Search

Your search keyword '"Beby-Defaux, Agnès"' showing total 37 results
Start Over Author "Beby-Defaux, Agnès"
37 results on '"Beby-Defaux, Agnès"'

2. Impact of Human Immunodeficiency Virus Type 1 Minority Variants on the Virus Response to a Rilpivirine-Based First-line Regimen.

Author

Raymond, Stéphanie, Nicot, Florence, Pallier, Coralie, Bellecave, Pantxika, Maillard, Anne, Trabaud, Mary, Morand-Joubert, Laurence, Rodallec, Audrey, Amiel, Corinne, Mourez, Thomas, Bocket, Laurence, Beby-Defaux, Agnès, Bouvier-Alias, Magali, Lambert-Niclot, Sidonie, Charpentier, Charlotte, Malve, Brice, Mirand, Audrey, Dina, Julia, Le Guillou-Guillemette, Hélène, Marque-Juillet, Stéphanie, Signori-Schmuck, Anne, Barin, Francis, Si-Mohamed, Ali, Avettand Fenoel, Véronique, Roussel, Catherine, Calvez, Vincent, Saune, Karine, Marcelin, Anne, Rodriguez, Christophe, Descamps, Diane, and Izopet, Jacques

Subjects
Adult, Drug Resistance, Viral, Female, Genetic Variation, HIV Infections, HIV-1, Humans, Male, Mutation, Rilpivirine, Viral Load
Abstract

BACKGROUND: Minority resistant variants of human immunodeficiency virus type 1 (HIV-1) could influence the virological response to treatment based on nonnucleoside reverse transcriptase inhibitors (NNRTIs). Data on minority rilpivirine-resistant variants are scarce. This study used next-generation sequencing (NGS) to identify patients harboring minority resistant variants to nucleos(t)ide reverse transcriptase inhibitors and NNRTIs and to assess their influence on the virological response (VR). METHODS: All the subjects, 541 HIV-1-infected patients started a first-line regimen containing rilpivirine. VR was defined as a HIV-1 RNA load 20% in 29% of samples. We identified 43 (8.8%) and 36 (7.4%) patients who harbored rilpivirine-resistant variants with a 1% sensitivity threshold according to the French National Agency for Research on AIDS and Viral Hepatitis and Stanford algorithms, respectively. The VR was 96.9% at month 12. Detection of minority rilpivirine resistant variants was not associated with virological failure (VF). Multivariate analysis indicated that VF at month 12 was associated with a CD4 count

Published
2018

8. Pooling Rectal, Pharyngeal, and Urine Samples to Detect Neisseria gonorrhoeae, Chlamydia trachomatis, and Mycoplasma genitalium Using Multiplex Polymerase Chain Reaction Is as Effective as Single-Site Testing for Men Who Have Sex With Men

Author

Prazuck, Thierry, primary, Lanotte, Philippe, additional, Le Moal, Gwénaël, additional, Hocqueloux, Laurent, additional, Sunder, Simon, additional, Catroux, Mélanie, additional, Garcia, Magali, additional, Perfezou, Pascale, additional, Gras, Guillaume, additional, Plouzeau, Chloé, additional, Lévêque, Nicolas, additional, and Beby-Defaux, Agnès, additional

Published
2022
Full Text
View/download PDF

11. High levels of HPV16-L1 antibody but not HPV16 DNA load or integration predict oropharyngeal patient outcome: The Papillophar study

Author

Prétet, Jean-Luc, Dalstein, Véronique, Touzé, Antoine, Beby-Defaux, Agnès, Soussan, Patrick, Jacquin, Élise, Birembaut, Philippe, Clavel, Christine, Mougin, Christiane, Rousseau, Alexandra, Lacau Saint Guily, Jean, Agius, G., Albert, S., Babin, E., Badet, J., Badoual, C., Baglin, A., Blanc-Fournier, K., Cassagneau, E., Debry, C., de Raucourt, D., Diebold, M., Dufour, X., Hourseau, M., Lacave, R., Zalcman, E. Lechapt, Lefevre, M., Levillain, P., Malard, O., Mauvais, O., Mechine, A., Merol, J., Mirghani, H., Morinière, S., Périé, S., Rousselot, C., Simon, T., Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (UR 3181) (CEF2P / CARCINO), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), 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), Centre Hospitalier Universitaire de Reims (CHU Reims), Infectiologie et Santé Publique (UMR ISP), Université de Tours (UT)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Laboratoire Inflammation, Tissus épithéliaux et Cytokines (LITEC), Université de Poitiers, Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Service de virologie [Hôpital Tenon], CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Unité de Recherche Clinique de l’Est Parisien [CHU Saint-Antoine] (URC-EST), Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts (CHNO)-CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Rothschild [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Direction de la Recherche Clinique et de l'Innovation [AP-HP] (DRCI), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Oto-Rhino-Laryngologie Chirurgie cervico-faciale [CHU Tenon], Fondation Ophtalmologique Adolphe de Rothschild [Paris], and This work was funded by the Programme Hospitalier de Recherche Clinique, French Ministry of Health (Grant Numbers AOM 08104, AOM 11 293).

Subjects
stomatognathic diseases, Oropharyngeal cancer, viruses, [SDV]Life Sciences [q-bio], virus diseases, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biomarker, General Medicine, Papillomavirus, Prognosis, neoplasms, female genital diseases and pregnancy complications, General Biochemistry, Genetics and Molecular Biology
Abstract

International audience; The incidence of oropharyngeal cancers (OPC) is increasing in the world. Among OPC, those induced by human papillomaviruses have a better prognosis than non-HPV-associated OPC. The objective of this study was to highlight the relevance of HPV16 load, HPV16 DNA integration and HPV16-L1 serology on progression-free survival and overall survival of OPC patients. The PAPILLOPHAR cohort consists of 362 patients with oropharyngeal squamous cell carcinomas prospectively followed up for 5 years after treatment. Tumor biopsies and sera were collected at inclusion to investigate tumor HPV DNA/RNA characteristics and HPV16 L1 serology, respectively. Twenty-seven percent of tumor biopsies were HPV DNA- and RNA-positive and HPV16 represented 93% of HPV-positive cases. Among them, neither HPV16 viral load nor HPV16 DNA integration was associated with overall survival (OS) or progression-free survival (PFS). In contrast, high anti-HPV16 L1 antibody titers were significantly associated with a better OS and PFS. This study reveals that HPV16 load and integration are not relevant prognosis biomarkers in OPC patients. Clinical Relevance: High levels of HPV16 L1 antibodies may be useful to predict OPC patient outcome following treatment. ClinicalTrials.gov Identifier: NCT00918710, May 2017.

Published
2021
Full Text
View/download PDF

14. Drug-resistant cytomegalovirus in transplant recipients: a French cohort study

Author

Hantz, Sébastien, Garnier-Geoffroy, Françoise, Mazeron, Marie-Christine, Garrigue, Isabelle, Merville, Pierre, Mengelle, Catherine, Rostaing, Lionel, Saint Marcoux, Franck, Essig, Marie, Rerolle, Jean-Philippe, Cotin, Sébastien, Germi, Raphaëlle, Pillet, Sylvie, Lebranchu, Yvon, Turlure, Pascal, Alain, Sophie, Herbein, Georges, Coaquette, Alain, Lafon, Marie Edith, Garrigue, Isabelle, Archimbaud, Christine, Henquell, Cécile, Peigue-Lafeuille, Hélène, Pothier, Pierre, Bour, Jean Baptiste, Cesaire, Raymond, Majioullah, Fatimah, Morand, Patrice, Germi, Raphaëlle, Morel-Baccard, Christine, Signori-Schmuck, Anne, Alain, Sophie, Hantz, Sébastien, Grosjean, Jérôme, Morfin-Sherpa, Florence, Billaud, Geneviève, Domenach, Vinca, Andre, Patrice, Milon, Marie Paule, Segondy, Michel, Foulongne, Vincent, Agius, Gérard, Beby-Defaux, Agnès, Pozzetto, Bruno, Pillet, Sylvie, Mansuy, Jean Michel, Mengelle, Catherine, Gaudio-Castelain, Sandrine, Ducancelle, Alexandra, Lunel, Françoise, Payan, Christopher, Gouarin, Stéphanie, Dewilde, Anny, Bressolette, Céline, Coste-Burel, Marianne, Imbert-Marcille, Berthe-Marie, Andreoletti, Laurent, Leveque, Nicolas, Venard, Véronique, Jeulin, Hélène, Minjolle, Sophie, Gueudin, Marie, Colimon, Ronald, Stoll-Keller, Françoise, Fafi-Kremer, Samira, Dubois, F., Gaudy, Catherine, Deny, Paul, Vezinet, Françoise Brun, Houhou, Nadira, Honderlick, Patrick, Mazeron, Marie Christine, Leruez-Ville, Marianne, Vaghefi, Parissa, Dussaix, Elisabeth, Agut, Henri, Boutolleau, David, Deback, Claire, Scieux, Catherine, Le Goff, Jérôme, Ducloux, Didier, Vanlemmens, Claire, Larosa, Fabrice, Neau-Cransac, M., Dromer, C., Rosier, Emmanuelle, Merville, Pierre, Douillet, Marine, Morel, Delphine, Moreau, Karine, Martin, Séverine, Billes, Marc-Alain, Milpied, Noel, Tabrizi, Reza, Vigouroux, Stéphane, Melot, Cyril, Deteix, Patrice, Heng, Anne-Elisabeth, Mackaya, Léandre, Casanova, Sandrine, Bay, Jacques-Olivier, Demeocq, François, Duee, Frédéric, Mousson, Christiane, Hillon, Patrick, Minello, Anne, Charve, Philippe, Tanter, Yves, Bayle, François, Janbon, Bénédicte, Borrel, Elisabeth, Boignard, Aude, Neron, Linda, Pison, Christophe, Saint-Raymond, Christel, Brion, Jean Paul, Cahn, Jean Yves, Bordessoule, Dominique, Turlure, Pascal, Bompart, Frédérica, Philippon, Céline, Essig, Marie, Aldigier, Jean-Claude, Rerolle, Jean Philippe, Dickson, Zarah, Leprivey, Valérie, Roger-Rolle, Florence, Piguet, Christophe, Marquet, Pierre, Francois, Bruno, Pouteil-Noble, Claire, Mialou, Valérie, Mourad, Georges, Mariat, Christophe, Cornillon, Jérôme, Tavernie-Tardy, Emmanuelle, Attal, M., Huynh, Anne, Rostaing, Lionel, Kamar, Nassim, Mencia, Danièle, Crognier, Laure, de Ligny, Bruno Hurault, Hazzan, Marc, Bordigoni, Pierre, Pall-Kondolff, Sandrine, Salmon, Alexandra, Clement, Laurence, Chevallier, Patrice, Le Gouill, Steven, Gastinne, Thomas, Delaunay, Jacques, Ayari, Sameh, Guillaume, Thierry, Mohty, Mohammed, Moreau, Philippe, Robin, Marie-Aude, Le Houerou, Claire, Giral, Magali, Papuchon, Emmanuelle, Pattier, Sabine, Treilhaud, Michèle, Camus, Christophe, Etienne, Isabelle, Moulin, Bruno, Caillard-Ohlmann, Sophie, Lioure, Bruno, Cojean, Nadine, Lutz, Patrick, Uettwiller, Françoise, Entz-Werle, Natacha, Laplace, Annegret, Buchler, Matthias, Lebranchu, Yvon, Barbet, Christelle, Fourchy, Dominique, Stern, Marc, Grenet, Dominique, Delahousse, Michel, Karras, Alexandre, Saliba, Faouzi, Ichai, Philippe, Dhedin, Nathalie, Vernant, Jean-Paul, Uzunov, Madalina, Barrou, Benoît, Glotz, Denis, Peraldi, Marie-Noëlle, Langner, Nathalie, and Ribaud, Patricia

Published
2010
Full Text
View/download PDF

18. Emerging resistance mutations in PI-naive patients failing an atazanavir-based regimen (ANRS multicentre observational study)

Author

Lambert-Niclot, L, Grude, C, Chaix, L., Charpentier, L, Reigadas, C, Le Guillou-Guillemette, L, Rodallec, C, Maillard, Pascale, Dufayard, C, Mourez, C, Mirand, C, Guinard, L, Montes, S, Vallet, L, Marcelin, Marc, Descamps, L, Flandre, C, Delaugerre, L, Alloui, Chakib, Descamps, Diane, Charpentier, Charlotte, Visseaux, Benoit, Krivine, Anne, Bouviers-Alias, Ali, Pallier, Coralie, Soulié, Cathia, Wirden, Marc, Marcelin, Anne, Calvez, Vincent, Morand, Laurence, Lambert-Niclot, Sidonie, Fofana, Djeneba, Mahjoub, Nadia, Delaugerre, Constance, Chaix, Marie, Amiel, Corinne, Schneider, Veronique, Roussel, Catherine, Le Guillou-Guillemette, Hélène, Courdavault, Laurence, Reigadas, Sandrine, Recordon-Pinson, Patricia, Fleury, Hervé, Vallet, Sophie, Dina, Julia, Vabret, Astrid, Mirand, Audrey, Henquell, Cécile, Auvray, Christelle, de Rougemont, Alexis, Giraudon, Helene, Si-Mohammed, Ali, Mathez, Dominique, Signori-Schmuck, Anne, Morand, Patrice, Bocket, Laurence, Trabaud, Anne, Montes, Brigitte, Le Guen, Laura, Rodallec, Audrey, Ferré, Virginie, Jeulin, Hélène, SCHVOERER, Evelyne, Dufayard, Jacqueline, Allardet-Servent, Annick, carles, Marie, Guinard, Jérôme, Guigon, Aurélie, Giraudeau, Genevieve, Beby-Defaux, Agnès, Maillard, Anne, Plantier, Jean Christophe, Leoz, Marie, Mourez, Thomas, Bourlet, Thomas, Fafi-Kremer, Samira, Chiabrando, Julie, Raymond, Stéphanie, Izopet, Jacques, Barin, Francis, Marque-Juillet, Stéphanie, Yerly, Sabine, Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 - UFR de Médecine Pierre et Marie Curie (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Hôpital Pellegrin, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Centre hospitalier universitaire de Nantes (CHU Nantes), Hôpital Pontchaillou, Centre Hospitalier Universitaire de Nice (CHU Nice), CHU Rouen, Normandie Université (NU), CHU Clermont-Ferrand, Centre Hospitalier Régional d'Orléans (CHRO), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Hôpital de la Cavale Blanche - CHRU Brest (CHU - BREST ), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Laboratoire Bordelais de Recherche en Informatique (LaBRI), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), 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), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Service de virologie [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), Epidémiologie, stratégies thérapeutiques et virologie cliniques dans l'infection à VIH, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département de Mathématiques et Applications - ENS Paris (DMA), École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS), Département d'Astrophysique, de physique des Particules, de physique Nucléaire et de l'Instrumentation Associée (DAPNIA), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Laboratoire de Virologie [CHU Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Génétique et Ecologie des Virus, Génétique des Virus et Pathogénèse des Maladies Virales, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), UFR des Sciences de Santé (Université de Bourgogne), Université de Bourgogne (UB), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Centre Hospitalier Victor Dupouy, Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), CHU Bordeaux [Bordeaux], Laboratoire Universitaire de Biodiversité et Ecologie Microbienne (LUBEM), Université de Brest (UBO), Laboratoire de Virologie Humaine et Moléculaire [Caen], CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Groupe de Recherche sur l'Adaptation Microbienne (GRAM 2.0), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université de Caen Normandie (UNICAEN), Laboratoire Microorganismes : Génome et Environnement (LMGE), Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Laboratoire de sérologie-virologie (CHU de Dijon), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Hôpital Raymond Poincaré [AP-HP], Institut de biologie structurale (IBS - UMR 5075 ), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), 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)-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)-Centre National de la Recherche Scientifique (CNRS), Département de virologie [Grenoble], Centre Hospitalier Universitaire [Grenoble] (CHU), Service de Virologie [Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Epidémiologie, Démographie et Sciences Sociales: santé reproductive, sexualité et infection à VIH (Inserm U569), Epidémiologie, sciences sociales, santé publique (IFR 69), Université Paris 1 Panthéon-Sorbonne (UP1)-Université Paris-Sud - Paris 11 (UP11)-École des hautes études en sciences sociales (EHESS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris 1 Panthéon-Sorbonne (UP1)-Université Paris-Sud - Paris 11 (UP11)-École des hautes études en sciences sociales (EHESS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut national d'études démographiques (INED)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Chimie Physique et Microbiologie pour les Matériaux et l'Environnement (LCPME), Institut de Chimie du CNRS (INC)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Observatoire des Programmes Communautaires de Développement Rural (US ODR), Institut National de la Recherche Agronomique (INRA), Institut Pasteur de Nouvelle-Calédonie, Réseau International des Instituts Pasteur (RIIP), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Ecophysiologie Végétale, Agronomie et Nutritions (EVA), Institut National de la Recherche Agronomique (INRA)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU), Groupe Immunité des Muqueuses et Agents Pathogènes (GIMAP), Université Jean Monnet [Saint-Étienne] (UJM), Interaction virus-hôte et maladies du foie, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Claude de Préval (ICP), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Université de Tours (UT), Centre Hospitalier de Versailles André Mignot (CHV), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université de Bordeaux (UB)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB)-Centre National de la Recherche Scientifique (CNRS), 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), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), École normale supérieure - Paris (ENS-PSL), Microbiologie Fondamentale et Pathogénicité (MFP), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Recherche Agronomique (INRA), Université Jean Monnet - Saint-Étienne (UJM), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), Université de Tours, Service de Virologie [CHU Pitié-Salpêtrière], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Lycée agricole La Touche, Hôpital Bichat - Claude Bernard, Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB)-Université Sciences et Technologies - Bordeaux 1-Université Bordeaux Segalen - Bordeaux 2, Memo-Flu-ARDS Study Group, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Pitié-Salpêtrière [APHP], École normale supérieure - Paris (ENS Paris)-Centre National de la Recherche Scientifique (CNRS), CHU Pitié-Salpêtrière [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), CHU Tenon [APHP], Hôpital d'Argenteuil, Laboratoire Microorganismes : Génome et Environnement - Clermont Auvergne (LMGE), Université Clermont Auvergne (UCA)-Centre National de la Recherche Scientifique (CNRS), AP-HP Hôpital Raymond Poincaré [Garches], Unit for Virus Host-Cell Interactions [Grenoble] (UVHCI), Université Joseph Fourier - Grenoble 1 (UJF)-European Molecular Biology Laboratory [Grenoble] (EMBL)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de virologie moléculaire et structurale, CHU Grenoble, Laboratoire de virologie [CHU Lille], Université Panthéon-Sorbonne (UP1)-Université Paris-Sud - Paris 11 (UP11)-École des hautes études en sciences sociales (EHESS)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Panthéon-Sorbonne (UP1)-Université Paris-Sud - Paris 11 (UP11)-École des hautes études en sciences sociales (EHESS)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut national d'études démographiques (INED), Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Centre national de référence du VIH INSERM U966, Centre Hospitalier de Versailles (CHV), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
0301 basic medicine, Microbiology (medical), Adult, Male, medicine.medical_specialty, 030106 microbiology, Atazanavir Sulfate, HIV Infections, Emtricitabine, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Abacavir, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Internal medicine, Drug Resistance, Viral, medicine, Humans, Pharmacology (medical), 030212 general & internal medicine, Treatment Failure, Tenofovir, ComputingMilieux_MISCELLANEOUS, Retrospective Studies, Pharmacology, business.industry, virus diseases, Lamivudine, HIV Protease Inhibitors, Middle Aged, Viral Load, Resistance mutation, Dideoxynucleosides, 3. Good health, Atazanavir, Regimen, Drug Combinations, Infectious Diseases, Mutation, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, HIV-1, Ritonavir, business, Viral load, medicine.drug
Abstract

Background Atazanavir is a PI widely used as a third agent in combination ART. We aimed to determine the prevalence and the patterns of resistance in PI-naive patients failing on an atazanavir-based regimen. Methods We analysed patients failing on an atazanavir-containing regimen used as a first line of PI therapy. We compared the sequences of reverse transcriptase and protease before the introduction of atazanavir and at failure [two consecutive viral loads (VLs) >50 copies/mL]. Resistance was defined according to the 2014 Agence Nationale de Recherche sur le SIDA et les Hepatites Virales (ANRS) algorithm. Results Among the 113 patients, atazanavir was used in the first regimen in 71 (62.8%) patients and in the first line of a PI-based regimen in 42 (37.2%). Atazanavir was boosted with ritonavir in 95 (84.1%) patients and combined with tenofovir/emtricitabine or lamivudine (n = 81) and abacavir/lamivudine or emtricitabine (n = 22). At failure, median VL was 3.05 log10 copies/mL and the median CD4+ T cell count was 436 cells/mm3. The median time on atazanavir was 21.2 months. At failure, viruses were considered resistant to atazanavir in four patients (3.5%) with the selection of the following major atazanavir-associated mutations: I50L (n = 1), I84V (n = 2) and N88S (n = 1). Other emergent PI mutations were L10V, G16E, K20I/R, L33F, M36I/L, M46I/L, G48V, F53L, I54L, D60E, I62V, A71T/V, V82I/T, L90M and I93L/M. Emergent NRTI substitutions were detected in 21 patients: M41L (n = 2), D67N (n = 3), K70R (n = 1), L74I/V (n = 3), M184V/I (n = 16), L210W (n = 1), T215Y/F (n = 3) and K219Q/E (n = 2). Conclusions Resistance to atazanavir is rare in patients failing the first line of an atazanavir-based regimen according to the ANRS. Emergent NRTI resistance-associated mutations were reported in 18% of patients.

Published
2018
Full Text
View/download PDF

19. Acanthamoeba castellanii is not be an adequate model to study human adenovirus interactions with macrophagic cells

Author

Maisonneuve, Elodie, Cateau, Estelle, Leveque, Nicolas, Kaaki, Sihem, Beby-Defaux, Agnès, Rodier, Marie-Hélène, Ulasov, Ilya, Ecologie et biologie des interactions (EBI), Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Microbiologie de l'Eau (MDE), Université de Poitiers-Centre National de la Recherche Scientifique (CNRS)-Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Université de Reims Champagne-Ardenne (URCA), Service d'Anatomie et de Cytologie Pathologiques [Poitiers], and Centre hospitalier universitaire de Poitiers (CHU Poitiers)

Subjects
Adenoviruses, Immunofluorescence, lcsh:Medicine, Fluorescent Antibody Technique, Acanthamoeba, Pathology and Laboratory Medicine, White Blood Cells, Animal Cells, Medicine and Health Sciences, Amoebas, lcsh:Science, Protozoans, Acanthamoeba castellanii, Phagocytes, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Medical Microbiology, Viral Pathogens, Viruses, Cellular Types, Pathogens, Research Article, Cell Survival, Immune Cells, Immunology, Research and Analysis Methods, Microbiology, Cell Line, Virology, Parasite Groups, parasitic diseases, Humans, Trophozoites, Immunoassays, Microbial Pathogens, Blood Cells, Adenoviruses, Human, Macrophages, lcsh:R, Organisms, Biology and Life Sciences, Cell Biology, Coculture Techniques, Parasitic Protozoans, Viral Replication, DNA, Viral, Immunologic Techniques, lcsh:Q, Parasitology, DNA viruses, Apicomplexa
Abstract

International audience; Free living amoebae (FLA) including Acanthamoeba castellanii, are protozoa that feed on different microorganisms including viruses. These microorganisms show remarkable similarities with macrophages in cellular structures, physiology or ability to phagocyte preys, and some authors have therefore wondered whether Acanthamoeba and macrophages are evolutionary related. It has been considered that this amoeba may be an in vitro model to investigate relationships between pathogens and macrophagic cells. So, we intended in this study to compare the interactions between a human adenovirus strain and A. castellanii or THP-1 macrophagic cells. The results of molecular and microscopy techniques following co-cultures experiments have shown that the presence of the adenovirus decreased the viability of macrophages, while it has no effect on amoebic viability. On another hand, the viral replication occurred only in macrophages. These results showed that this amoebal model is not relevant to explore the relationships between adenoviruses and macrophages in in vitro experiments.

Published
2017
Full Text
View/download PDF

20. Differentiating Merkel cell carcinoma of lymph nodes without a detectable primary skin tumor from other metastatic neuroendocrine carcinomas: The ELECTHIP criteria

Author

Kervarrec, Thibault, primary, Zaragoza, Julia, additional, Gaboriaud, Pauline, additional, Le Gouge, Amélie, additional, Beby-Defaux, Agnès, additional, Le Corre, Yannick, additional, Hainaut-Wierzbicka, Ewa, additional, Aubin, Francois, additional, Bens, Guido, additional, Michenet, Patrick, additional, Maillard, Hervé, additional, Touzé, Antoine, additional, Samimi, Mahtab, additional, and Guyétant, Serge, additional

Published
2018
Full Text
View/download PDF

21. Epithelial to mesenchymal transition and HPV infection in squamous cell oropharyngeal carcinomas: the papillophar study.

Author

Lefevre, Marine, Rousseau, Alexandra, Rayon, Thomas, Dalstein, Véronique, Clavel, Christine, Beby-Defaux, Agnès, Pretet, Jean-Luc, Soussan, Patrick, Polette, Myriam, Lacau Saint Guily, Jean, Birembaut, Philippe, Dalstein, Véronique, Beby-Defaux, Agnès, and Papillophar Study Group

Abstract

Background: Human Papillomavirus (HPV) infection is recognised as aetiological factor of carcinogenesis in oropharyngeal squamous cell carcinomas (OPC). HPV-related OPC respond better to treatments and have a significantly favourable outcome. Epithelial to mesenchymal transition (EMT) implicated in tumour invasion, is a hallmark of a poor prognosis in carcinomas.Methods: We have studied the relationship of EMT markers (E-cadherin, β-catenin and vimentin) with HPV infection (DNA and E6/E7 mRNA detection), p16INK4a expression and survival outcomes in a cohort of 296 patients with OPC.Results: Among the 296 OPSSC, 26% were HPV positive, 20.3% had overt EMT (>25% of vimentin positive tumour cells). Lower E-cadherin expression was associated with a higher risk of distant metastasis in univariate (P=0.0110) and multivariate analyses (hazard ratios (HR)=6.86 (1.98; 23.84)). Vimentin expression tends towards worse metastasis-free survival (MFS; HR=2.53 (1.00; 6.41)) and was an independent prognostic factor of progression-free survival (HR=1.55 (1.03; 2.34)).Conclusions: There was a non significant association of EMT with HPV status. This may be explained by a mixed subpopulation of patients HPV positive with associated risk factors (HPV, tobacco and alcohol). Thus, the detection of EMT in OPC represents another reliable approach in the prognosis and the management of OPC whatever their HPV status. [ABSTRACT FROM AUTHOR]

Published
2017
Full Text
View/download PDF

26. Human papillomavirus genotype distribution in oropharynx and oral cavity cancer in France—The EDiTH VI study

Author

St Guily, Jean Lacau, primary, Jacquard, Anne-Carole, additional, Prétet, Jean-Luc, additional, Haesebaert, Julie, additional, Beby-Defaux, Agnès, additional, Clavel, Christine, additional, Agius, Gérard, additional, Birembaut, Philippe, additional, Okaïs, Claire, additional, Léocmach, Yann, additional, Soubeyrand, Benoît, additional, Pradat, Pierre, additional, Riethmuller, Didier, additional, Mougin, Christiane, additional, and Denis, François, additional

Published
2011
Full Text
View/download PDF

27. Human papillomavirus genotype distribution in tonsil cancers

Author

St Guily, Jean Lacau, primary, Clavel, Christine, additional, Okaïs, Claire, additional, Prétet, Jean-Luc, additional, Beby-Defaux, Agnès, additional, Agius, Gérard, additional, Birembaut, Philippe, additional, Jacquard, Anne-Carole, additional, Léocmach, Yann, additional, Soubeyrand, Benoît, additional, Riethmuller, Didier, additional, Denis, François, additional, and Mougin, Christiane, additional

Published
2011
Full Text
View/download PDF

29. Human Papillomavirus 16 Oncoprotein E7 Stimulates UBF1-Mediated rDNA Gene Transcription, Inhibiting a p53-Independent Activity of p14ARF.

Author

Dichamp, Isabelle, Séité, Paule, Agius, Gérard, Barbarin, Alice, and Beby-Defaux, Agnès

Subjects
PAPILLOMAVIRUS diseases, CANCER research, STATHMIN, RECOMBINANT DNA, GENETIC transcription, P53 antioncogene, DISEASE risk factors
Abstract

High-risk human papillomavirus oncoproteins E6 and E7 play a major role in HPV-related cancers. One of the main functions of E7 is the degradation of pRb, while E6 promotes the degradation of p53, inactivating the p14ARF-p53 pathway. pRb and p14ARF can repress ribosomal DNA (rDNA) transcription in part by targeting the Upstream Binding Factor 1 (UBF1), a key factor in the activation of RNA polymerase I machinery. We showed, through ectopic expression and siRNA silencing of p14ARF and/or E7, that E7 stimulates UBF1-mediated rDNA gene transcription, partly because of increased levels of phosphorylated UBF1, preventing the inhibitory function of p14ARF. Unexpectedly, activation of rDNA gene transcription was higher in cells co-expressing p14ARF and E7, compared to cells expressing E7 alone. We did not find a difference in P-UBF1 levels that could explain this data. However, p14ARF expression induced E7 to accumulate into the nucleolus, where rDNA transcription takes place, providing an opportunity for E7 to interact with nucleolar proteins involved in this process. GST-pull down and co-immunoprecipitation assays showed interactions between p14ARF, UBF1 and E7, although p14ARF and E7 are not able to directly interact. Co-expression of a pRb-binding-deficient mutant (E7C24G) and p14ARF resulted in EC24G nucleolar accumulation, but not in a significant higher activation of rDNA transcription, suggesting that the inactivation of pRb is involved in this phenomenon. Thus, p14ARF fails to prevent E7-mediated UBF1 phosphorylation, but could facilitate nucleolar pRb inactivation by targeting E7 to the nucleolus. While others have reported that p19ARF, the mouse homologue of p14ARF, inhibits some functions of E7, we showed that E7 inhibits a p53-independent function of p14ARF. These results point to a mutually functional interaction between p14ARF and E7 that might partly explain why the sustained p14ARF expression observed in most cervical pre-malignant lesions and malignancies may be ineffective. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

30. Lack of correlation between nutritional status and seroprotection against influenza in a long term care facility.

Author

Paccalin, Marc, Plouzeau, Chloé, Bouche, Gauthier, Guillard, Olivier, Beby-Defaux, Agnès, Mauco, Gérard, and Agius, Gérard

Subjects
NUTRITIONAL assessment, INFLUENZA, LONG-term care facilities, POLYMERASE chain reaction, VIRUS diseases, MEDICAL care
Abstract

We conducted a prospective study in a long-term care facility. Virologic diagnosis was assessed using viral isolation, polymerase chain reaction and serology for all patients with a flu-like syndrome. Albumin, vitamins and trace elements were also measured. Results. The risk of influenza increased 6.5-fold in patients with an antibody titer of 40 during the influenza outbreak ( P =0.04). Micronutriments and vitamins deficiencies were important. Patients with antibody titer >1:40 could still be infected by the virus without correlation with the nutritional status. Conclusion. Humoral protection with a titer >1:40 might not be protective in the elderly. Nutritional deficiencies were too prevalent to detect any effect on the results. [ABSTRACT FROM AUTHOR]

Published
2006
Full Text
View/download PDF

33. Human Papillomavirus 16 Oncoprotein E7 Stimulates UBF1-Mediated rDNA Gene Transcription, Inhibiting a p53-Independent Activity of p14ARF.

Author

Dichamp, Isabelle, Séité, Paule, Agius, Gérard, Barbarin, Alice, and Beby-Defaux, Agnès

Subjects
*PAPILLOMAVIRUS diseases, *CANCER research, *STATHMIN, *RECOMBINANT DNA, *GENETIC transcription, *P53 antioncogene, *DISEASE risk factors
Abstract

High-risk human papillomavirus oncoproteins E6 and E7 play a major role in HPV-related cancers. One of the main functions of E7 is the degradation of pRb, while E6 promotes the degradation of p53, inactivating the p14ARF-p53 pathway. pRb and p14ARF can repress ribosomal DNA (rDNA) transcription in part by targeting the Upstream Binding Factor 1 (UBF1), a key factor in the activation of RNA polymerase I machinery. We showed, through ectopic expression and siRNA silencing of p14ARF and/or E7, that E7 stimulates UBF1-mediated rDNA gene transcription, partly because of increased levels of phosphorylated UBF1, preventing the inhibitory function of p14ARF. Unexpectedly, activation of rDNA gene transcription was higher in cells co-expressing p14ARF and E7, compared to cells expressing E7 alone. We did not find a difference in P-UBF1 levels that could explain this data. However, p14ARF expression induced E7 to accumulate into the nucleolus, where rDNA transcription takes place, providing an opportunity for E7 to interact with nucleolar proteins involved in this process. GST-pull down and co-immunoprecipitation assays showed interactions between p14ARF, UBF1 and E7, although p14ARF and E7 are not able to directly interact. Co-expression of a pRb-binding-deficient mutant (E7C24G) and p14ARF resulted in EC24G nucleolar accumulation, but not in a significant higher activation of rDNA transcription, suggesting that the inactivation of pRb is involved in this phenomenon. Thus, p14ARF fails to prevent E7-mediated UBF1 phosphorylation, but could facilitate nucleolar pRb inactivation by targeting E7 to the nucleolus. While others have reported that p19ARF, the mouse homologue of p14ARF, inhibits some functions of E7, we showed that E7 inhibits a p53-independent function of p14ARF. These results point to a mutually functional interaction between p14ARF and E7 that might partly explain why the sustained p14ARF expression observed in most cervical pre-malignant lesions and malignancies may be ineffective. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

34. Stable prevalence of transmitted drug resistance mutations and increased circulation of non-B subtypes in antiretroviral-naive chronically HIV-infected patients in 2015/2016 in France.

Author

Assoumou L, Bocket L, Pallier C, Grude M, Ait-Namane R, Izopet J, Raymond S, Charpentier C, Visseaux B, Wirden M, Trabaud MA, Le Guillou-Guillemette H, Allaoui C, Henquell C, Krivine A, Dos Santos G, Delamare C, Bouvier-Alias M, Montes B, Ferre V, De Monte A, Signori-Schmuck A, Maillard A, Morand-Joubert L, Tumiotto C, Fafi-Kremer S, Amiel C, Barin F, Marque-Juillet S, Courdavault L, Vallet S, Beby-Defaux A, de Rougemont A, Fenaux H, Avettand-Fenoel V, Allardet-Servent A, Plantier JC, Peytavin G, Calvez V, Chaix ML, and Descamps D

Subjects
Adult, CD4 Lymphocyte Count, Chronic Disease epidemiology, Female, France epidemiology, Genotype, HIV Infections drug therapy, HIV Infections epidemiology, HIV Seropositivity epidemiology, HIV-1 classification, HIV-1 drug effects, Humans, Male, Middle Aged, Prevalence, RNA, Viral blood, Anti-HIV Agents therapeutic use, Drug Resistance, Viral genetics, HIV Infections transmission, HIV-1 genetics, Mutation
Abstract

Objectives: We estimated the prevalence of transmitted-drug-resistance-associated mutations (TDRAMs) in antiretroviral-naive chronically HIV-1-infected patients., Patients and Methods: TDRAMs were sought in samples from 660 diagnosed HIV-1-infected individuals in 2015/2016 in 33 HIV clinical centres. Weighted analyses, considering the number of patients followed in each centre, were used to derive representative estimates of the percentage of individuals with TDRAMs. Results were compared with those of the 2010/2011 survey (n = 661) using the same methodology., Results: At inclusion, median CD4 cell counts and plasma HIV-1 RNA were 394 and 350/mm3 (P = 0.056) and 4.6 and 4.6 log10 copies/mL (P = 0.360) in the 2010/2011 survey and the 2015/2016 survey, respectively. The frequency of non-B subtypes increased from 42.9% in 2010/2011 to 54.8% in 2015/2016 (P < 0.001), including 23.4% and 30.6% of CRF02&#95;AG (P = 0.004). The prevalence of virus with protease or reverse-transcriptase TDRAMs was 9.0% (95% CI = 6.8-11.2) in 2010/2011 and 10.8% (95% CI = 8.4-13.2) in 2015/2016 (P = 0.269). No significant increase was observed in integrase inhibitor TDRAMs (6.7% versus 9.2%, P = 0.146). Multivariable analysis showed that men infected with the B subtype were the group with the highest risk of being infected with a resistant virus compared with others (adjusted OR = 2.2, 95% CI = 1.3-3.9)., Conclusions: In France in 2015/2016, the overall prevalence of TDRAMs was 10.8% and stable compared with 9.0% in the 2010/2011 survey. Non-B subtypes dramatically increased after 2010. Men infected with B subtype were the group with the highest risk of being infected with a resistant virus, highlighting the need to re-emphasize safe sex messages., (© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2019
Full Text
View/download PDF

35. Acanthamoeba castellanii is not be an adequate model to study human adenovirus interactions with macrophagic cells.

Author

Maisonneuve E, Cateau E, Leveque N, Kaaki S, Beby-Defaux A, and Rodier MH

Subjects
Adenoviruses, Human ultrastructure, Cell Line, Cell Survival, Coculture Techniques, DNA, Viral metabolism, Fluorescent Antibody Technique, Humans, Macrophages ultrastructure, Phagocytes cytology, Trophozoites ultrastructure, Acanthamoeba castellanii physiology, Adenoviruses, Human physiology, Macrophages parasitology, Macrophages virology
Abstract

Free living amoebae (FLA) including Acanthamoeba castellanii, are protozoa that feed on different microorganisms including viruses. These microorganisms show remarkable similarities with macrophages in cellular structures, physiology or ability to phagocyte preys, and some authors have therefore wondered whether Acanthamoeba and macrophages are evolutionary related. It has been considered that this amoeba may be an in vitro model to investigate relationships between pathogens and macrophagic cells. So, we intended in this study to compare the interactions between a human adenovirus strain and A. castellanii or THP-1 macrophagic cells. The results of molecular and microscopy techniques following co-cultures experiments have shown that the presence of the adenovirus decreased the viability of macrophages, while it has no effect on amoebic viability. On another hand, the viral replication occurred only in macrophages. These results showed that this amoebal model is not relevant to explore the relationships between adenoviruses and macrophages in in vitro experiments.

Published
2017
Full Text
View/download PDF

37. Virologic diagnosis and follow-up of children born to mothers infected by HIV-1 group O.

Author

Gueudin M, Lemée V, Ferre V, Beby-Defaux A, Pathé JP, Guist'hau O, Braun J, Simon F, and Plantier JC

Subjects
DNA, Viral blood, Female, HIV Infections virology, Humans, Infant, Newborn, Infectious Disease Transmission, Vertical, Polymerase Chain Reaction methods, Proviruses, RNA, Viral blood, Viral Load, HIV Infections diagnosis, HIV Infections transmission, HIV-1 classification
Published
2004
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results