Author: "Baillat, V." - Searchworks@Jio Institute Digital Library Search Results

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37 results on '"Baillat, V."'

1. Immunovirological status in people with perinatal and adult-acquired HIV-1 infection: a multi-cohort analysis from France

Author: Aumaitre, H., Froguel, E., Caby, F., Dellion, S., Gerard, L., Lucht, F., Chirouze, C., Dupon, M., Schmit, Jl, Goujard, C., Allegre, T., Cazenave, B., Hittinger, G., De Truchis, P., Cailhol, J., Duvivier, C., Canestri, A., Bouchaud, O., Karmochkine, M., Salmon-Ceron, D., Zucman, D., Mortier, E., Tubiana, R., Girard, P.M., Pintado, C., Cabie, A., Rabier, V., Morlat, P., Neau, D., Genet, C., Makhloufi, D., Ronot, S Bregigeon, Ghosn, J., Reliquet, V., Perré, P., Pellegrin, Jl, Arvieux, C., Cheneau, C., Bernard, L., Delobel, P., Verdon, R., Jacomet, C., Piroth, L., Ajana, F., Bevilacqua, S., Debab, Y., Lecapitaine, A.L., Cotte, L., Mokhtari, S., Mercie, P., Poubeau, P., Garrait, V., Khuong, Ma, Beck-Wirth, G., Blum, L., Blanche, S., Boccara, F., Prazuck, T., Barbuat, C., Viard, J.P., Stegmann-Planchard, S., Martha, B., Treluyer, J.M., Dore, E., Gaud, C., Niault, M., Fernandes, E., Hitoto, H., Compagnucci, A., Elenga, N., Faye, A., Dollfus, C., Chace, A., Levine, M., Martha, S.A., Floch-Tudal, C., Kebaïli, K., Entz-Werle, N., Tricoire, J., Mazingue, F., Bolot, P., Brazille, P., Goetghebuer, T., Gennotte, A.F., Van Der Linden, D., Schmitz, V., Moutschen, M., Crenn-Hebert, C., Habibi, F., Coursol, A., Guesdon, E., Ceccaldi, P.F., Dehlinger – Paul, M., Pannier, E., Marcou, V., Elleau, C., Achkar, M., Vareil, M.O., Couderc, S., Routier, C., Bouldouyre, M.A., Selleret, L., Chabrol, A., Bellahcene, C., Pluchart, C., Yangui, A., Vignes, D., Alissa, A., Johnson, A., Lachassinne, E., Benbara, A., Karaoui, L., Bongain, A., Yakeu, B., Schmit, J.L., Cravello, L., Hubert, C., Faucher, P., Pinquier, D., Borie, C., Rocchi, D., Brunet-Cartier, C., Briandet, C., Brouard, J., Chalvon-Demersay, A., Rajguru, M., Billiemaz, K., Fresard, A., Moulin, A., Fialaire, P., Mesnard, L., Werner, E., Vintejoux, E., Marian, J., Ranaivojaona, S., Bissuel, F., Abdelhadi, M., Hammou, Y., Genet-Villeger, C., Hatchuel, Y., Bachelard, G., Medus, M., Dendale – Nguyen, J., Guimard, T.S., Martha, A., Rouha, M., Perfezou, P., De Saint Martin, L., Jaffuel, S., Buzele, R., Gousseff, M., Cudeville, C., Vitrat, V., Michau, C., Palenzuela, G., Driessen, M., Heller-Roussin, B., Labaune, J.M., Muanza, B., Massardier, J., Partisani, M., Hau, I., Runel-Belliard, C., Brehin, C., Kebaili, K., Lalande, M., Lagree, M., Lacombe, K., Molina, J.-M., Reynes, J., Robineau, O., Raffi, F., Becker, A., Weiss, L., Allègre, T., Pialoux, G., Souala, F., Rami, A., Katlama, C., Cabié, A., Viard, J.-P., Bastides, F., Michel, C., Salmon, D., Lièvre, J-D Le, Sotto, A., Rouveix, E., Naqvi, A., Brégigeon, S., Rodet, R., Simon-Coutelier, A., Esnault, J.-L., Buzelé, R., Stein, A., Godin-Colet, C., Pichancourt, G., Caraux-Paz, P., Zadeh, M Mohseni, Gérard, L., Lascaux-Cametz, C., Bodard, L., Pellegrin, J.-L., Ettahar, N., Uludag, A., Rosenthal, E., Prevoteau du Clary, F., Jaureguiberry, S., Philibert, P., Lecapitaine, A.-L., Chakvetadze, E., Champagne, H., Daneluzzi, V., Goupil de Bouillé, J., Leprêtre, A., Lamaury, I., Darasteanu, I., Abraham, B., Garipuy, D., Berger, J.-L., Schmit, J.-L., Diallo, K., Gourdon, F., Vaillant, O., Gaborieau, V., Doll, J., Quinsat, D., Geffray, L., Girard, J.-J., Houlbert, D., Perronne, V., Klement, E., Antioniotti, O., Rouzioux, C., Avettand-Fenoel, V., Lortholary, O., Boucly, S., Maignan, A., Thiebaut, R., Meyer, L., Boufassa, F., Charles, M.A., Dray-Spira, R., Legeai, C., Amon, V., Benammar, N., Seng, R., Slama, L., Bonnard, P., Chakvetadze, C., L’Yavanc, T., Capeau, J., Vigouroux, C., Fellahi, S., Bastard, J.P., Oksenhendler, E., Bourge, J.F., Bajzik, V., Sereni, D., Lascoux-Combe, C., Taulera, O., Dien, L.V., Delgado, J., Molina, J.M., Saint-Marc, T., Ferret, S., Pavie, J., Bergmann, J.F., Parrinello, M., BLefebvre, Boudraa, C., Diallo, B., Lupin, C., Herson, S., Simon, A., Edeb, N., Guillevin, L., Tahi, T., Pietri, M.P., Tisne-Dessus, D., Jalbert, C., Yeni, P., Matheron, S., Pahlavan, G., Phung, B., El-Alami Talbi, N., Ramani, Z., Catalano, G., Godard, C., Boue, F., Chambrin, V., Bornarel, D., Schoen, H., Carlier, R., Fantin, B., Poder, C., Dhote, R., Bentata, M., Honore, P., Tuyet, Xuan, Delfraissy, J.F., Chaix, F., Rannou, M.T., Levy, Y., Sobel, A., Dumont, C., Abel, S., Pierre-François, S., Beaujolais, V., Poizot-Martin, I., Zaegel-Faucher, O., Debreux, C., Moreau, J., Van Der Gheynst, E., Thiebaut-Drobacheff, M.C., Foltzer, A., Hoen, B., Faucher, J.F., Gil, H., Ragnaud, J.M., Raymond, I., Louis, I., Hessamfar, M., Baillat, V., De Boever, C Merle, Tramoni, C., Soufflet, A., Guadagnin, P., Choutet, P., Mounoury, O., Brosseau, D., Hue, H., May, T., Wassoumbou, S., Stenzel, M., Bouillon, M.P., Yazdanpanah, Y., Huleux, T., Aissi, E., Pavel, S., Rey, D., Fischer, P., Blaison, G., Martinot, M., Pachart, A., Jeanblanc, F., Touraine, J.L., Trepo, C., Miailhes, P., Kouadjo, K., Thoirain, V., Brochier, C., Perre, P., Leautez, S., Esnault, J.L., Suaud, I., Seng, Rémonie, Frange, Pierre, Faye, Albert, Dollfus, Catherine, le Chenadec, Jérôme, Boufassa, Faroudy, Essat, Asma, Goetghebuer, Tessa, Arezes, Elisa, Avettand-Fènoël, Véronique, Bigna, Jean-Joël, Blanche, Stéphane, Goujard, Cécile, Meyer, Laurence, Warszawski, Josiane, and Viard, Jean-Paul
Published: 2024
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2. Levels and determinants of breast and cervical cancer screening uptake in HIV‐infected women compared with the general population in France

Author: Tron, L, Lert, F, Spire, B, DraySpira, R, Allègre, T, Mours, P., Riou, J.M., Sordage, M., Chennebault, J. M., Fialaire, P., Rabier, V., Froidure, M., Huguet, D., Leduc, D., Pichancourt, G., Wajsbrot, A., Bourdeaux, C., Foltzer, A., Hoen, B., HustacheMathieu, L., Abgrall, S., Barruet, R., Bouchaud, O., Chabrol, A., Mattioni, S, Mechai, F., Jeantils, V., Bernard, N., Bonnet, F., Hessamfar, M., Lacoste, D., Malvy, D., Mercié, P., Morlat, P., Paccalin, F., Pertusa, M. C., Pistone, T., Receveur, M. C., Vandenhende, M. A., Dupont, C., Freire Maresca, A., Leporrier, J., Rouveix, E., Dargere, S., de la Blanchardière, ., Martin, A., Noyon, V., Verdon, R., Rogeaux, O., Beytout, J., Gourdon, F., Laurichesse, H., Meier, F., Mortier, E., Simonpoli, A. M., Cordier, F., Delacroix, I., Garrait, V., Elharrar, B., Dominguez, S., Lascaux, A. S., Lelièvre, J. D., Levy, Y., Melica, G., Buisson, M., Piroth, L., Waldner, A., Gruat, N., Leprêtre, A., de Truchis, P., Le Du, D, Melchior, J. Cl., Sehouane, R., Troisvallets, D., Blanc, M., BocconGibod, I., Bosseray, A., Brion, J. P., Durand, F., Leclercq, P., Marion, F., Pavese, P., BrottierMancini, E., Faba, L., RoncatoSaberan, M., BollengierStragier, O., Esnault, J. L., LeautezNainville, S., Perré, P., Froguel, E., Nguessan, M., Simon, P., Colardelle, P., Doll, J., GodinCollet, C., RoussinBretagne, S., Delfraissy, J. F., Duracinsky, M., Goujard, C., Peretti, D., Quertainmont, Y., Marionneau, J., Aissi, E., Van Grunderbeeck, N, Denes, E., DucroixRoubertou, S., Genet, C., Weinbreck, P., AugustinNormand, C., Boibieux, A., Cotte, L., Ferry, T., Koffi, J., Miailhes, P., Perpoint, T., Peyramond, D., Schlienger, I., Brunel, J. M., Carbonnel, E., Chiarello, P., Livrozet, J. M., Makhloufi, D., Dhiver, C., Husson, H., Madrid, A., Ravaux, I., de Severac, M.L., Thierry Mieg, M., Tomei, C., Hakoun, S., Moreau, J., Mokhtari, S., Soavi, M. J., Faucher, O., Ménard, A., Orticoni, M., PoizotMartin, I., Soavi, M. J., Atoui, N., Baillat, V., Faucherre, V., Favier, C., Jacquet, J. M., Le Moing, V, Makinson, A., Mansouri, R., Merle, C., Elforzli, N., Allavena, C., Aubry, O., Besnier, M., Billaud, E., Bonnet, B., Bouchez, S., Boutoille, D., Brunet, C., Feuillebois, N., Lefebvre, M., MorineauLe Houssine, P, Mounoury, O., Point, P., Raffi, F., Reliquet, V., Talarmin, J. P., Ceppi, C., Cua, E., Dellamonica, P., De SalvadorGuillouet, Durant, J., Ferrando, S., MondainMiton, V., Perbost, I., Pillet, S., ProuvostKeller, B., Pradier, C., Pugliese, P., Roger, P. M., Rosenthal, E., Sanderson, F., Hocqueloux, L., Niang, M., Prazuck, T., Arsac, P., BarraultAnstett, M.F., Ahouanto, M., Bouvet, E., Castanedo, G., CharloisOu, C., Dia Kotuba, A., EidAntoun, Z., Jestin, C., Jidar, K., Joly, V., KhuongJosses, M. A., Landgraf, N., Landman, R., Lariven, S., Leprêtre, A., Lʼhériteau, F., Machado, M., Matheron, S., Michard, F., Morau, G., Pahlavan, G., Phung, B. C., Prévot, M. H., Rioux, C., Yéni, P., BaniSadr, F., Calboreanu, A., Chakvetadze, E., Salmon, D., Silbermann, B., Batisse, D., Beumont, M., Buisson, M., Castiel, P., Derouineau, J., Eliaszewicz, M., Gonzalez, G., Jayle, D., Karmochkine, M., Kousignian, P., Pavie, J., Pierre, I., Weiss, L., Badsi, E., Bendenoun, M., Cervoni, J., Diemer, M., Durel, A., Rami, A., Sellier, P., AitMohand, H., Amirat, N., Bonmarchand, M., Bourdillon, F., Breton, G., Caby, F., Grivois, J. P., Katlama, C., Kirstetter, M., Paris, L., Pichon, F., Roudière, L., Schneider, L., Samba, M. C., Seang, S., Simon, A., Stitou, H., Tubiana, R., Valantin, M. A., Bollens, D., Bottero, J., Bui, E., Campa, P., Fonquernie, L., Fournier, S., Girard, P. M., Goetschel, A., Guyon, H. F., Lacombe, K., Lallemand, F., Lefebvre, B., Maynard, J. L., Meyohas, M. C., Ouazene, Z., Pacanowski, J., Picard, O., Raguin, G., Roussard, P., Tourneur, M., Tredup, J., Valin, N., Balkan, S., Clavel, F., Colin de Verdière, N, De Castro, N., de Lastours, V., Ferret, S., Gallien, S., Garrait, V., Gérard, L., Goguel, J., Lafaurie, M., LascouxCombe, C., Molina, J. M., Oksenhendler, E., Pavie, J., Pintado, C., Ponscarme, D., Rozenbaum, W., Scemla, A., Bonnard, P., Lassel, L., Lebrette, M. G., Lyavanc, T., Mariot, P., Missonnier, R., Ohayon, M., Pialoux, G., Treilhou, M. P., Vincensini, J. P., Gilquin, J., Hadacek, B., NaitIghil, L., Nguyen, T. H., Pintado, C., Sobel, A., Viard, J. P., Zak Dit Zbar, O., Aumaître, H., Eden, A., Ferreyra, M., Lopez, F., Medus, M., Neuville, S., Saada, M., Blum, L., Perfezou, P., Arvieux, C., Chapplain, J. M., Revest, M., Souala, F., Tattevin, P., Bord, S., BorsaLebas, F., Caron, F., Chapuzet, C., Debab, Y., Gueit, I., Etienne, M., Fartoukh, C., Feltgen, K., Joly, C., RobadayVoisin, S., Suel, P., Khuong, M. A., Krausse, J., Poupard, M., Tran Van, G., Cazorla, C., Daoud, F., Fascia, P., Frésard, A., Guglielminotti, C., Lucht, F., BernardHenry, C., Cheneau, C., Lang, J. M., de Mautort, E., Partisani, M., Priester, M., Rey, D., Majerholc, C., Zucman, D., Assi, A., Lafeuillade, A., de Jaureguiberry, J. P., Gisserot, O., Aquilina, C., Prevoteau du Clary, F., Alvarez, M., Chauveau, M., Cuzin, L., Delobel, P., Garipuy, D., Labau, E., Marchou, B., Massip, P., Mularczyk, M., Obadia, M., Ajana, F., Allienne, C., Baclet, V., de la Tribonnière, X, Huleux, T., Melliez, H., Meybeck, A., Riff, B., Valette, M., Viget, N., Bastides, F., Bernard, L., Gras, G., Guadagnin, P., May, T., Rabaud, C., Dos Santos, A, P oinsignon, Y., Derradji, O., Escaut, L., Teicher, E., Vittecoq, D., Bantsima, J., CarauxPaz, P., and Patey, O.
Published: 2017
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3. Opportunistic infections and AIDS malignancies early after initiating combination antiretroviral therapy in high-income countries

Author: Lodi, Sara, Del Amo, Julia, Moreno, Santiago, Bucher, H. C., Furrer, Hansjakob, Logan, Roger, Sterne, Jonathan, Pérez-Hoyos, Santiago, Jarrín, Inma, Phillips, Andrew, Olson, Ashley, Van Sighem, Ard, Reiss, Peter, Sabin, C., Jose, Sophie, Justice, Amy, Goulet, Joseph, Miró, José M., Ferrer, Elena, Meyer, Laurence, Seng, Rémonie, Vourli, Georgia, Antoniadou, Anastasia, Dabis, Francois, Vandenhede, Mari Anne, Costagliola, Dominique, Abgrall, S., Hernán, Miguel A., Hernan, Miguel, Bansi, L., Hill, T., Dunn, D., Porter, K., Glabay, A., Orkin, C., Thomas, R., Jones, K., Fisher, M., Perry, N., Pullin, A., Churchill, D., Gazzard, B., Nelson, M., Asboe, D., Bulbeck, S., Mandalia, S., Clarke, J., Delpech, V., Anderson, J., Munshi, S., Post, F., Easterbrook, P., Khan, Y., Patel, P., Karim, F., Duffell, S., Gilson, R., Man, S. L., Williams, I., Gompels, M., Dooley, D., Schwenk, A., Ainsworth, J., Johnson, M., Youle, M., Lampe, F., Smith, C., Grabowska, H., Chaloner, C., Ismajani Puradiredja, D., Phillips, A., Walsh, J., Weber, J., Kemble, C., Mackie, N., Winston, A., Leen, C., Wilson, A., Bezemer, D. O., Gras, L. A.J., Kesselring, A. M., Van Sighem, A. I., Zaheri, S., Van Twillert, G., Kortmann, W., Branger, J., Prins, J. M., Kuijpers, T. W., Scherpbier, H. J., Van Der Meer, J. T.M., Wit, F. W.M.N., Godfried, M. H., Reiss, P., Van Der Poll, T., Nellen, F. J.B., Lange, J. M.A., Geerlings, S. E., Van Vugt, M., Pajkrt, D., Bos, J. C., Van Der Valk, M., Grijsen, M. L., Wiersinga, W. J., Brinkman, K., Blok, W. L., Frissen, P. H.J., Schouten, W. E.M., Van Den Berk, G. E.L., Veenstra, J., Lettinga, K. D., Mulder, J. W., Vrouenraets, S. M.E., Lauw, F. N., Van Eeden, A., Verhagen, D. W.M., Van Agtmael, M. A., Perenboom, R. M., Claessen, F. A.P., Bomers, M., Peters, E. J.G., Richter, C., Van Der Berg, J. P., Gisolf, E. H., Schippers, E. F., Van Nieuwkoop, C., Van Elzakker, E. P., Leyten, E. M.S., Gelinck, L. B.S., Pronk, M. J.H., Bravenboer, B., Kootstra, G. J., Delsing, C. E., Sprenger, H. G., Doedens, R., Scholvinck, E. H., Van Assen, S., Bierman, W. F.W., Soetekouw, R., Ten Kate, R. W., Van Vonderen, M. G.A., Van Houte, D. P.F., Kroon, F. P., Van Dissel, J. T., Arend, S. M., De Boer, M. G.J., Jolink, H., Ter Vollaard, H. J.M., Bauer, M. P., Weijer, S., El Moussaoui, R., Lowe, S., Schreij, G., Oude Lashof, A., Posthouwer, D., Koopmans, P. P., Keuter, M., Van Der Ven, A. J.A.M., Ter Hofstede, H. J.M., Dofferhoff, A. S.M., Warris, A., Van Crevel, R., Van Der Ende, M. E., De Vries-Sluijs, T. E.M.S., Schurink, C. A.M., Nouwen, J. L., Nispen Tot Pannerden, M. H., Verbon, A., Rijnders, B. J.A., Van Gorp, E. C.M., Hassing, R. J., Smeulders, A. W.M., Hartwig, N. G., Driessen, G. J.A., Den Hollander, J. G., Pogany, K., Juttmann, J. R., Van Kasteren, M. E.E., Hoepelman, A. I.M., Mudrikova, T., Schneider, M. M.E., Jaspers, C. A.J.J., Ellerbroek, P. M., Oosterheert, J. J., Arends, J. E., Wassenberg, M. W.M., Barth, R. E., Geelen, S. P.M., Wolfs, T. F.W., Bont, L. J., Van Den Berge, M., Stegeman, A., Groeneveld, P. H.P., Alleman, M. A., Bouwhuis, J. W., Barin, F., Burty, C., Duvivier, C., Enel, P., Fredouille-Heripret, L., Gasnault, J., Khuong, M. A., Mahamat, A., Pilorgé, F., Tattevin, P., Salomon, Valérie, Jacquemet, N., Costagliola, D., Grabar, S., Guiguet, M., Lanoy, E., Lièvre, L., Mary-Krause, M., Selinger-Leneman, H., Lacombe, J. M., Potard, V., Bricaire, F., Herson, S., Katlama, C., Simon, A., Desplanque, N., Girard, P. M., Meynard, J. L., Meyohas, M. C., Picard, O., Cadranel, J., Mayaud, C., Pialoux, G., Clauvel, J. P., Decazes, J. M., Gérard, L., Molina, J. M., Diemer, M., Sellier, P., Bentata, M., Honoré, P., Jeantils, V., Tassi, S., Mechali, D., Taverne, B., Bouvet, E., Crickx, B., Ecobichon, J. L., Matheron, S., Picard-Dahan, C., Yeni, P., Berthé, H., Dupont, C., Chandemerle, C., Mortier, E., De Truchis, P., Tisne-Dessus, D., Weiss, L., Salmon, D., Auperin, I., Gilquin, J., Roudière, L., Viard, J. P., Boue, F., Fior, R., Delfraissy, J. F., Goujard, C., Jung, C., Lesprit, Ph, Vittecoq, D., Fraisse, P., Lang, J. M., Rey, D., Beck-Wirth, G., Stahl, J. P., Lecercq, P., Gourdon, F., Laurichesse, H., Fresard, A., Lucht, F., Bazin, C., Verdon, R., Chavanet, P., Arvieux, C., Michelet, C., Choutet, P., Goudeau, A., Maître, M. F., Hoen, B., Eglinger, P., Faller, J. P., Borsa-Lebas, F., Caron, F., Reynes, J., Daures, J. P., May, T., Rabaud, C., Berger, J. L., Rémy, G., Arlet-Suau, E., Cuzin, L., Massip, P., Thiercelin Legrand, M. F., Pontonnier, G., Viget, N., Yasdanpanah, Y., Dellamonica, P., Pradier, C., Pugliese, P., Aleksandrowicz, K., Quinsat, D., Ravaux, I., Tissot-Dupont, H., Delmont, J. P., Moreau, J., Gastaut, J. A., Poizot Martin, I., Retornaz, F., Soubeyrand, J., Galinier, A., Ruiz, J. M., Allegre, T., Blanc, P. A., Bonnet-Montchardon, D., Lepeu, G., Granet-Brunello, P., Esterni, J. P., Pelissier, L., Cohen-Valensi, R., Nezri, M., Chadapaud, S., Laffeuillade, A., Billaud, E., Raffi, F., Boibieux, A., Peyramond, D., Livrozet, J. M., Touraine, J. L., Cotte, L., Trepo, C., Strobel, M., Bissuel, F., Pradinaud, R., Sobesky, M., Cabié, A., Gaud, C., Contant, M., Aubert, V., Barth, J., Battegay, M., Bernasconi, E., Böni, J., Burton-Jeangros, C., Calmy, A., Cavassini, M., Egger, M., Elzi, L., Fehr, J., Fellay, J., Furrer, H., Haerry, D., Fux, C. A., Gorgievski, M., Günthard, H., Hasse, B., Hirsch, H. H., Hösli, I., Kahlert, C., Kaiser, L., Keiser, O., Klimkait, T., Kovari, H., Ledergerber, B., Martinetti, G., Martinez De Tejada, B., Metzner, K., Müller, N., Nadal, D., Pantaleo, G., Rauch, A., Regenass, S., Rickenbach, M., Rudin, C., Schmid, P., Schultze, D., Schöni-Affolter, F., Schüpbach, J., Speck, R., Taffé, P., Tarr, P., Telenti, A., Trkola, A., Vernazza, P., Weber, R., Yerly, S., Casabona, J., Gallois, A., Esteve, A., Podzamczer, D., Murillas, J., Gatell, J. M., Manzardo, C., Tural, C., Clotet, B., Ferrer, E., Riera, M., Segura, F., Navarro, G., Force, L., Vilaró, J., Masabeu, A., García, I., Guadarrama, M., Cifuentes, C., Dalmau, D., Jaen, Agustí, C., Montoliu, A., Pérez, I., Gargoulas, Freyra, Blanco, J. L., Garcia-Alcaide, F., Martínez, E., Mallolas, J., López-Dieguez, M., García-Goez, J. F., Sirera, G., Romeu, J., Jou, A., Negredo, E., Miranda, C., Capitan, M. C., Saumoy, M., Imaz, A., Tiraboschi, J. M., Murillo, O., Bolao, F., Peña, C., Cabellos, C., Masó, M., Vila, A., Sala, M., Cervantes, M., Jose Amengual, Ma, Navarro, M., Penelo, E., Barrufet, P., Bejarano, G., Molina, J., Alvaro, M., Mercadal, J., Fernandez, Juanse, Ospina, Jesus E., Muñoz, M. A., Caro-Murillo, A. M., Sobrino, P., Jarrín, I., Gomez Sirvent, J. L., Rodríguez, P., Aleman, M. R., Alonso, M. M., Lopez, A. M., Hernandez, M. I., Soriano, V., Labarga, P., Barreiro, P., Medrano, J., Rivas, P., Herrero, D., Blanco, F., Vispo, M. E., Martín, L., Ramírez, G., De Diego, M., Rubio, R., Pulido, F., Moreno, V., Cepeda, C., Hervás, Rl, Iribarren, J. A., Arrizabalaga, J., Aramburu, M. J., Camino, X., Rodrí-guez-Arrondo, F., Von Wichmann, M. A., Pascual, L., Goenaga, M. A., Gutierrez, F., Masia, M., Ramos, J. M., Padilla, S., Sanchez-Hellín, V., Bernal, E., Escolano, C., Montolio, F., Peral, Y., Berenguer, J., Lopez, J. 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A., Guerrero, R., Rivera, E., Marco, A., Quintana, M., Gonzalez, C., Castilla, J., Guevara, M., De Mendoza, C., Zahonero, N., Ortíz, M., Paraskevis, D., Touloumi, G., Pantazis, N., Bakoyannis, G., Gioukari, V., Antoniadou, A., Papadopoulos, A., Petrikkos, G., Daikos, G., Psichogiou, M., Gargalianos-Kakolyris, P., Xylomenos, G., Katsarou, O., Kouramba, A., Ioannidou, P., Kordossis, T., Kontos, A., Lazanas, M., Chini, M., Tsogas, N., Panos, G., Paparizos, V., Leuow, K., Kourkounti, S., Sambatakou, H., Mariolis, I., Skoutelis, A., Papastamopoulos, V., Baraboutis, I., Internal medicine, APH - Aging & Later Life, Pediatric surgery, CCA - Innovative therapy, ICaR - Circulation and metabolism, ICaR - Ischemia and repair, Graduate School, Paediatric Infectious Diseases / Rheumatology / Immunology, Landsteiner Laboratory, AII - Amsterdam institute for Infection and Immunity, Infectious diseases, Global Health, Center of Experimental and Molecular Medicine, APH - Amsterdam Public Health, AII - Inflammatory diseases, and ARD - Amsterdam Reproduction and Development
Subjects: Adult, Male, medicine.medical_specialty, Adolescent, Opportunistic infection, AIDS-Related Opportunistic Infections, Immunology, Population, Retinitis, HIV Infections, Article, 17 Psychology And Cognitive Sciences, Young Adult, Immune reconstitution inflammatory syndrome, Antiretroviral Therapy, Highly Active, Neoplasms, Virology, Internal medicine, medicine, Humans, Immunology and Allergy, education, Inverse probability weighting, Aged, education.field_of_study, business.industry, Developed Countries, Incidence, Progressive multifocal leukoencephalopathy, Hazard ratio, HIV, virus diseases, 11 Medical And Health Sciences, Middle Aged, 06 Biological Sciences, medicine.disease, United States, Europe, Infectious Diseases, Anti-Retroviral Agents, Unmasking, Female, Cytomegalovirus retinitis, business
Abstract: Background: There is little information on the incidence of AIDS-defining events which have been reported in the literature to be associated with immune reconstitution inflammatory syndrome (IRIS) after combined antiretroviral therapy (cART) initiation. These events include tuberculosis, mycobacterium avium complex (MAC), cytomegalovirus (CMV) retinitis, progressive multifocal leukoencephalopathy (PML), herpes simplex virus (HSV), Kaposi sarcoma, non-Hodgkin lymphoma (NHL), cryptococcosis and candidiasis.Methods: We identified individuals in the HIV-CAUSAL Collaboration, which includes data from six European countries and the US, who were HIV-positive between 1996 and 2013, antiretroviral therapy naive, aged at least 18 years, hadCD4+ cell count and HIV-RNA measurements and had been AIDS-free for at least 1 month between those measurements and the start of follow-up. For each AIDS-defining event, we estimated the hazard ratio for no cART versus less than 3 and at least 3 months since cART initiation, adjusting for time-varying CD4+ cell count and HIV-RNA via inverse probability weighting.Results: Out of 96 562 eligible individuals (78% men) with median (interquantile range) follow-up of 31 [13,65] months, 55 144 initiated cART. The number of cases varied between 898 for tuberculosis and 113 for PML. Compared with non-cART initiation, the hazard ratio (95% confidence intervals) up to 3 months after cART initiation were 1.21 (0.90-1.63) for tuberculosis, 2.61 (1.05-6.49) for MAC, 1.17 (0.34-4.08) for CMV retinitis, 1.18 (0.62-2.26) for PML, 1.21 (0.83-1.75) for HSV, 1.18 (0.87-1.58) for Kaposi sarcoma, 1.56 (0.82-2.95) for NHL, 1.11 (0.56-2.18) for cryptococcosis and 0.77 (0.40-1.49) for candidiasis.Conclusion: With the potential exception of mycobacterial infections, unmasking IRIS does not appear to be a common complication of cART initiation in high-income countries.
Published: 2014
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4. Opportunistic infections and AIDS malignancies early after initiating combination antiretroviral therapy in high-income countries

Author: Lodi, S. Del Amo, J. Moreno, S. Bucher, H.C. Furrer, H. Logan, R. Sterne, J. Pérez-Hoyos, S. Jarrín, I. Phillips, A. Olson, A. Van Sighem, A. Reiss, P. Sabin, C. Jose, S. Justice, A. Goulet, J. Miró, J.M. Ferrer, E. Meyer, L. Seng, R. Vourli, G. Antoniadou, A. Dabis, F. Vandenhede, M.-A. Costagliola, D. Abgrall, S. Hernán, M.A. Hernan, M. Bansi, L. Hill, T. Sabin, C. Dunn, D. Porter, K. Glabay, A. Orkin, C. Thomas, R. Jones, K. Fisher, M. Perry, N. Pullin, A. Churchill, D. Gazzard, B. Nelson, M. Asboe, D. Bulbeck, S. Mandalia, S. Clarke, J. Delpech, V. Anderson, J. Munshi, S. Post, F. Easterbrook, P. Khan, Y. Patel, P. Karim, F. Duffell, S. Gilson, R. Man, S.-L. Williams, I. Gompels, M. Dooley, D. Schwenk, A. Ainsworth, J. Johnson, M. Youle, M. Lampe, F. Smith, C. Grabowska, H. Chaloner, C. Ismajani Puradiredja, D. Bansi, L. Hill, T. Phillips, A. Sabin, C. Walsh, J. Weber, J. Kemble, C. Mackie, N. Winston, A. Leen, C. Wilson, A. Bezemer, D.O. Gras, L.A.J. Kesselring, A.M. Van Sighem, A.I. Zaheri, S. Van Twillert, G. Kortmann, W. Branger, J. Prins, J.M. Kuijpers, T.W. Scherpbier, H.J. Van Der Meer, J.T.M. Wit, F.W.M.N. Godfried, M.H. Reiss, P. Van Der Poll, T. Nellen, F.J.B. Lange, J.M.A. Geerlings, S.E. Van Vugt, M. Pajkrt, D. Bos, J.C. Van Der Valk, M. Grijsen, M.L. Wiersinga, W.J. Brinkman, K. Blok, W.L. Frissen, P.H.J. Schouten, W.E.M. Van Den Berk, G.E.L. Veenstra, J. Lettinga, K.D. Mulder, J.W. Vrouenraets, S.M.E. Lauw, F.N. Van Eeden, A. Verhagen, D.W.M. Van Agtmael, M.A. Perenboom, R.M. Claessen, F.A.P. Bomers, M. Peters, E.J.G. Richter, C. Van Der Berg, J.P. Gisolf, E.H. Schippers, E.F. Van Nieuwkoop, C. Van Elzakker, E.P. Leyten, E.M.S. Gelinck, L.B.S. Pronk, M.J.H. Bravenboer, B. Kootstra, G.J. Delsing, C.E. Sprenger, H.G. Doedens, R. Scholvinck, E.H. Van Assen, S. Bierman, W.F.W. Soetekouw, R. Ten Kate, R.W. Van Vonderen, M.G.A. Van Houte, D.P.F. Kroon, F.P. Van Dissel, J.T. Arend, S.M. De Boer, M.G.J. Jolink, H. Ter Vollaard, H.J.M. 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Arlet-Suau, E. Cuzin, L. Massip, P. Thiercelin Legrand, M.F. Pontonnier, G. Viget, N. Yasdanpanah, Y. Dellamonica, P. Pradier, C. Pugliese, P. Aleksandrowicz, K. Quinsat, D. Ravaux, I. Tissot-Dupont, H. Delmont, J.P. Moreau, J. Gastaut, J.A. Poizot-Martin, I. Retornaz, F. Soubeyrand, J. Galinier, A. Ruiz, J.M. Allegre, T. Blanc, P.A. Bonnet-Montchardon, D. Lepeu, G. Granet-Brunello, P. Esterni, J.P. Pelissier, L. Cohen-Valensi, R. Nezri, M. Chadapaud, S. Laffeuillade, A. Billaud, E. Raffi, F. Boibieux, A. Peyramond, D. Livrozet, J.M. Touraine, J.L. Cotte, L. Trepo, C. Strobel, M. Bissuel, F. Pradinaud, R. Sobesky, M. Cabié, A. Gaud, C. Contant, M. Aubert, V. Barth, J. Battegay, M. Bernasconi, E. Böni, J. Bucher, H.C. Burton-Jeangros, C. Calmy, A. Cavassini, M. Egger, M. Elzi, L. Fehr, J. Fellay, J. Furrer, H. Haerry, D. Fux, C.A. Gorgievski, M. Günthard, H. Hasse, B. Hirsch, H.H. Hösli, I. Kahlert, C. Kaiser, L. Keiser, O. Klimkait, T. Kovari, H. Ledergerber, B. Martinetti, G. Martinez De Tejada, B. Metzner, K. Müller, N. Nadal, D. Pantaleo, G. Rauch, A. Regenass, S. Rickenbach, M. Rudin, C. Schmid, P. Schultze, D. Schöni-Affolter, F. Schüpbach, J. Speck, R. Taffé, P. Tarr, P. Telenti, A. Trkola, A. Vernazza, P. Weber, R. Yerly, S. Casabona, J. Gallois, A. Esteve, A. Podzamczer, D. Murillas, J. Gatell, J.M. Manzardo, C. Tural, C. Clotet, B. Ferrer, E. Riera, M. Segura, F. Navarro, G. Force, L. Vilaró, J. Masabeu, A. García, I. Guadarrama, M. Cifuentes, C. Dalmau, D. Jaen, À. Agustí, C. Montoliu, A. Pérez, I. Gargoulas, F. Blanco, J.L. Garcia-Alcaide, F. Martínez, E. Mallolas, J. López-Dieguez, M. García-Goez, J.F. Sirera, G. Romeu, J. Jou, A. Negredo, E. Miranda, C. Capitan, M.C. Saumoy, M. Imaz, A. Tiraboschi, J.M. Murillo, O. Bolao, F. Peña, C. Cabellos, C. Masó, M. Vila, A. Sala, M. Cervantes, M. Jose Amengual, Ma. Navarro, M. Penelo, E. Barrufet, P. Bejarano, G. Molina, J. Guadarrama, M. Alvaro, M. Mercadal, J. Fernandez, J. Ospina, J.E. Muñoz, M.A. Caro-Murillo, A.M. Sobrino, P. Jarrín, I. Gomez Sirvent, J.L. Rodríguez, P. Aleman, M.R. Alonso, M.M. Lopez, A.M. Hernandez, M.I. Soriano, V. Labarga, P. Barreiro, P. Medrano, J. Rivas, P. Herrero, D. Blanco, F. Vispo, M.E. Martín, L. Ramírez, G. De Diego, M. Rubio, R. Pulido, F. Moreno, V. Cepeda, C. Hervás, Rl. Iribarren, J.A. Arrizabalaga, J. Aramburu, M.J. Camino, X. Rodrí-guez-Arrondo, F. Von Wichmann, M.A. Pascual, L. Goenaga, M.A. Gutierrez, F. Masia, M. Ramos, J.M. Padilla, S. Sanchez-Hellín, V. Bernal, E. Escolano, C. Montolio, F. Peral, Y. Berenguer, J. Lopez, J.C. Miralles, P. Cosín, J. Sanchez, M. Gutierrez, I. Ramírez, M. Padilla, B. Vidal, F. Sanjuan, M. Peraire, J. Veloso, S. Vilades, C. Lopez-Dupla, M. Olona, M. Vargas, M. Aldeguer, J.L. Blanes, M. Lacruz, J. Salavert, M. Montero, M. Cuéllar, S. De Los Santos, I. Sanz, J. Oteo, J.A. Blanco, J.R. Ibarra, V. Metola, L. Sanz, M. Pérez-Martínez, L. Sola, J. Uriz, J. Castiello, J. Reparaz, J. Arriaza, M.J. Irigoyen, C. Moreno, S. Antela, A. Casado, J.L. Dronda, F. Moreno, A. Pérez, M.J. López, D. Gutiérrez, C. Hernández, B. Pumares, M. Martí, P. García, L. Page, C. García, F. Hernández, J. Peña, A. Muñoz, L. Parra, J. Viciana, P. Leal, M. López-Cortés, L.F. Trastoy, M. Mata, R. Justice, A.C. Fiellin, D.A. Rimland, D. Jones-Taylor, C. Oursler, K.A. Titanji, R. Brown, S. Garrison, S. Rodriguez-Barradas, M. Masozera, N. Goetz, M. Leaf, D. Simberkoff, M. Blumenthal, D. Leung, J. Butt, A. Hoffman, E. Gibert, C. Peck, R. Mattocks, K. Braithwaite, S. Brandt, C. Bryant, K. Cook, R. Conigliaro, J. Crothers, K. Chang, J. Crystal, S. Day, N. Erdos, J. Freiberg, M. Kozal, M. Gandhi, N. Gaziano, M. Gerschenson, M. Good, B. Gordon, A. Goulet, J.L. Kraemer, K. Lim, J. Maisto, S. Miller, P. Mole, L. O'Connor, P. Papas, R. Robins, J.M. Rinaldo, C. Roberts, M. Samet, J. Tierney, B. Whittle, J. Babiker, A. Brettle, R. Darbyshire, J. Gilson, R. Goldberg, D. Hawkins, D. Jaffe, H. Johnson, A. McLean, K. Pillay, D. Cursley, A. Ewings, F. Fairbrother, K. Louisa Gnatiuc, S.L. Murphy, B. Douglas, G. Kennedy, N. Pritchard, J. Andrady, U. Rajda, N. Maw, R. McKernan, S. Drake, S. Gilleran, G. White, D. Ross, J. Toomer, S. Hewart, R. Wilding, H. Woodward, R. Dean, G. Heald, L. Horner, P. Glover, S. Bansaal, D. Eduards, S. Carne, C. Browing, M. Das, R. Stanley, B. Estreich, S. Magdy, A. O'Mahony, C. Fraser, P. Hayman, B. Jebakumar, S.P.R. Joshi, U. Ralph, S. Wade, A. Mette, R. Lalik, J. Summerfield, H. El-Dalil, A. France, J.A. White, C. Robertson, R. Gordon, S. McMillan, S. Morris, S. Lean, C. Vithayathil, K. McLean, L. Winter, A. Gale, D. Jacobs, S. Tayal, S. Short, L. Roberts, M. Green, S. Williams, G. Sivakumar, K. Bhattacharyya, N.D. Monteiro, E. Minton, J. Dhar, J. Nye, F. De Souza, C.B. Isaksen, A. McDonald, L. McLean, K. Franca, A. Hawkins, D. William, L. Jendrulek, I. Peters, B. Shaunak, S. El-Gadi, S. Easterbrook, P.J. Mazhude, C. Gilson, R. Johnstone, R. Fakoya, A. McHale, J. Waters, A. Kegg, S. Mitchell, S. Byrne, P. Johnson, M. Rice, P. Fidler, S. Mullaney, S.A. McCormack, S. David, D. Melville, R. Phillip, K. Balachandran, T. Mabey-Puttock, S. Sukthankar, A. Murphy, C. Wilkins, E. Ahmad, S. Tayal, S. Haynes, J. Evans, E. Ong, E. Das, R. Grey, R. Meaden, J. Bignell, C. Loay, D. Peacock, K. Girgis, M.R. Morgan, B. Palfreeman, A. Wilcox, J. Tobin, J. Tucker, L. Saeed, A.M. Chen, F. Deheragada, A. Williams, O. Lacey, H. Herman, S. Kinghorn, D. Devendra, V.S. Wither, J. Dawson, S. Rowen, D. Harvey, J. Wilkins, E. Bridgwood, A. Singh, G. Chauhan, M. Kellock, D. Young, S. Dannino, S. Kathir, Y. Rooney, G. Currie, J. Fitzgerald, M. Devendra, S. Keane, F. Booth, G. Green, T. Arumainayyagam, J. Chandramani, S. Rajamanoharan, S. Robinson, T. Curless, E. Gokhale, R. Tariq, A. Roberts, M. Williams, O. Luzzi, G. FitzGerald, M. Fairley, I. Wallis, F. Smit, E. Ward, F. Molina, J.M. Loze, B. Morlat, P. Bonarek, M. Bonnet, F. Nouts, C. Louis, I. Raffi, F. Reliquet, V. Sauser, F. Biron, C. Mounoury, O. Hue, H. Brosseau, D. Delfraissy, J.F. Goujard, C. Ghosn, J. Rannou, M.T. Bergmann, J.F. Badsi, E. Rami, A. Diemer, M. Parrinello, M. Girard, P.M. Samanon-Bollens, D. Campa, P. Tourneur, M. Desplanques, N. Livrozet, J.M. Jeanblanc, F. Chiarello, P. Makhloufi, D. Blanc, A.P. Allègre, T. Reynes, J. Baillat, V. Lemoing, V. Merle De Boever, C. Tramoni, C. Cabié, A. Sobesky, G. Abel, S. Beaujolais, V. Pialoux, G. Slama, L. Chakvetadze, C. Berrebi, V. Yeni, P. Bouvet, E. Fournier, I. Gerbe, J. Trepo, C. Koffi, K. Augustin-Normand, C. Miailhes, P. Thoirain, V. Brochier, C. Thomas, R. Souala, F. Ratajczak, M. Beytoux, J. Jacomet, C. Gourdon, F. Rouveix, E. Morelon, S. Dupont, C. Olivier, C. Lortholary, O. Dupont, B. Viard, J.P. Maignan, A. Ragnaud, J.M. Raymond, I. Leport, C. Jadand, C. Jestin, C. Longuet, P. Boucherit, S. Sereni, D. Lascoux, C. Prevoteau, F. Sobel, A. Levy, Y. Lelièvre, J.D. Lascaux, A.S. Dominguez, S. Dumont, C. Aumâitre, H. Delmas, B. Saada, M. Medus, M. Guillevin, L. Salmon, D. Tahi, T. Yazdanpanah, Y. Pavel, S. Marien, M.C. Drenou, B. Beck-Wirth, G. Beck, C. Benomar, M. Katlama, C. Tubiana, R. Ait Mohand, H. Chermak, A. Ben Abdallah, S. Bentata, M. Touam, F. Hoen, B. Drobacheff, C. Folzer, A. Massip, P. Obadia, M. Prudhomme, L. Bonnet, E. Balzarin, F. Pichard, E. Chennebault, J.M. Fialaire, P. Loison, J. Galanaud, P. Boué, F. Bornarel, D. Verdon, R. Bazin, C. Six, M. Ferret, P. Weiss, L. Batisse, D. Gonzales-Canali, G. Tisne-Dessus, D. Devidas, A. Chevojon, P. Turpault, I. Lafeuillade, A. Cheret, A. Philip, G. Morel, P. Timsit, J. Herson, S. Amirat, N. Simon, A. Brancion, C. Cabane, J. Picard, O. Tredup, J. Stein, A. Ravault, I. Chavanet, C. Buisson, M. Treuvetot, S. Choutet, P. Nau, P. Bastides, F. May, T. Boyer, L. Wassoumbou, S. Oksenhendeler, E. Gérard, L. Bernard, L. De Truchis, P. Berthé, H. Domart, Y. Merrien, D. Greder Belan, A. Gayraud, M. Bodard, L. Meudec, A. Beuscart, C. Daniel, C. Pape, E. Vinceneux, P. Simonpoli, A.M. Zeng, A. Fournier, L. Fuzibet, J.G. Sohn, C. Rosenthal, E. Quaranta, M. Dellamonica, P. Chaillou, S. Sabah, M. Audhuy, B. Schieber, A. Moreau, P. Niault, M. Vaillant, O. Huchon, G. Compagnucci, A. De Lacroix Szmania, I. Richier, L. Lamaury, I. Saint-Dizier, F. Garipuy, D. Gastaut, J.A. Drogoul, M.P. Poizot Martin, I. Fabre, G. Lambert De Cursay, G. Abraham, B. Perino, C. Lagarde, P. David, F. Roche-Sicot, J. Saraux, J.L. Leprêtre, A. Fampin, B. Uludag, A. Morin, A.S. Bletry, O. Zucman, D. Regnier, A. Girard, J.J. Quinsat, D.T. Heripret, L. Grihon, F. Houlbert, D. Ruel, M. Chemlal, K. Caron, F. Debab, Y. Tremollieres, F. Perronne, V. Lepeu, G. Slama, B. Perré, P. Miodovski, C. Guermonprez, G. Dulioust, A. Boudon, P. Malbec, D. Patey, O. Semaille, C. Deville, J. Remy, G. Béguinot, I. Galanaud, P. Boue, F. Chambrin, V. Pignon, C. Estocq, G.A. Levy, A. Delfraissy, J.F. Goujard, C. Duracinsky, M. Le Bras, P. Ngussan, M.S. Peretti, D. Medintzeff, N. Lambert, T. Segeral, O. Lezeau, P. Laurian, Y. Weiss, L. Buisson, M. Piketty, C. Karmochkine, M. Batisse, D. Eliaszewitch, M. Jayle, D. Tisne-Dessus, D. Kazatchkine, M. Leport, C. Colasante, U. Jadand, C. Jestin, C. Duval, X. Nouaouia, W. Boucherit, S. Vilde, J.L. Girard, P.M. Bollens, D. Binet, D. Diallo, B. Meyohas, M.C. Fonquernie, L. Lagneau, J.L. Salmon, D. Guillevin, L. Tahi, T. Launay, O. Pietrie, M.P. Sicard, D. Stieltjes, N. Michot, J. Sobel, A. Levy, Y. Bourdillon, F. Lascaux, A.S. Lelievre, J.D. Dumont, C. Dupont, B. Obenga, G. Viard, J.P. Maignan, A. Vittecoq, D. Escaut, L. Bolliot, C. Bricaire, F. Katlama, C. Schneider, L. Herson, S. Simon, A. Iguertsira, M. Stein, A. Tomei, C. Ravaux, I. Dhiver, C. Tissot Dupont, H. Vallon, A. Gallais, J. Gallais, H. Gastaut, J.A. Drogoul, M.P. Fabre, G. Dellamonica, P. Durant, J. Mondain, V. Perbost, I. Cassuto, J.P. Karsenti, J.M. Venti, H. Fuzibet, J.G. Rosenthal, E. Ceppi, C. Quaranta, M. Krivitsky, J.A. Bentata, M. Bouchaud, O. Honore, P. Sereni, D. Lascoux, C. Delgado, J. Rouzioux, C. Burgard, M. Boufassa, L. Peynet, J. Pérez-Hoyos, S. Del Amo, J. Alvarez, D. Monge, S. Muga, R. Sanvisens, A. Clotet, B. Tor, J. Bolao, F. Rivas, I. Vallecillo, G. Del Romero, J. Raposo, P. Rodríguez, C. Vera, M. Hurtado, I. Belda, J. Fernandez, E. Alastrue, I. Santos, C. Tasa, T. Juan, A. Trullen, J. Garcia De Olalla, P. Cayla, J. Masdeu, E. Knobel, H. Mirò, J.M. Sambeat, M.A. Guerrero, R. Rivera, E. Guerrero, R. Marco, A. Quintana, M. Gonzalez, C. Castilla, J. Guevara, M. De Mendoza, C. Zahonero, N. Ortíz, M. Paraskevis, D. Touloumi, G. Pantazis, N. Bakoyannis, G. Gioukari, V. Antoniadou, A. Papadopoulos, A. Petrikkos, G. Daikos, G. Psichogiou, M. Gargalianos-Kakolyris, P. Xylomenos, G. Katsarou, O. Kouramba, A. Ioannidou, P. Kordossis, T. Kontos, A. Lazanas, M. Chini, M. Tsogas, N. Panos, G. Paparizos, V. Leuow, K. Kourkounti, S. Sambatakou, H. Mariolis, I. Skoutelis, A. Papastamopoulos, V. Baraboutis, I. The HIV-CAUSAL Collaboration
Subjects: virus diseases
Abstract: Background: There is little information on the incidence of AIDS-defining events which have been reported in the literature to be associated with immune reconstitution inflammatory syndrome (IRIS) after combined antiretroviral therapy (cART) initiation. These events include tuberculosis, mycobacterium avium complex (MAC), cytomegalovirus (CMV) retinitis, progressive multifocal leukoencephalopathy (PML), herpes simplex virus (HSV), Kaposi sarcoma, non-Hodgkin lymphoma (NHL), cryptococcosis and candidiasis. Methods: We identified individuals in the HIV-CAUSAL Collaboration, which includes data from six European countries and the US, who were HIV-positive between 1996 and 2013, antiretroviral therapy naive, aged at least 18 years, hadCD4+ cell count and HIV-RNA measurements and had been AIDS-free for at least 1 month between those measurements and the start of follow-up. For each AIDS-defining event, we estimated the hazard ratio for no cART versus less than 3 and at least 3 months since cART initiation, adjusting for time-varying CD4+ cell count and HIV-RNA via inverse probability weighting. Results: Out of 96 562 eligible individuals (78% men) with median (interquantile range) follow-up of 31 [13,65] months, 55 144 initiated cART. The number of cases varied between 898 for tuberculosis and 113 for PML. Compared with non-cART initiation, the hazard ratio (95% confidence intervals) up to 3 months after cART initiation were 1.21 (0.90-1.63) for tuberculosis, 2.61 (1.05-6.49) for MAC, 1.17 (0.34-4.08) for CMV retinitis, 1.18 (0.62-2.26) for PML, 1.21 (0.83-1.75) for HSV, 1.18 (0.87-1.58) for Kaposi sarcoma, 1.56 (0.82-2.95) for NHL, 1.11 (0.56-2.18) for cryptococcosis and 0.77 (0.40-1.49) for candidiasis. Conclusion: With the potential exception of mycobacterial infections, unmasking IRIS does not appear to be a common complication of cART initiation in high-income countries. © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Published: 2014

5. Physiological suppression of microRNA-silencing pathway by HIV-1 during virus replication

Author: Triboulet, R., Mari, B., Lin, Yea-Lih, Chable-Bessia, C., Bennasser, Y., Lebrigand, K., Cardinaud, B., Maurin, T., Barbry, P., Baillat, V., Reynes, J., Corbeau, P., Jeang, Kt, Benkirane, M., Institut de génétique humaine (IGH), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)
Subjects: [SDV.GEN]Life Sciences [q-bio]/Genetics, ComputingMilieux_MISCELLANEOUS
Abstract: International audience
Published: 2007
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6. Balance des substrats à l’exercice chez des patients infectés par le VIH 1 et présentant un syndrome lipodystrophique: Effet d’un réentraînement ciblé par la calorimétrie d’effort

Author: Fédou, C., Fabre, J., Baillat, V., Reynes, J., Brun, J.F., and Mercier, J.
Published: 2008
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7. Vitamin E supplementation increases the expression of the CCR5 coreceptor in HIV-1 infected subjects

Author: PORTALES, P, primary, GUERRIER, T, additional, CLOT, J, additional, CORBEAU, P, additional, METTLING, C, additional, LIN, Y, additional, BAILLAT, V, additional, MERLEDEBOEVER, C, additional, MOING, V, additional, and TRAMONI, C, additional
Published: 2004
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8. Decrease in LDL size in HIV-positive adults before and after lopinavir/ritonavir-containing regimen: an index of atherogenicity?

Author: Badiou, S, primary, Merle De Boever, C, additional, Dupuy, A.M, additional, Baillat, V, additional, Cristol, J.P, additional, and Reynes, J, additional
Published: 2003
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9. Impact of Insertions in the HIV-1 P6 Ptapp Region on the Virological Response to Amprenavir

Author: Lastere, Stephane, Dalban, Cecile, Collin, Gilles, Descamps, Diane, Girard, Pierre-Marie, Clavel, Francois, Costagliola, Dominique, Brun-Vezinet, Francoise, Brun-Vezinet, F, Clavel, F, Costagliola, D, Dalban, C, Girard, PM, Matheron, S, Meynard, JL, Morand-Joubert, L, Peytavin, G, Vray, M, Beguinot, I, Waldner, A, Beumont, M, Semaille, C, Bentata, M, Berlureau, P, Gérard, L, Molina, JM, Hor, R, Bayol-Honnet, G, Lascoux-Combe, C, Drobacheff, C, Hoen, B, Dupon, M, Lacut, JY, Goujard, C, Rousseau, C, Vincent, V, Diemer, M, Lepeu, G, Zerazhi, H, de Truchis, P, Berthé, H, Jeantils, V, Tazi, C Taleb, Vittecoq, D, Escaut, L, Dupont, B, Nait-Ighil, L, Rozenbaum, W, Nguyen, T Huyen, Boué, F, Galanaud, P, Kazatchkine, M, Piketty, C, Bernasconi, C, Salmon-Ceron, D, Michon, C, Chandemerle, C, Lascaux, AS, Magnier, JD, Schneider, L, Ait-Mohand, H, Simon, A, Herson, S, Bollens, D, Picard, O, Tangre, P, Bonarek, M, Morlat, P, Trépo, C, Cotte, L, Gastaut, JA, Poizot-Martin, I, Moran, G, Masson, S, Bennai, Y, Belarbi, L, Prevot, MH, Fournier, I, Reynes, J, Baillat, V, Raffi, F, Esnault, JL, Ceppi, C, Cassuto, JP, Arvieux, C, Chapplain, JM, Rey, D, Krantz, V, Besnier, JM, Bastides, F, Obadia, M, Aquilina, C, Bazin, C, Verdon, R, Piroth, L, Grappin, M, Sissoko, D, Valette, M, May, T, Burty, C, Debab, Y, Caron, F, Elharrar, B, Launay, O, Winter, C, Chapuis, L, Auperin, I, and Gilquin, J
Abstract: We evaluated the impact of genetic changes within p6Gaggene on the virological response (VR, mean decrease in plasma viral load at week 12) to unboosted amprenavir (APV). Gag-protease fragments, including gag p2, p7, p1, p6 regions and whole protease (PR) were sequenced from baseline plasma specimens of 84 highly pre-treated but APV-naive patients included in the NARVAL (ANRS 088) trial. The correlation between baseline p6Gagpolymorphism, PR mutations, baseline characteristics and VR to APV was analysed in univariate analysis. Insertions (P459Ins) within p6 protein, leading to partial or complete duplication of the PTAPP motif, were significantly associated with a decreased VR (P459Ins versus wild-type; –0.3 ±0.8 vs –1.1 ±1.2 log copies/ml, P=0.007) and were more frequent when the V82A/F/T/S PR mutation was present (P=0.020). In multivariate analysis, after adjustment on the predictive factors of the VR in the NARVAL trial and on the PR mutations linked with response, there was a strong trend to an association (P=0.058) between the presence of P459Ins and an altered VR. In conclusion, these results suggest that insertions in the p6 region of HIV-1 gag gene may affect the VR, in highly pre-treated patients receiving an unboosted APV-containing regimen.
Published: 2004
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10. Relationship between CCR5 density and viral load after discontinuation of antiretroviral therapy.

Author: Reynes J, Baillat V, Portales P, Clot J, Corbeau P, Reynes, Jacques, Baillat, Vincent, Portales, Pierre, Clot, Jacques, and Corbeau, Pierre
Published: 2004
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11. Assessement of Awareness of, Concerns and Attitudes Towards HIV-Related Court-Case Sentences in France in a Representative Sample of People Living with HIV (ANRS VESPA2 Survey)

Author: Marie Suzan-Monti, Bruno Spire, Antoine Vilotitch, Rosemary Dray-Spira, Patrick Yeni, Michel Celse, Baptiste Demoulin, Observatoire régional de la santé Provence-Alpes-Côte d'Azur [Marseille] (ORS PACA), 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), Conseil national du sida et des hépatites virales [Paris, France], Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Paris Diderot - Paris 7 (UPD7), Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), The VESPA2 survey was sponsored and funded by the French National Agency for Research on Aids and Viral Hepatitis (ANRS), Grant No. 2010-176., ANRS VESPA2 study group : Lert F, Spire B, Carrieri P, Dray-Spira R, Hamelin C, Lorente N, Préau M, Suzan-Monti M, Mora M, Le Strat Y, Cuzin L, Meyer L, Rojas-Castro D, Fischer H, Allègre T, Mours P, Riou JM, Sordage M, Chennebault JM, Fialaire P, Rabier V, Froidure M, Huguet D, Leduc D, Pichancourt G, Wajsbrot A, Bourdeaux C, Foltzer A, Hoen B, Hustache-Mathieu L, Abgrall S, Barruet R, Bouchaud O, Chabrol A, Mattioni S, Mechai F, Jeantils V, Bernard N, Bonnet F, Hessamfar M, Lacoste D, Malvy D, Mercié P, Morlat P, Paccalin F, Pertusa MC, Pistone T, Receveur MC, Vandenhende MA, Dupont C, Freire Maresca A, Leporrier J, Rouveix E, Dargere S, de la Blanchardière A, Martin A, Noyon V, Verdon R, Rogeaux O, Beytout J, Gourdon F, Laurichesse H, Meier F, Mortier E, Simonpoli AM, Cordier F, Delacroix I, Garrait V, Elharrar B, Dominguez S, Lascaux AS, Lelièvre JD, Levy Y, Melica G, Buisson M, Piroth L, Waldner A, Gruat N, Leprêtre A, de Truchis P, Le Du D, Melchior JC, Sehouane R, Troisvallets D, Blanc M, Boccon-Gibod I, Bosseray A, Brion JP, Durand F, Leclercq P, Marion F, Pavese P, Brottier-Mancini E, Faba L, Roncato-Saberan M, Bollengier-Stragier O, Esnault JL, Leautez-Nainville S, Perré P, Froguel E, Nguessan M, Simon P, Colardelle P, Doll J, Godin-Collet C, Roussin-Bretagne S, Delfraissy JF, Duracinsky M, Goujard C, Peretti D, Quertainmont Y, Marionneau J, Aissi E, Van Grunderbeeck N, Denes E, Ducroix-Roubertou S, Genet C, Weinbreck P, Augustin-Normand C, Boibieux A, Cotte L, Ferry T, Koffi J, Miailhes P, Perpoint T, Peyramond D, Schlienger I, Brunel JM, Carbonnel E, Chiarello P, Livrozet JM, Makhloufi D, Dhiver C, Husson H, Madrid A, Ravaux I, de Severac ML, Thierry Mieg M, Tomei C, Hakoun S, Moreau J, Mokhtari S, Soavi MJ, Faucher O, Ménard A, Orticoni M, Poizot-Martin I, Atoui N, Baillat V, Faucherre V, Favier C, Jacquet JM, Le Moing V, Makinson A, Mansouri R, Merle C, Elforzli N, Allavena C, Aubry O, Besnier M, Billaud E, Bonnet B, Bouchez S, Boutoille D, Brunet C, Feuillebois N, Lefebvre M, Morineau-Le Houssine P, Mounoury O, Point P, Raffi F, Reliquet V, Talarmin JP, Ceppi C, Cua E, Dellamonica P, De Salvador-Guillouet F, Durant J, Ferrando S, Mondain-Miton V, Perbost I, Pillet S, Prouvost-Keller B, Pradier C, Pugliese P, Rahelinirina V, Roger PM, Rosenthal E, Sanderson F, Hocqueloux L, Niang M, Prazuck T, Arsac P, Barrault-Anstett MF, Ahouanto M, Bouvet E, Castanedo G, Charlois-Ou C, Dia Kotuba A, Eid-Antoun Z, Jestin C, Jidar K, Joly V, Khuong-Josses MA, Landgraf N, Landman R, Lariven S, L'hériteau F, Machado M, Matheron S, Michard F, Morau G, Pahlavan G, Phung BC, Prévot MH, Rioux C, Yéni P, Bani-Sadr F, Calboreanu A, Chakvetadze E, Salmon D, Silbermann B, Batisse D, Beumont M, Castiel P, Derouineau J, Eliaszewicz M, Gonzalez G, Jayle D, Karmochkine M, Kousignian P, Pavie J, Pierre I, Weiss L, Badsi E, Bendenoun M, Cervoni J, Diemer M, Durel A, Rami A, Sellier P, Ait-Mohand H, Amirat N, Bonmarchand M, Bourdillon F, Breton G, Caby F, Grivois JP, Katlama C, Kirstetter M, Paris L, Pichon F, Roudière L, Schneider L, Samba MC, Seang S, Simon A, Stitou H, Tubiana R, Valantin MA, Bollens D, Bottero J, Bui E, Campa P, Fonquernie L, Fournier S, Girard PM, Goetschel A, Guyon HF, Lacombe K, Lallemand F, Lefebvre B, Maynard JL, Meyohas MC, Ouazene Z, Pacanowski J, Picard O, Raguin G, Roussard P, Tourneur M, Tredup J, Valin N, Balkan S, Clavel F, de Verdière NC, De Castro N, de Lastours V, Ferret S, Gallien S, Gérard L, Goguel J, Lafaurie M, Lascoux-Combe C, Molina JM, Oksenhendler E, Pintado C, Ponscarme D, Rozenbaum W, Scemla A, Bonnard P, Lassel L, Lebrette MG, Lyavanc T, Mariot P, Missonnier R, Ohayon M, Pialoux G, Treilhou MP, Vincensini JP, Gilquin J, Hadacek B, Nait-Ighil L, Nguyen TH, Sobel A, Viard JP, Zak Dit Zbar O, Aumaître H, Eden A, Ferreyra M, Lopez F, Medus M, Neuville S, Saada M, Blum L, Perfezou P, Arvieux C, Chapplain JM, Revest M, Souala F, Tattevin P, Bord S, Borsa-Lebas F, Caron F, Chapuzet C, Debab Y, Gueit I, Etienne M, Fartoukh C, Feltgen K, Joly C, Robaday-Voisin S, Suel P, Khuong MA, Krausse J, Poupard M, Tran Van G, Cazorla C, Daoud F, Fascia P, Frésard A, Guglielminotti C, Lucht F, Bernard-Henry C, Cheneau C, Lang JM, de Mautort E, Partisani M, Priester M, Rey D, Majerholc C, Zucman D, Assi A, Lafeuillade A, de Jaureguiberry JP, Gisserot O, Aquilina C, du Clary FP, Alvarez M, Chauveau M, Delobel P, Garipuy D, Labau E, Marchou B, Massip P, Mularczyk M, Obadia M, Ajana F, Allienne C, Baclet V, de la Tribonnière X, Huleux T, Melliez H, Meybeck A, Riff B, Valette M, Viget N, Bastides F, Bernard L, Gras G, Guadagnin P, May T, Rabaud C, Dos Santos A, Poinsignon Y, Derradji O, Escaut L, Teicher E, Vittecoq D, Bantsima J, Caraux-Paz P, Patey O., Lissalde, Claire, and 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)
Subjects: Adult, Male, medicine.medical_specialty, Adolescent, Social Psychology, Social stigma, Cross-sectional study, Social Stigma, Stigma (botany), HIV Infections, 03 medical and health sciences, Discrimination, Psychological, 0302 clinical medicine, Criminalization, 5. Gender equality, Criminal Law, Surveys and Questionnaires, medicine, Humans, 030212 general & internal medicine, 10. No inequality, Psychiatry, Prejudice (legal term), Transients and Migrants, Depressive Disorder, Major, Stereotyping, 030505 public health, Public health, Public Health, Environmental and Occupational Health, HIV, Awareness, Middle Aged, 16. Peace & justice, Health psychology, Cross-Sectional Studies, Sexual Partners, Infectious Diseases, Attitude, Socioeconomic Factors, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Criminal law, Female, Key population, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, France, 0305 other medical science, Psychology, Prejudice
Abstract: International audience; Some of the 12 criminal trials and sentences in France for HIV transmission in 1998-2011 attracted substantial public attention , with a possible negative impact on people living with HIV (PLWH) through reinforced stigma and discrimination. This analysis aimed to characterize PLWH enrolled in the representative ANRS-VESPA2 survey, aware of and concerned about convictions for HIV transmission. Being a migrant from Sub-Saharan Africa, having difficult socioeconomic conditions, having unprotected sex with one's main partner and concealing one's HIV status were all factors statistically associated with concern about the sentences. Participants tempted to press charges against someone for infecting them were more likely to be younger, women, not living in a couple, unemployed, and to report a major depressive disorder. Concern about HIV-related criminal proceedings among the most vulnerable PLWH do not reflect the actual risk of prosecution they are exposed to. Resumen En Francia, algunos de los 12 juicios y sentencias relacionados con la contaminación del VIH en 1998-2011 suscitaron con-siderablemente el interés público. Esto pudo impactar negativamente las personas viviendo con VIH (PVVIH) aumentando su estigmatización y discriminación. Este análisis busca caracterizar las PVVIH, de la encuesta ANRS-VESPA2, informadas acerca de esos juicios e inquietos por la posibilidad de implicación en uno de ellos. Ser inmigrante subsahariano, las con-diciones socio-económicas desfavorables, las relaciones sexuales no protegidas con la pareja principal, y ocultar el VIH, están asociados a la posibilidad de ser implicados en un juicio. Por otro lado, aquellos que han intentado presentar cargos por contaminación del VIH fueron mayoritariamente jóvenes, mujeres, personas viviendo solas, desempleados, y personas en depresión. Los juicios por contaminación del VIH entre las PVVIH más vulnerables no reflejan el riesgo de acusación al que están expuestos.
Published: 2018
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12. Lopinavir/ritonavir monotherapy versus current treatment continuation for maintenance therapy of HIV-1 infection: the KALESOLO trial.

Author: Meynard JL, Bouteloup V, Landman R, Bonnard P, Baillat V, Cabie A, Kolta S, Izopet J, Taburet AM, Mercie P, Chene G, and Girard PM
Subjects: Adult, Antiretroviral Therapy, Highly Active methods, Female, France, HIV Infections virology, HIV-1 isolation & purification, Humans, Lopinavir, Male, Middle Aged, RNA, Viral blood, Treatment Outcome, Viral Load, Anti-HIV Agents administration & dosage, HIV Infections drug therapy, Pyrimidinones administration & dosage, Ritonavir administration & dosage
Abstract: Objectives: We evaluated a monotherapy maintenance regimen with lopinavir/ritonavir versus continuing current combined antiretroviral treatment (cART) in HIV patients with suppressed plasma HIV-1 RNA., Patients and Methods: This was an open-label, non-inferiority, multicentre trial in 23 sites in France. Adults were randomized if they had no history of virological failure while receiving a protease inhibitor, maintained HIV-1 RNA <50 copies/mL for at least 6 months and did not change cART during the last 3 months. The primary endpoint was the proportion of patients with HIV-1 RNA <50 copies/mL at Week 48 (non-inferiority margin set at -12%) with missing data and treatment modification considered as failure. The trial has been registered in ClinicalTrials.gov under the identifier NCT00140751., Results: At Week 48, 84% (73/87) of patients in the lopinavir/ritonavir monotherapy group met the primary endpoint compared with 88% (87/99) in the cART group [difference, -4.0%, lower limit of 90% two-sided confidence interval (CI) for difference, -12.4%]. In secondary analysis with success defined as plasma HIV-1 RNA <400 copies/mL, 87% (76/87) of patients in the lopinavir/ritonavir monotherapy group were virologically suppressed compared with 88% (87/99) in the cART group (difference, -0.5%, lower limit of 90% two-sided CI for difference, -8.5%). If antiretroviral treatment intensification was taken into account, 91% (79/87) of patients in the lopinavir/ritonavir monotherapy group met the primary endpoint compared with 88% (87/99) in the cART group (difference, +2.9%, lower limit of 90% two-sided CI for difference, -4.5%). Failures of lopinavir/ritonavir monotherapy did not show acquired resistance mutations in the protease gene., Conclusions: Lopinavir/ritonavir monotherapy did not achieve non-inferiority versus cART for maintaining plasma HIV-1 RNA <50 copies/mL. Nevertheless, the incidence of virological failure was low (mostly with HIV-1 RNA <400 copies/mL) and easily managed by treatment intensification.
Published: 2010
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13. Close association of CD8+/CD38 bright with HIV-1 replication and complex relationship with CD4+ T-cell count.

Author: Tuaillon E, Al Tabaa Y, Baillat V, Segondy M, Picot MC, Reynes J, and Vendrell JP
Subjects: Anti-Retroviral Agents therapeutic use, Biomarkers analysis, Biomarkers blood, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes metabolism, CD8-Positive T-Lymphocytes metabolism, Case-Control Studies, Female, HIV Infections drug therapy, HIV Infections pathology, HIV Infections virology, HIV-1 immunology, Humans, Longitudinal Studies, Lymphocyte Activation immunology, Lymphocyte Activation physiology, Male, RNA, Viral analysis, RNA, Viral blood, Sensitivity and Specificity, Viral Load, ADP-ribosyl Cyclase 1 metabolism, CD4-Positive T-Lymphocytes pathology, CD8-Positive T-Lymphocytes cytology, HIV Infections immunology, HIV-1 physiology, Membrane Glycoproteins metabolism, Virus Replication immunology
Abstract: Background: Measuring lymphocyte activation provides information in addition to CD4(+) T-cell count for immune monitoring of HIV-1 infected patients. CD38 is a well-established activation marker that is generally analyzed on the whole population of CD8(+) T-cells. Focusing specifically on CD38 high expression (CD8(+)/CD38(bright)) may be an interesting surrogate gating strategy because CD38(bright) characterizes principally activated memory cells., Methods: CD8(+)/CD38(bright) was investigated in 1,353 HIV-1 infected patients over a one-year period to establish relevant cutoff values and clarify the relationships of this marker with HIV-1 RNA viral load (VL) and CD4(+) T-cell count., Results: The CD8(+)/CD38(bright) (>8,500 CD38 binding site per cells) is well correlated with HIV-1 VL (r = 0.87, P < 0.001) in this longitudinal follow-up of nonimmunodepressed patients that initiated antiviral therapy (ART). In aviremic patients on ART, the marker was highly predictive of VL rebound (sensitivity 93%, specificity 64% for a VL level of detection >200 copies/ml). While the CD8(+)/CD38(bright) moderately correlated with CD4(+) T-cell count independently of the VL (r = -0.37, P < 0.001), it increased dramatically in aviremic patient groups that exhibited profound CD4(+) T-cell depletion (median 39% for CD4(+) T-cell counts <50/mm(3)). This result indicates that other additional immunological and/or viral factors than readily detectable HIV-1 replication appears to be involved in T-cell activation of immunodepressed individuals., Conclusions: CD8(+)/CD38(bright) is an effective marker for monitoring T-cell activation, which is a central factor of HIV-1 pathogenesis. This gating strategy requires only a single additional staining in conventional four color CD4 protocols., ((c) 2008 Clinical Cytometry Society.)
Published: 2009
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14. Long-term persistence of memory B cells specific for hepatitis B surface antigen in HIV-1-infected patients.

Author: Tuaillon E, Tabaa YA, Baillat V, Petitjean G, Reynes J, and Vendrell JP
Subjects: Anti-HIV Agents therapeutic use, Antibodies, Viral analysis, B-Lymphocytes virology, Case-Control Studies, Enzyme-Linked Immunosorbent Assay, HIV Infections drug therapy, HIV Infections virology, Hepatitis B Surface Antigens immunology, Hepatitis B Vaccines administration & dosage, Hepatitis B, Chronic prevention & control, Hepatitis B, Chronic virology, Humans, Immunologic Memory, Lymphocyte Activation, Lymphocyte Count, Statistics, Nonparametric, Time Factors, B-Lymphocytes immunology, HIV Infections immunology, HIV-1, Hepatitis B Surface Antigens blood, Hepatitis B virus immunology, Hepatitis B, Chronic immunology
Abstract: To investigate the maintenance of long-term memory B cells specific for hepatitis B surface antigen (HBsAg), purified blood B cells were polyclonally stimulated and cells secreting antibodies directed to HBsAg (HBs-SC) enumerated by ELISpot. HBs-SC were found in 18/20 HIV-1-infected patients with either natural or vaccinal immunity to hepatitis B virus, including six subjects with serum anti-hepatitis B surface antibody levels less than 10 mIU/ml. A lower number of HBs-SC was found in HBsAg-vaccinated patients compared with vaccinated controls.
Published: 2007
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15. Unintegrated HIV-1 provides an inducible and functional reservoir in untreated and highly active antiretroviral therapy-treated patients.

Author: Petitjean G, Al Tabaa Y, Tuaillon E, Mettling C, Baillat V, Reynes J, Segondy M, and Vendrell JP
Subjects: CD4-Positive T-Lymphocytes virology, DNA, Viral, HIV Infections drug therapy, Humans, Virus Activation, Virus Integration, Virus Replication, Anti-HIV Agents therapeutic use, Antiretroviral Therapy, Highly Active, HIV Infections virology, HIV-1 physiology, Virus Latency
Abstract: Background: The presence of HIV-1 preintegration reservoir was assessed in an in vitro experimental model of latent HIV-1 infection, and in patients treated or not with highly active antiretroviral therapy (HAART)., Results: In resting CD4+ T lymphocytes latently infected in vitro with HIV-1, we demonstrated that the polyclonal activation induced a HIV-1 replication, which could be prevented by the use of an HIV-1 integrase inhibitor. We also showed that this reservoir was labile since the rescuable HIV-1-antigens production from unintegrated HIV-1 genomes declined over time. These data confirm that our experimental approach allows the characterization of a functional unintegrated HIV-1 reservoir. We then explored the preintegration reservoir in HIV-1-infected patients. This reservoir was detected in 11 of 12 untreated patients, in 4 of 10 sustained responders to HAART, and in one incomplete responder. This reservoir was also inducible, labile, and anti-HIV-1 integrase drug inhibited its induction. Finally, this reservoir was associated with the presence of spontaneous HIV-1 antigens producing CD4+ T cells in blood from 3 of 3 untreated patients and 2 of 2 sustained responders to HAART harboring a preintegration reservoir., Conclusion: This preintegration phase of HIV-1 latency could be a consequence of the ongoing viral replication in untreated patients and of a residual viral replication in treated patients.
Published: 2007
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16. Suppression of microRNA-silencing pathway by HIV-1 during virus replication.

Author: Triboulet R, Mari B, Lin YL, Chable-Bessia C, Bennasser Y, Lebrigand K, Cardinaud B, Maurin T, Barbry P, Baillat V, Reynes J, Corbeau P, Jeang KT, and Benkirane M
Subjects: 3' Untranslated Regions, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Cell Line, Gene Expression Regulation, Gene Products, tat metabolism, HIV-1 genetics, HeLa Cells, Histone Acetyltransferases genetics, Histone Acetyltransferases metabolism, Humans, Jurkat Cells, Leukocytes, Mononuclear enzymology, Oligonucleotide Array Sequence Analysis, RNA, Small Interfering genetics, Ribonuclease III genetics, Ribonuclease III metabolism, Transcription Factors genetics, Transcription Factors metabolism, Transfection, Virus Latency, p300-CBP Transcription Factors, tat Gene Products, Human Immunodeficiency Virus, HIV-1 physiology, Leukocytes, Mononuclear virology, MicroRNAs genetics, RNA Interference, Virus Replication
Abstract: MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 19 to 25 nucleotides that function as gene regulators and as a host cell defense against both RNA and DNA viruses. We provide evidence for a physiological role of the miRNA-silencing machinery in controlling HIV-1 replication. Type III RNAses Dicer and Drosha, responsible for miRNA processing, inhibited virus replication both in peripheral blood mononuclear cells from HIV-1-infected donors and in latently infected cells. In turn, HIV-1 actively suppressed the expression of the polycistronic miRNA cluster miR-17/92. This suppression was found to be required for efficient viral replication and was dependent on the histone acetyltransferase Tat cofactor PCAF. Our results highlight the involvement of the miRNA-silencing pathway in HIV-1 replication and latency.
Published: 2007
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17. Suv39H1 and HP1gamma are responsible for chromatin-mediated HIV-1 transcriptional silencing and post-integration latency.

Author: du Chéné I, Basyuk E, Lin YL, Triboulet R, Knezevich A, Chable-Bessia C, Mettling C, Baillat V, Reynes J, Corbeau P, Bertrand E, Marcello A, Emiliani S, Kiernan R, and Benkirane M
Subjects: Cell Cycle Proteins physiology, Cells, Cultured, HIV Long Terminal Repeat, HeLa Cells, Histone Acetyltransferases physiology, Histone Methyltransferases, Histone-Lysine N-Methyltransferase metabolism, Histones metabolism, Humans, Jurkat Cells, Models, Biological, Positive Transcriptional Elongation Factor B physiology, Protein Methyltransferases, Sp1 Transcription Factor physiology, Transcription Factors physiology, Transcription, Genetic, Transcriptional Activation, p300-CBP Transcription Factors, Chromatin physiology, Chromosomal Proteins, Non-Histone physiology, Gene Silencing, HIV-1 physiology, Methyltransferases physiology, Repressor Proteins physiology, Virus Integration, Virus Latency
Abstract: HIV-1 gene expression is the major determinant regulating the rate of virus replication and, consequently, AIDS progression. Following primary infection, most infected cells produce virus. However, a small population becomes latently infected and constitutes the viral reservoir. This stable viral reservoir seriously challenges the hope of complete viral eradication. Viewed in this context, it is critical to define the molecular mechanisms involved in the establishment of transcriptional latency and the reactivation of viral expression. We show that Suv39H1, HP1gamma and histone H3Lys9 trimethylation play a major role in chromatin-mediated repression of integrated HIV-1 gene expression. Suv39H1, HP1gamma and histone H3Lys9 trimethylation are reversibly associated with HIV-1 in a transcription-dependent manner. Finally, we show in different cellular models, including PBMCs from HIV-1-infected donors, that HIV-1 reactivation could be achieved after HP1gamma RNA interference.
Published: 2007
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18. The immunological response to highly active antiretroviral therapy is linked to CD4+ T-cell surface CCR5 density.

Author: Vincent T, Portalès P, Baillat V, Eden A, Clot J, Reynes J, and Corbeau P
Subjects: HIV Infections drug therapy, HIV Infections virology, HIV-1 physiology, Humans, Antiretroviral Therapy, Highly Active, CD4-Positive T-Lymphocytes immunology, HIV Infections immunology, Receptors, CCR5 metabolism
Published: 2006
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19. Is tenofovir involved in hypophosphatemia and decrease of tubular phosphate reabsorption in HIV-positive adults?

Author: Badiou S, De Boever CM, Terrier N, Baillat V, Cristol JP, and Reynes J
Subjects: Adenine adverse effects, Adenine therapeutic use, Adult, Anti-HIV Agents therapeutic use, Cross-Sectional Studies, Female, Humans, Kidney Tubules, Proximal metabolism, Male, Middle Aged, Organophosphonates therapeutic use, Phosphates metabolism, Tenofovir, Adenine analogs & derivatives, Anti-HIV Agents adverse effects, HIV Infections drug therapy, Hypophosphatemia chemically induced, Kidney Tubules, Proximal drug effects, Organophosphonates adverse effects
Abstract: Objectives: Tubulopathy with hypophosphatemia have been observed in HIV-positive patients receiving a tenofovir-containing regimen. However, the real incidence and prevalence of hypophosphatemia and their relation to tubular reabsorption disorders in tenofovir-treated patients remain uncertain. The aim of our study was to explore the effect of tenofovir on phosphatemia and on tubular phosphate reabsorption., Methods: In a first transversal study, 145 HIV-positive adults (44+/-9 years) receiving tenofovir 300 mg daily with a mean exposure of 11+/-9 months were included. In a second prospective study, 29 HIV-positive antiretroviral experienced adults (44+/-10 years) were evaluated before introduction of tenofovir 300 mg daily (M0) and at 3 months (M3) and 6 months (M6), thereafter. Phosphate, creatinine, glucose and protein levels were determined in plasma and urine. The ratio of maximal reabsorption capacity (TmPO4)/glomerular filtration rate (GFR) was determined by using the normogramm of Walton and Bijvoet., Results: In the transversal study, 26% of patients had hypophosphatemia (<0.84 mmol/l) while 47% of patients had a decreased TmPO4/GFR (<0.8 mmol/l). In the prospective study, baseline prevalence of hypophosphatemia (<0.84 mmol/l) and decreased TmPO4/GFR (<0.8mmol/l) was 31 and 41%, respectively. Three and 6 months after starting tenofovir, there is no significant change in mean phosphate levels (M0:0.91 mmol/l, M3:0.97 mmol/l, M6:0.98 mmol/l) and mean TmPO4/GFR (M0:0.80 mmol/l, M3:0.88 mmol/l, M6:0.84 mmol/l). Moreover, prevalence of hypophosphatemia (M3:28%, M6:28%) and decreased TmPO4/GFR (M3:41%, M6:45%) remained stable., Conclusion: Hypophosphatemia linked to a decreased proximal tubular reabsorption was frequently observed in HIV-positive adults independently of the use of tenofovir. In this preliminary study, no worsening effect on phosphatemia and tubular phosphate reabsorption was observed 6 months after introduction of tenofovir in treatment experienced patients.
Published: 2006
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20. CXCR4 overexpression during the course of HIV-1 infection correlates with the emergence of X4 strains.

Author: Lin YL, Portales P, Segondy M, Baillat V, de Boever CM, Le Moing V, Réant B, Montes B, Clot J, Reynes J, and Corbeau P
Subjects: Adolescent, Adult, Aged, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes metabolism, Chemokine CCL5 blood, Female, Gene Expression, Humans, Interleukin-7 blood, Male, Middle Aged, Phenotype, Receptors, CXCR4 blood, Viral Load, Virus Replication, HIV Infections blood, HIV Infections virology, HIV-1 genetics, Receptors, CXCR4 biosynthesis
Abstract: The factors that determine the emergence of X4 isolates in some HIV-1-infected subjects are unknown. As the level of expression of CXCR4 could favor an R5 to X4 switch, quantitative flow cytometry was used to measure CXCR4 density on CD4 T cells in 200 HIV-1-positive adults, and this was compared with CD4 counts, interleukin-7 (IL-7), and RANTES (regulated on activation, normal T expressed and secreted) plasma levels and the R5/X4 virus phenotype. CD4 T-cell surface CXCR4 densities were increased in infected subjects and inversely correlated with CD4 T-cell count (r=-0.548, P<0.001). Yet, in vitro infection with either R5 or X4 strains and in vivo increases in viral load following interruption of antiretroviral treatment did not induce CXCR4 overexpression. The plasma levels of IL-7 and RANTES, 2 cytokines able to induce CXCR4 expression, did not correlate with CXCR4 density. Finally, higher CXCR4 densities were observed in patients harboring X4 strains (3300, 95% CI 2431-4169 CXCR4 molecules per cell) than in patients harboring only R5 strains (2406, 95% CI 2135-2677, P=0.027). These data suggest that CXCR4 overexpression during the course of the disease in some patients could favor the emergence of X4 strains.
Published: 2005

21. T-Cell surface CCR5 density is not correlated with hepatitis severity in hepatitis C virus/HIV-coinfected individuals: implications for the therapeutic use of CCR5 antagonists.

Author: Vincent T, Portales P, Baillat V, de Boever CM, Le Moing V, Vidal M, Ducos J, Clot J, Reynes J, and Corbeau P
Subjects: Adult, CCR5 Receptor Antagonists, CD4 Antigens analysis, CD4-Positive T-Lymphocytes immunology, CD8 Antigens analysis, CD8-Positive T-Lymphocytes immunology, Female, Flow Cytometry, HIV Infections drug therapy, HIV Infections immunology, HLA-DR Antigens analysis, Hepacivirus isolation & purification, Hepacivirus physiology, Hepatitis C pathology, Hepatitis C virology, Humans, Liver pathology, Liver Cirrhosis pathology, Male, Middle Aged, Transaminases blood, Viral Load, HIV Infections complications, Hepatitis C complications, Hepatitis C immunology, Receptors, CCR5 analysis, T-Lymphocytes immunology
Abstract: CCR5 antagonists represent promising anti-HIV agents. Yet, if the CCR5 chemokine receptor plays a positive role in hepatitis C virus (HCV) infection, CCR5 antagonists might be contraindicated in HCV/HIV-coinfected subjects. Therefore, we tested the hypothesis that the level of T-cell surface CCR5 expression, which might determine the intensity of HCV-specific T-cell recruitment into the liver, and thereby the efficiency of the anti-HCV response, could determine HCV disease evolution. For this purpose, we compared CCR5 density, measured by quantitative flow cytometry at the surface of nonactivated (human leukocyte antigen-D-related [HLA-DR]-) T cells of 51 HCV/HIV patients, with HCV load, serum aminotransferase levels, and liver histology (inflammatory activity, fibrosis, and rate of fibrosis progression). DR-CD4+ T-cell surface CCR5 density, which correlated with DR-CD8+ T-cell surface CCR5 density and was stable over time in HCV/HIV-coinfected individuals, did not correlate with any of the biologic parameters of HCV infection analyzed and was not linked to the capacity to clear the virus. In conclusion, we failed to demonstrate any impact of interindividual variability in T-cell surface CCR5 density on HCV infection, which would have argued against the use of CCR5 antagonists in HIV/HCV-coinfected subjects.
Published: 2005

22. Human immunodeficiency virus type 1 (HIV-1) antigen secretion by latently infected resting CD4+ T lymphocytes from HIV-1-infected individuals.

Author: Fondere JM, Petitjean G, Huguet MF, Salhi SL, Baillat V, Macura-Biegun A, Becquart P, Reynes J, and Vendrell JP
Subjects: Antiretroviral Therapy, Highly Active, CD4-Positive T-Lymphocytes metabolism, DNA, Viral analysis, HIV Infections drug therapy, HIV-1 immunology, Humans, Time Factors, Viral Load, Viremia, Virus Replication, CD4-Positive T-Lymphocytes virology, HIV Antigens metabolism, HIV Infections virology, HIV-1 physiology, Virus Activation, Virus Latency
Abstract: In resting CD4(+) T lymphocytes harboring human immunodeficiency virus type 1 (HIV-1), replication-competent virus persists in patients responding to highly active antiretroviral therapy (HAART). This small latent reservoir represents between 10(3) and 10(7) cells per patient. However, the efficiency of HIV-1 DNA-positive resting CD4(+) T cells in converting to HIV-1-antigen-secreting cells (HIV-1-Ag-SCs) after in vitro CD4(+)-T-cell polyclonal stimulation has not been satisfactorily evaluated. By using an HIV-1-antigen enzyme-linked immunospot assay, 8 HIV-1-Ag-SCs per 10(6) CD4(+) resting T cells were quantified in 25 patients with a plasma viral load of <20 copies/ml, whereas 379 were enumerated in 10 viremic patients. In parallel, 369 and 1,238 copies of HIV-1 DNA per 10(6) CD4(+) T cells were enumerated in the two groups of patients, respectively. Only a minority of latently HIV-1 DNA-infected CD4(+) T cells could be stimulated in vitro to become HIV-1-Ag-SCs, particularly in aviremic patients. The difference between the number of HIV-1 immunospots in viremic versus aviremic patients could be explained by HIV-1 unintegrated viral DNA that gave additional HIV-1-Ag-SCs after in vitro CD4(+)-T-cell polyclonal stimulation. The ELISPOT approach to targeting the HIV-1-Ag-SCs could be a useful method for identifying latently HIV-1-infected CD4(+) T cells carrying replication-competent HIV-1 in patients responding to HAART.
Published: 2004
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23. Fenofibrate improves the atherogenic lipid profile and enhances LDL resistance to oxidation in HIV-positive adults.

Author: Badiou S, Merle De Boever C, Dupuy AM, Baillat V, Cristol JP, and Reynes J
Subjects: Adult, Anti-Retroviral Agents therapeutic use, Apolipoprotein A-I blood, Apolipoprotein C-III, Apolipoproteins B, Apolipoproteins C blood, Cholesterol blood, Cholesterol, HDL blood, Cholesterol, LDL blood, Female, Fenofibrate administration & dosage, Humans, Hypertriglyceridemia blood, Hypertriglyceridemia complications, Hypolipidemic Agents administration & dosage, Lipoproteins blood, Male, Middle Aged, Oxidation-Reduction drug effects, Triglycerides blood, Vitamin E administration & dosage, Vitamin E therapeutic use, Copper pharmacology, Fenofibrate therapeutic use, HIV Infections blood, Hypolipidemic Agents therapeutic use, Lipoproteins, LDL blood
Abstract: Background: Low HDL-cholesterol, hypertriglyceridemia (HTG) and occurrence of small dense LDL could be involved in increased cardiovascular risk in HIV-infected patients. This study evaluates the effects of fenofibrate and/or Vitamin E on lipoprotein profile., Design: Thirty-six HIV-positive adults with fasting triglycerides (TGs) > or =2 mmol/l and stable antiretroviral therapy (ART) were randomly assigned to receive either micronised fenofibrate (200 mg/day) or Vitamin E (500 mg/day) for a first period of 3 months and the association of both for an additional 3-month period., Methods and Results: Total cholesterol, HDL-C, LDL-C, triglycerides, apoA1, apoB, apoCIII, lipoprotein composition, LDL size and LDL resistance to copper-induced oxidation were determined before initiation of fenofibrate or Vitamin E, and 3 and 6 months thereafter. Three months of fenofibrate treatment results in a significant decrease in triglycerides (-40%), apoCIII (-21%), total cholesterol (-14%), apoB (-17%) levels, non-HDL-C (-17%), TG/apoA1 ratio in HDL (-27%) associated with an increase in HDL-C (+15%) and apoA1 (+11%) levels. Moreover, fenofibrate increases LDL size and enhances LDL resistance to oxidation. Three months of Vitamin E supplementation only improves LDL resistance to oxidation and addition to fenofibrate results in a slightly greater effect., Conclusion: Fenofibrate therapy improves the atherogenic lipid profile in HIV-positive adults with hypertriglyceridemia.
Published: 2004
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24. Detection and enumeration of circulating HIV-1-specific memory B cells in HIV-1-infected patients.

Author: Fondere JM, Huguet MF, Macura-Biegun A, Baillat V, Ohayon V, Reynes J, and Vendrell JP
Subjects: Antibody Specificity, Antigens, CD blood, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, HIV Antibodies blood, HIV-1 isolation & purification, Humans, Immunoglobulin D blood, Tumor Necrosis Factor Receptor Superfamily, Member 7 blood, Viremia blood, Viremia immunology, Acquired Immunodeficiency Syndrome immunology, Acquired Immunodeficiency Syndrome virology, B-Lymphocytes immunology, HIV-1 immunology, Immunologic Memory immunology
Abstract: Memory B cells are long-living cells that circulate throughout the body and differentiate into plasma cells after stimulation by antigens, cytokines, and direct cell-to-cell interaction in lymphoid tissues. For HIV-1-infected patients, we assessed whether in vitro polyclonal B cell activation that induces immunoglobulin secreting cells (SCs) also generates HIV-1-specific resting B cells to synthesize antibodies specific to HIV-1. To this end, highly purified B cells from 10 HIV-1-untreated patients were cultured with or without mouse fibroblastic cells expressing the CD40 ligand in the presence of IL-2 and IL-10. The percentage of immunoglobulin SCs we obtained by using the B cell-CD40L stimulation system was equal to 55% to 98% of the circulating memory B cells. Moreover, the anti-HIV-1 IgG, IgA, or IgM antibody SCs represented 1 x 10-2 to 1 x 10-3 of the total immunoglobulin SCs. The anti-HIV-1-specific antibodies detected in cell culture supernatants were directed to gag-, pol-, and env-encoded viral proteins. We found that in AIDS patients, HIV-1-specific resting memory B cells circulate in the blood and can be quantified by their anti-HIV-1 antibody secretion after strong B cell polyclonal stimulation.
Published: 2004
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25. Enumeration of latently infected CD4+ T cells from HIV-1-infected patients using an HIV-1 antigen ELISPOT assay.

Author: Fondere JM, Planas JF, Huguet MF, Baillat V, Bolos F, Reynes J, and Vendrell JP
Subjects: CD4 Lymphocyte Count, Cells, Cultured, Enzyme-Linked Immunosorbent Assay methods, Female, HIV Antigens immunology, HIV Infections drug therapy, HIV-1 isolation & purification, Humans, Lymphocyte Activation, Male, CD4-Positive T-Lymphocytes virology, HIV Infections immunology, HIV Infections virology, HIV-1 physiology, Virus Latency
Abstract: Background: Latently infected resting CD4(+) T cells carrying replication-competent HIV-1 are present in naive, chronically infected individuals as well as in those who are receiving highly active antiretroviral therapy (HAART). These cells serve as a potential source of reactivation of viral replication and remain a major obstacle for the eradication of HIV-1., Objectives: The enzyme-linked immunospot (ELISPOT) assay was adapted to the detection and the enumeration of HIV-1 antigen-secreting cells at the single cell level. We applied this test to count latently HIV-1-infected CD4(+) T cells., Study Design: Latently infected CD4(+) T cells were assessed in an in vitro model of HIV-1-infected resting CD4(+) T cells as well as in eighteen HAART-treated and in four HIV-1-infected untreated patients. Enriched CD4(+) T cells were cultured with or without antibodies against CD3 and CD28 T cell receptors and with irradiated peripheral blood mononuclear cells from HIV-1 seronegative individuals. At the term of the cell culture, CD4(+) T lymphocytes were tested using the HIV-1 antigen ELISPOT assay., Results: In the experimental HIV-1 infection model, 5579+/-4190 CD4(+) T cells secreting HIV-1 antigen were enumerated after polyclonal activation. In contrast, only 15+/-6 HIV-1 immunospots were obtained from unstimulated T cells. In all patients tested, induced HIV-1 antigen-secreting cells were measured at a frequency of 55+/-108/10(6) CD4(+) T cells., Conclusion: As each immunospot represents one HIV-1 antigen-secreting cell, the HIV-1 ELISPOT assay is a powerful to enumerate circulating CD4(+) T lymphocytes latently infected with HIV-1.
Published: 2004
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26. Detection of peripheral HIV-1-specific memory B cells in patients untreated or receiving highly active antiretroviral therapy.

Author: Fondere JM, Huguet MF, Yssel H, Baillat V, Reynes J, van de Perre P, and Vendrell JP
Subjects: Anti-HIV Agents therapeutic use, Antibody Specificity, B-Lymphocytes drug effects, CD40 Ligand immunology, Cells, Cultured, Chronic Disease, HIV Antibodies biosynthesis, HIV Infections drug therapy, HIV Infections virology, HIV-1 physiology, Humans, Immunologic Memory immunology, Lymphocyte Activation immunology, Viral Load, Virus Replication, Antiretroviral Therapy, Highly Active, B-Lymphocytes immunology, HIV Infections immunology, HIV-1 immunology
Abstract: Objectives: To examine whether polyclonal activation of circulating B cells, in a process that involves CD40-CD40 ligand and cytokine interactions, could induced HIV-1-specific memory B cells to synthesize HIV-1-specific antibodies., Methods: B cells from 26 HIV-1-infected patients were cultured with a CD40L-transfected cell line plus interleukins 2 and 10 and tested for their secretion of HIV-1- and Toxoplasma gondii-specific antibodies., Results: In vitro activated B lymphocytes from HIV-1-infected patients secreted anti-HIV-1-specific antibodies. B cells from HIV-1-infected patients as well as those from controls chronically infected by T. gondii synthesized T. gondii-specific antibodies. HIV-1-specific IgG-, IgA- or IgM-secreting B cells represented approximately 1 x 10(-4) to 1 x 10(-5) of total circulating B cells and 1 x 10(-2) to 1 x 10(-3) of immunoglobulin-secreting cells. HIV-1-specific memory B cells were found in 9/9 untreated patients and in 8/17 patients receiving highly active antiretroviral therapy (HAART). The other nine patients showed a normal CD40-CD40L B cell response and six of them produced T. gondii-specific antibody B cells. The follow-up of seven patients indicated that HIV-1-specific memory B cells became undetectable after 8 to 46 months of HAART, whereas T. gondii-specific memory B cells persisted in parasite coinfected patients., Conclusions: Circulating memory HIV-1-specific B cells were detected in untreated patients and in about half of the patients taking HAART, suggesting that persistent low-level ongoing viral replication is not sufficient to maintain HIV-1-specific memory B cells.
Published: 2003
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27. Reasons for early abacavir discontinuation in HIV-infected patients.

Author: Peyriere H, Guillemin V, Lotthe A, Baillat V, Fabre J, Favier C, Atoui N, Hansel S, Hillaire-Buys D, and Reynes J
Subjects: Adult, Adverse Drug Reaction Reporting Systems, Dideoxynucleosides administration & dosage, Drug Hypersensitivity epidemiology, Female, France, Humans, Male, Middle Aged, Retrospective Studies, Risk Factors, Time Factors, Dideoxynucleosides adverse effects, Dideoxynucleosides therapeutic use, Drug Hypersensitivity complications, HIV Infections complications, HIV Infections drug therapy
Abstract: Objective: To determine incidence of and reasons for discontinuation of abacavir within the first 6 months of therapy., Methods: Retrospective study performed in the cohort of HIV-infected adults who started abacavir in a medical unit between 1997 and December 2000. All adverse drug reactions (ADRs) (especially hypersensitivity) observed in this cohort were reported. The association between drugs and complications were evaluated, using the French method to assess unexpected and toxic drug reactions. According to the variables studied, statistical analysis was performed using the chi2 test, Fisher's exact test, Mann-Whitney, Wilcoxon, or Kruskal-Wallis tests., Results: All 331 patients treated with abacavir during this time period were included in this study. Early discontinuation of abacavir was observed in 34.1% of patients, the main reasons being adverse effects (20.8%), virologic failure (3.3%), drug holidays (2.7%), poor adherence (2.7%), and death (1.8%). Adverse effects were mostly represented by hypersensitivity reactions. After retrospective analysis, abacavir was stopped for likely hypersensitivity in 8.5% of patients, for doubtful hypersensitivity in 4.2%, and for other adverse effects in 8.1% of patients., Conclusions: This study shows that abacavir is mainly stopped during the first 6 months of therapy for ADRs. The rate of likely hypersensitivity reaction observed in this study (8.5%) is higher than that observed in clinical trials (5%). After retrospective evaluation, the causality assessment of abacavir is not always certain.
Published: 2003
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28. Low CD4+ T-cell surface CCR5 density as a cause of resistance to in vivo HIV-1 infection.

Author: Reynes J, Baillat V, Portales P, Clot J, and Corbeau P
Subjects: Female, HIV Seronegativity, HIV-1 pathogenicity, Humans, Male, CD4-Positive T-Lymphocytes metabolism, HIV Infections immunology, Immunity, Innate, Receptors, CCR5 metabolism
Published: 2003
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29. Small dense LDL and atherogenic lipid profile in HIV-positive adults: influence of lopinavir/ritonavir-containing regimen.

Author: Badiou S, De Boever CM, Dupuy AM, Baillat V, Cristol JP, and Reynes J
Subjects: Adult, Antiretroviral Therapy, Highly Active adverse effects, Arteriosclerosis chemically induced, HIV Protease Inhibitors adverse effects, Humans, Lipids blood, Lopinavir, HIV Infections drug therapy, Hyperlipidemias chemically induced, Lipoproteins, LDL blood, Pyrimidinones adverse effects, Ritonavir adverse effects
Published: 2003
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30. Perforin expression in T cells and virological response to PEG-interferon alpha2b in HIV-1 infection.

Author: Portales P, Reynes J, Rouzier-Panis R, Baillat V, Clot J, and Corbeau P
Subjects: Adult, Antiviral Agents therapeutic use, CD4-CD8 Ratio, CD8-Positive T-Lymphocytes drug effects, CD8-Positive T-Lymphocytes immunology, Case-Control Studies, Drug Therapy, Combination, Flow Cytometry methods, Follow-Up Studies, HIV Infections immunology, HIV Infections virology, Humans, Interferon alpha-2, Perforin, Polyethylene Glycols therapeutic use, Pore Forming Cytotoxic Proteins, Recombinant Proteins, Statistics, Nonparametric, Viral Load, CD8-Positive T-Lymphocytes metabolism, HIV Infections drug therapy, HIV-1, Interferon-alpha therapeutic use, Membrane Glycoproteins metabolism
Abstract: Objective and Design: Interferon alpha (IFNalpha), which is known to directly inhibit the HIV-1 replicative cycle and to increase the activity of cytotoxic T lymphocytes (CTL), is being tested as an anti-HIV agent. As CTL play a major role in immune defence against HIV, we wanted to further characterize CTL activity and the effect of IFNalpha on it., Methods: We followed by flow cytometry the intracellular expression of the key mediator of cytotoxicity, perforin, in peripheral blood T cells of patients treated with IFNalpha., Results: We observed that the percentage of T cells harbouring perforin was higher in infected subjects than in non-infected controls. Administration of IFNalpha2b attached to polyethylene glycol increased this perforin expression further and reduced viral load (P = 0.010). The increase in the percentage of T cells expressing perforin correlated with IFNalpha-induced decrease in viral load (r, 0.753; P = 0.003). In addition, the level of perforin expression before IFNalpha administration was inversely correlated with viral load remaining after IFNalpha administration (r, -0.647; P= 0.017)., Conclusion: The pre-therapeutic percentage of perforin-positive T cells might be a predictive marker of the virological response to IFNalpha in HIV-1-infected patients.
Published: 2003
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31. Interferon-alpha restores HIV-induced alteration of natural killer cell perforin expression in vivo.

Author: Portales P, Reynes J, Pinet V, Rouzier-Panis R, Baillat V, Clot J, and Corbeau P
Subjects: Adult, CD4 Lymphocyte Count, Case-Control Studies, Cytotoxicity Tests, Immunologic, Female, Granzymes, HIV Infections immunology, Humans, Intracellular Fluid metabolism, Killer Cells, Natural immunology, Lymphocyte Activation, Male, Middle Aged, Perforin, Pore Forming Cytotoxic Proteins, Serine Endopeptidases metabolism, Viremia, HIV Infections drug therapy, HIV-1, Interferon-alpha therapeutic use, Killer Cells, Natural metabolism, Membrane Glycoproteins metabolism
Abstract: Objective: The percentage and the activity of natural killer (NK) cells are known to be decreased in HIV-infected patients. However, the mechanisms responsible for this NK deficiency are poorly understood. Because of the role of NK cells in the host defence against microbial infections, this defect contributes to the virus-induced immune deficiency. The aim of the present study was to better understand this defect in order to be able to restore NK function in HIV infection., Design and Methods: The expression of the cytolytic mediators perforin and granzyme A was analysed by flow cytometry, the lytic activity of peripheral blood NK cells of HIV-infected patients was analysed by cytotoxic assay, and the expression of perforin was followed during administration of interferon (IFN)alpha attached to polyethylene glycol (PEG)-IFNalpha., Results: The lytic activity and the expression of perforin and granzyme A was low in NK cells of infected individuals in comparison with normal control volunteers. In both groups NK cytotoxic capacity was linked to perforin expression. The low perforin expression in HIV-infected subjects negatively correlated with HIV RNA plasma level. administration of PEG-IFNalpha restored perforin expression even in patients whose viral load was not reduced by this treatment., Conclusions: These results suggest that HIV-induced NK deficiency could be partly mediated by a defect in perforin and granzyme A expression, and that PEG-IFNalpha could be used in infected subjects to directly improve their natural immunity in addition to eventually reducing their viraemia.
Published: 2003
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32. Apolipoprotein CIII and highly active antiretroviral therapy (HAART)-induced hypertriglyceridemia.

Author: Badiou S, Dupuy AM, Baillat V, Fabre J, Tur MD, Cristol JP, and Reynes J
Subjects: Adult, Apolipoprotein C-III, HIV Infections blood, Humans, Hypertriglyceridemia blood, Middle Aged, Triglycerides blood, Anti-HIV Agents adverse effects, Antiretroviral Therapy, Highly Active adverse effects, Apolipoproteins C blood, HIV Infections drug therapy, Hypertriglyceridemia chemically induced
Published: 2003

33. Dynamics of spontaneous HIV-1 specific and non-specific B-cell responses in patients receiving antiretroviral therapy.

Author: Fournier AM, Baillat V, Alix-Panabieres C, Fondere JM, Merle C, Segondy M, Huguet MF, Reynes J, and Vendrell JP
Subjects: Adult, Drug Therapy, Combination, Female, HIV Antibodies blood, HIV Infections immunology, Humans, Immunoglobulin G blood, Lymphocyte Activation, Lymphocyte Count, Male, Middle Aged, Viral Load, Anti-HIV Agents therapeutic use, B-Lymphocytes immunology, HIV Infections drug therapy, HIV-1 immunology, Reverse Transcriptase Inhibitors therapeutic use
Abstract: Objectives: As spontaneous anti-HIV-1 antibody and IgG secretion by peripheral blood mononuclear cells (PBMC) reflect immune system activation by HIV-1 antigens, we evaluated the impact of antiretroviral therapies on HIV-1 specific and non-specific B cell responses., Methods: Anti-HIV-1 antibody and non-specific IgG were measured by ELISA in supernatants of PBMC cultured during 7 day from 30 patients initiating an antiretroviral therapy at baseline, 8, 16, 24, 36 and 48 weeks., Results: An early and sustained fall in plasma viral load to below the detection limit (20 copies/ml) was observed in 17 sustained responder patients (SR), whereas HIV-1 RNA remained detectable in 13 others incomplete responders. In both groups, HIV-1 specific antibody secretion decreased significantly in parallel with plasma viral load and polyclonal immunoglobulin production became similar to that of PBMC controls. However, HIV-1 specific antibody production became negative in only six SR, exhibiting a greater increase of CD4 T-cell counts and higher levels of the spontaneous HIV-1 specific IgA secretion at baseline than the other SR., Conclusions: Antiretroviral therapy induced a rapid and dramatic decrease of spontaneous HIV-1 specific and non-specific B cell responses. These results pointed out that HIV-1 specific antibody secretion persisted in 11 out of 17 SR patients, suggesting persistent immune system activation by residual HIV-1 antigens., (Copyright 2002 Lippincott Williams & Wilkins)
Published: 2002
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34. Spontaneous secretion of immunoglobulins and anti-HIV-1 antibodies by in vivo activated B lymphocytes from HIV-1-infected subjects: monocyte and natural killer cell requirement for in vitro terminal differentiation into plasma cells.

Author: Fournier AM, Fondere JM, Alix-Panabieres C, Merle C, Baillat V, Huguet MF, Taïb J, Ohayon V, Zembala M, Reynes J, and Vendrell JP
Subjects: Antigens, CD analysis, Antigens, Differentiation, B-Lymphocyte analysis, B-Lymphocytes immunology, CD40 Antigens physiology, Cell Adhesion Molecules physiology, Cell Communication, Cell Differentiation, Cells, Cultured, Humans, Interleukin-6 pharmacology, Lymphocyte Activation, Receptors, Transferrin, Acquired Immunodeficiency Syndrome immunology, B-Lymphocytes physiology, HIV Antibodies biosynthesis, HIV-1 immunology, Immunoglobulins biosynthesis, Killer Cells, Natural physiology, Monocytes physiology, Plasma Cells physiology
Abstract: Peripheral blood mononuclear cells from HIV-1-infected subjects secrete spontaneously in vitro immunoglobulins (Ig) and anti-HIV-1 antibodies (Ab). Purified B lymphocytes secrete only minute amounts of Ig and anti-HIV-1 Ab compared with unfractionated cells. Monocytes and natural killer cells enhanced both secretions by cell-to-cell contacts, involving adhesion and CD27, CD80 costimulatory molecules and IL-6. Cell interactions prolonged the survival and allowed the terminal maturation of in vivo activated B cells. The secreting cell precursors were highly differentiated B cells expressing a broad diversity of maturation markers (CD27(+), CD38(+), CD20(+/-), CD37(+/-), CD71(+/-), HLA-DQ(+/-), sIg(+/-)) but not sIgD, CD28, or CD40. This phenotype and the cytologic aspect of purified B cells suggest that these cells are early plasma cells originated from germinal center. Ex vivo secreting peripheral B cells had probably gone beyond the CD40/CD40 ligand interaction; then following CD28/CD80 and CD27/CD27 ligand (CD70) interactions in the presence of IL-6, they achieved in vitro their differentiation into plasma cells.
Published: 2002
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35. CD4 T cell surface CCR5 density as a host factor in HIV-1 disease progression.

Author: Reynes J, Portales P, Segondy M, Baillat V, André P, Avinens O, Picot MC, Clot J, Eliaou JF, and Corbeau P
Subjects: Adult, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes immunology, Disease Progression, Female, HIV Infections virology, HIV Long-Term Survivors, Humans, Male, Middle Aged, Receptors, CCR5 genetics, CD4-Positive T-Lymphocytes metabolism, HIV Infections immunology, HIV Infections physiopathology, HIV-1 physiology, Receptors, CCR5 metabolism
Abstract: Objective and Design: We have recently shown that the number of CCR5 molecules at the surface of peripheral blood CD4 T cells (CCR5 density) correlates with the viral RNA plasma level in HIV-1-infected individuals. As viral load is a strong predictor of outcome in HIV infection, the present study examines the correlation between CCR5 density and HIV-1 disease progression., Methods: Using a quantitative flow cytometry assay, we measured CCR5 density in HIV-1-infected adults and control healthy volunteers. The CCR5 genotype (presence of a Delta 32 allele) was also determined., Results: CCR5 density was stable over time on non-activated, HLA-DR(-)CD4 T cells of infected individuals. In a study cohort of 25 patients, asymptomatic and non-treated, we observed a correlation between CCR5 density on HLA-DR(-)CD4 T cells and the CD4 T cell slope (P = 0.026), which was independent of the presence or absence of the Delta 32CCR5 deletion. In particular, slow progressors expressed lower CCR5 densities than non-slow progressors (P = 0.004) and non-infected control subjects (P = 0.002)., Conclusion: These results are compatible with the hypothesis that CCR5 density, which is a key factor of HIV-1 infectability, determines in-vivo HIV production, and thereby the rate of CD4 cell decline. Consequently, CCR5 density quantitation could be a new valuable prognostic tool in HIV-1 infection. Moreover, these data emphasize the therapeutic potential of treatments that reduce functional CCR5 density.
Published: 2001
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36. In vitro anti-Toxoplasma gondii antibody production by peripheral blood mononuclear cells in the diagnosis and the monitoring of toxoplasmic encephalitis in AIDS-related brain lesions.

Author: Lacascade C, Conge AM, Baillat V, Pages I, Huguet MF, Reynes J, and Vendrell JP
Subjects: AIDS-Related Opportunistic Infections diagnosis, Adult, Aged, Antiprotozoal Agents therapeutic use, Encephalitis diagnosis, France, Humans, Male, Middle Aged, Pyrimethamine therapeutic use, Retrospective Studies, Toxoplasmosis, Cerebral diagnosis, Trimethoprim, Sulfamethoxazole Drug Combination therapeutic use, AIDS-Related Opportunistic Infections immunology, Antibodies, Protozoan biosynthesis, Encephalitis immunology, Leukocytes, Mononuclear immunology, Toxoplasmosis, Cerebral immunology
Abstract: The spontaneous secretion in vitro of anti-Toxoplasma gondii antibodies by peripheral blood mononuclear cells was assessed in 69 patients with AIDS-related brain lesions. The sensitivity and specificity of this assay in the diagnosis of toxoplasmic encephalitis (TE) were found to be 85.4% and 92.8%, respectively. Twenty-four patients with TE were observed during 1-year follow-up after initiation of anti-Toxoplasma treatment and classified on the basis of their clinical and radiologic responses as sustained responders (SR; n = 11), incomplete responders (IR; n = 7) or transient responders (TR; n = 6). In vitro anti-T. gondii antibody secretion decreased as early as the first month after initiation of treatment and disappeared within the year in SRs, persisted in IRs, and decreased but rebounded at relapse in the TR patients. In vitro anti-T. gondii antibody, which reflects immune system activation by parasitic antigens, could be a surrogate marker of TE in AIDS patients.
Published: 2000
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37. CD4+ T cell surface CCR5 density as a determining factor of virus load in persons infected with human immunodeficiency virus type 1.

Author: Reynes J, Portales P, Segondy M, Baillat V, André P, Réant B, Avinens O, Couderc G, Benkirane M, Clot J, Eliaou JF, and Corbeau P
Subjects: Acquired Immunodeficiency Syndrome virology, Adult, HLA-DR Antigens analysis, Humans, Acquired Immunodeficiency Syndrome immunology, CD4-Positive T-Lymphocytes chemistry, HIV-1 isolation & purification, Receptors, CCR5 analysis, Viremia virology
Abstract: The intensity of expression of the chemokine receptor CCR5 is involved in in vitro cell infectability by human immunodeficiency virus (HIV)-1 R5 isolates. Because CCR5 expression varies among individuals, the hypothesis that this expression could determine virus load in HIV-1-infected persons was tested. The mean number of CCR5 molecules per cell was measured on peripheral blood CD4+ T lymphocytes (CCR5 density) from HIV-1-infected, asymptomatic, nontreated adults. There was a strong correlation between HIV RNA plasma level and CCR5 density (P=.009) that was independent of cell activation and was not due to an HIV-induced CCR5 up-regulation. These data are compatible with the hypothesis that CCR5 density is a key factor governing cell infectability and in vivo virus production and explain the protective effect of the Delta32CCR5 deletion, which results in low CCR5 expression. CCR5 density might be of critical predictive value in HIV infection.
Published: 2000
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