Research, Royal Surrey County Hospital, Guildford, United Kingdom., Participants: Fifteen men and women with insulin resistance participated in the study., Intervention: The intervention included 40 g/d HAM-RS2 compared with a matched placebo for 8 wk., Main Outcome Measures: After each supplement, participants underwent a two-step hyperinsulinemic-euglycemic clamp study with the addition of glucose tracers; a meal tolerance test; arteriovenous sampling across forearm muscle tissue; and a sc adipose tissue biopsy for assessment of gene expression., Results: There was enhanced uptake of glucose into the forearm muscle measured by arteriovenous sampling (65 ± 15% increase after resistant starch; P < 0.001). Adipose tissue function was also affected, with enhanced fatty acid suppression after HAM-RS2 treatment and an increase in gene expression for hormone sensitive lipase (P = 0.005), perilipin (P = 0.011), lipoprotein lipase (P = 0.014), and adipose triglyceride lipase (P = 0.03) in biopsy samples. There was no effect on the insulin sensitivity of hepatic glucose production or plasma lipids after HAM-RS2., Conclusion: HAM-RS2 improved peripheral but not hepatic insulin resistance and requires further study as an intervention in patients with or at risk for type 2 diabetes.

Published
2012
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50. Oil composition of high-fat diet affects metabolic inflammation differently in connection with endotoxin receptors in mice.

Author

Laugerette F, Furet JP, Debard C, Daira P, Loizon E, Géloën A, Soulage CO, Simonet C, Lefils-Lacourtablaise J, Bernoud-Hubac N, Bodennec J, Peretti N, Vidal H, and Michalski MC

Subjects
3T3-L1 Cells, Acute-Phase Proteins, Adipose Tissue, White metabolism, Animals, Biomarkers blood, Biomarkers metabolism, Carrier Proteins blood, Cytokines blood, Fatty Acids, Monounsaturated, Fatty Acids, Nonesterified adverse effects, Fatty Acids, Nonesterified blood, Gram-Negative Bacteria immunology, Gram-Negative Bacteria isolation & purification, Gram-Positive Bacteria immunology, Gram-Positive Bacteria isolation & purification, Intestines immunology, Intestines microbiology, Intestines pathology, Lipopolysaccharide Receptors blood, Lipopolysaccharide Receptors metabolism, Male, Membrane Glycoproteins blood, Metabolic Diseases metabolism, Metabolic Diseases microbiology, Mice, Mice, Inbred C57BL, Palm Oil, Plant Oils adverse effects, Random Allocation, Rapeseed Oil, Sunflower Oil, Toll-Like Receptor 4 metabolism, Adipose Tissue, White immunology, Cytokines metabolism, Diet, High-Fat adverse effects, Metabolic Diseases etiology, Metabolic Diseases immunology, Receptors, Immunologic metabolism
Abstract

Low-grade inflammation observed in obesity is a risk factor for cardiovascular disease. Recent studies revealed that this would be linked to gut-derived endotoxemia during fat digestion in high-fat diets, but nothing is known about the effect of lipid composition. The study was designed to test the impact of oil composition of high-fat diets on endotoxin metabolism and inflammation in mice. C57/Bl6 mice were fed for 8 wk with chow or isocaloric isolipidic diets enriched with oils differing in fatty acid composition: milk fat, palm oil, rapeseed oil, or sunflower oil. In vitro, adipocytes (3T3-L1) were stimulated or not with lipopolysaccharide (LPS; endotoxin) and incubated with different fatty acids. In mice, the palm group presented the highest level of IL-6 in plasma (P < 0.01) together with the highest expression in adipose tissue of IL-1β and of LPS-sensing TLR4 and CD14 (P < 0.05). The higher inflammation in the palm group was correlated with a greater ratio of LPS-binding protein (LBP)/sCD14 in plasma (P < 0.05). The rapeseed group resulted in higher sCD14 than the palm group, which was associated with lower inflammation in both plasma and adipose tissue despite higher plasma endotoxemia. Taken together, our results reveal that the palm oil-based diet resulted in the most active transport of LPS toward tissues via high LBP and low sCD14 and the greatest inflammatory outcomes. In contrast, a rapeseed oil-based diet seemed to result in an endotoxin metabolism driven toward less inflammatory pathways. This shows that dietary fat composition can contribute to modulate the onset of low-grade inflammation through the quality of endotoxin receptors.

Published
2012
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