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348 results on '"Brun-Vezinet, F."'

101. Interactions between nevirapine resistance mutations and NRTI resistance mutations

Author

Deforche, K., Camacho, R., Grossman, Z., Silander, T., Soares, Ma, Shafer, Rw, Laethem, K., Carvalho, Ap, Wynhoven, B., Cane, P., Clarke, J., Snoeck, J., Sirivichayakul, S., Ariyoshi, K., Holguin, A., Rudich, H., Rodrigues, R., Bouzas, Mb, Brun-Vezinet, F., Cahn, P., Brigido, Lf, Soriano, V., Sugiura, W., Phanuphak, P., Morris, L., Weber, J., Pillay, D., Tanuri, A., Harrigan, Pr, Schapiro, Jm, Katzenstein, D., Kantor, R., and Anne-Mieke Vandamme

102. HIV-1 RNA response to antiretroviral treatment in 1280 participants in the Delta Trial: an extended virology study

Author

Aboulker, J. P., Babiker, A. G., Brun-Vezinet, F., Darbyshire, J. H., Flandre, P., Gazzard, B., Nunn, A. J., Goodall, R., Aber, V., Bragman, K., Breckenridge, A. M., Carbon, C., Charreau, I., Chene, G., Collis, P., Cooper, D., Dormont, J., Fiddian, P., Flepp, M., Goebel, F. D., Hooker, M., Lange, J., Luthy, R., Peto, T. E. A., Reiss, P., Seligmann, M., Stone, A. B., Thomis, J., STEFANO VELLA, Walckenaer, G., Warrell, D., Weller, I. V. D., Wilber, R., Yeni, P., Yeo, J., Withnall, R., Goudsmit, J., Huraux, J. M., Noorda, J., Weiss, R., Boucher, C., Schuurman, R., Descamps, D., Jeffries, D., Tedder, R., Weber, J., Krzyanowski, C., Weverling, G., Delta Coordinating, Comm, and Delta Virology, Commg

106. Clinical and laboratory guidelines for the use of HIV-1 drug resistance testing as part of treatment management: recommendations for the European setting

Author

Miller, V., Anne-Mieke Vandamme, Loveday, C., Staszewski, S., Lundgren, J., Youle, M., Ait-Khaled, M., Boucher, C., Brun-Vezinet, F., Dedes, N., Giaquinto, C., Hertogs, K., Houyez, F., Perrin, L., Pillay, D., Schmit, Jc, Schuurman, R., Lange, J., Banhegyi, D., Biondi, G., Broekhuizen, A., Bush-Donovan, C., Camacho, R., Carlier, H., Clavel, F., Clotet, B., Clumeck, N., Colebunders, R., Clerq, K., Jaegher, Jj, Schrijver, G., Smet, K., Hall, W., Harrigan, R., Hatzakis, A., Hellmann, N., Hoetelmans, R., Holtzer, C., Katlama, C., Larder, D., Loriaux, E., Mccreedy, B., Mulcahy, F., Opravil, M., Phillips, A., Ruiz, N., Shulse, E., Sonnerborg, A., Soriano, V., Steel, H., Vella, S., Williams, A., and Hiv, Euroguidelines Grp Resistance

107. Prediction of response to antiretroviral therapy by human experts and by the EuResist data-driven expert system (the EVE study)

Author

Maurizio Zazzi, Kaiser, R., Sönnerborg, A., Struck, D., Altmann, A., Prosperi, M., Rosen Zvi, M., Petroczi, A., Peres, Y., Schülter, E., Boucher, Ca, Brun Vezinet, F., Harrigan, Pr, Morris, L., Obermeier, M., Perno, Cf, Phanuphak, P., Pillay, D., Shafer, Rw, Vandamme A, M., Laethem, K., Wensing, Amj, Lengauer, T., and Incardona, F.

Subjects
Male, Treatment Outcome, Databases, Factual, HIV-1, Humans, Expert Systems, Female, HIV Infections, Viral Load, Settore MED/07 - Microbiologia e Microbiologia Clinica, Probability
Abstract

The EuResist expert system is a novel data-driven online system for computing the probability of 8-week success for any given pair of HIV-1 genotype and combination antiretroviral therapy regimen plus optional patient information. The objective of this study was to compare the EuResist system vs. human experts (EVE) for the ability to predict response to treatment.The EuResist system was compared with 10 HIV-1 drug resistance experts for the ability to predict 8-week response to 25 treatment cases derived from the EuResist database validation data set. All current and past patient data were made available to simulate clinical practice. The experts were asked to provide a qualitative and quantitative estimate of the probability of treatment success.There were 15 treatment successes and 10 treatment failures. In the classification task, the number of mislabelled cases was six for EuResist and 6-13 for the human experts [mean±standard deviation (SD) 9.1±1.9]. The accuracy of EuResist was higher than the average for the experts (0.76 vs. 0.64, respectively). The quantitative estimates computed by EuResist were significantly correlated (Pearson r=0.695, P0.0001) with the mean quantitative estimates provided by the experts. However, the agreement among experts was only moderate (for the classification task, inter-rater κ=0.355; for the quantitative estimation, mean±SD coefficient of variation=55.9±22.4%).With this limited data set, the EuResist engine performed comparably to or better than human experts. The system warrants further investigation as a treatment-decision support tool in clinical practice.

108. Comparison of five interpretation algorithms for the prediction of protease inhibitor susceptibility in HIV-1 non-B subtypes

Author

Snoeck, J., Kantor, R., Shafer, Rw, Derdelinckx, I., Carvalho, Ap, Wynhoven, B., Soares, Ma, Cane, P., Clarke, J., Pillay, C., Sirivichayakul, S., Ariyoshi, K., Holguin, A., Rudich, H., Rodrigues, R., Bouzas, Mb, Laethem, K., Brun-Vezinet, F., Reid, C., Cahn, P., Brigido, Lf, Grossman, Z., Soriano, V., Sugiura, W., Phanuphak, P., Morris, L., Weber, J., Pillay, D., Tanuri, A., Harrigan, Pr, Camacho, R., Schapiro, Jm, Katzenstein, D., and Anne-Mieke Vandamme

109. Virological and immunological outcomes at 3 years after starting antiretroviral therapy with regimens containing non-nucleoside reverse transcriptase inhibitor, protease inhibitor, or both in INITIO: open-label randomised trial

Author

Yeni, P., Cooper, D. A., Aboulker, J. P., Babiker, A. G., Carey, D., Darbyshire, J. H., Marco Floridia, Girard, P. M., Goodall, L., Hooker, M. H., Mijch, A., Meiffredy, V., Salzberger, B., Antunes, F., Babiker, A., Becker, M., Boukli, N., Brun-Vezinet, F., Churchill, D., Conway, B., Chazallon, C., Darbyshire, J., Wit, S., Dusak, B., Emery, S., Flepp, M., Gatell, J., Goodall, R. L., Hemmer, R., Hooker, M., Law, M., Loveday, C., Lundgren, J., Manion, D., Mulcahy, F., Orani, A., Pharo, C., Ristola, M., Sandstrom, E., Schechter, M., Schnittman, S., Seligmann, M., Staszewski, S., Stek, M., Verbiest, W., Weber, J., Withnall, R., and Initio Trial Int Co-ordinating

110. Mapping nevirapine and efavirenz resistance using Bayesian networks of HIV-1 pol sequences of subtypes A, B, C, F and G

Author

Deforche, K., Camacho, R., Grossman, Z., Silander, T., Soares, M., Shafer, Rw, Laethem, K., Carvalho, Ap, Wynhoven, B., Cane, P., Clarke, J., Snoeck, J., Sirivichayakul, S., Ariyoshi, K., Holguin, A., Rudich, H., Rodrigues, R., Bouzas, M., Brun-Vezinet, F., Cahn, P., Brigido, Lf, Soriano, V., Sugiura, W., Phanuphak, P., Morris, L., Weber, J., Pillay, D., Tanuri, A., Harrigan, Pr, Schapiro, Jm, Katzenstein, D., Kantor, R., and Anne-Mieke Vandamme

111. HIV-1 integrase variability and relationship with drug resistance in antiretroviral-naive and -experienced patients with different HIV-1 subtypes

Author

Reigadas, S., Marcelin, A. G., Houssaïni, A., Yerly, S., Descamps, D., Plantier, J. C., Ruffault, A., Amiel, C., Trabaud, M. A., Flandre, Philippe, Fleury, H., Masquelier, B., Roussel, C., Alloui, C., Leguillou-Guillemette, H., Bettinger, D., Pallier, C., Brun-Vezinet, F., Peytavin, G., Pinson, P., Vallet, S., Poveda, J. D., Mirand, A., Krivine, A., Auvray, C., de Rougemont, A., Signori-Schmuck, A., Bocket, L., Rogez, S., Tamalet, C., Schneider, V., Bouvier-Alias, M., Montes, B., Schvoerer, E., Ferré, V., Chaix, M. L., Guinard, J., Haim-Boukobza, S., Soulié, C., Flandre, P., Assoumou, L., Calvez, V., Maillard, A., Morand-Joubert, L., Chaplain, C., Delaugerre, C., Bourlet, T., Bertsch, S., Raymond, S., Marque-Juillet, S., Reigadas, S., Marcelin, A. G., Houssaïni, A., Yerly, S., Descamps, D., Plantier, J. C., Ruffault, A., Amiel, C., Trabaud, M. A., Flandre, Philippe, Fleury, H., Masquelier, B., Roussel, C., Alloui, C., Leguillou-Guillemette, H., Bettinger, D., Pallier, C., Brun-Vezinet, F., Peytavin, G., Pinson, P., Vallet, S., Poveda, J. D., Mirand, A., Krivine, A., Auvray, C., de Rougemont, A., Signori-Schmuck, A., Bocket, L., Rogez, S., Tamalet, C., Schneider, V., Bouvier-Alias, M., Montes, B., Schvoerer, E., Ferré, V., Chaix, M. L., Guinard, J., Haim-Boukobza, S., Soulié, C., Flandre, P., Assoumou, L., Calvez, V., Maillard, A., Morand-Joubert, L., Chaplain, C., Delaugerre, C., Bourlet, T., Bertsch, S., Raymond, S., and Marque-Juillet, S.

126. Prevalence of hepatitis E virus (HEV) antibodies according to HIV status

Author

Bissuel, F., Houhou, N., Leport, C., Brun-Vezinet, F., and Vilde, J.L.

Subjects
HIV infection -- Complications, Hepatitis E -- Demographic aspects
Abstract

According to an abstract submitted by the authors to the 11th International Conference on AIDS, held July 7-12, 1996, in Vancouver, British Columbia, "OBJECTIVE: To assess the prevalence of Hepatitis [...]

Published
1996

139. Issues for the FDA.

Author

Loussert-Ajaka, I, Simon, F, and Brun-Vezinet, F

Published
1995

141. CD4 cell count response to first-line combination ART in HIV-2+ patients compared with HIV-1+ patients: A multinational, multicohort European study

Author

Wittkop, Linda, Arsandaux, Julie, Trevino, Ana, van der Loeff, Maarten Schim, Anderson, Jane, van Sighem, Ard, Böni, Jürg, Brun-Vezinet, Françoise, Soriano, Vicente, Boufassa, Faroudy, Brockmeyer, Norbert, Calmy, Alexandra, Dabis, François, Jarrin, Inma, Dorrucci, Maria, Duque, Vitor, Fätkenheuer, Gerd, Zangerle, Robert, Ferrer, Elena, Porter, Kholoud, Judd, Ali, Sipsas, Nikolaos V., Lambotte, Olivier, Shepherd, Leah, Leport, Catherine, Morrison, Charles, Mussini, Cristina, Obel, Niels, Ruelle, Jean, Schwarze-Zander, Carolyne, Sonnerborg, Anders, Teira, Ramon, Torti, Carlo, Valadas, Emilia, Colin, Celine, Friis-Møller, Nina, Costagliola, Dominique, Thiebaut, Rodolphe, Chene, Geneviève, Matheron, Sophie, Touloumi, Giota, Warszawski, Josiane, Meyer, Laurence, Krause, Murielle Mary, Ghosn, Jade, Reiss, Peter, Wit, Ferdinand, Prins, Maria, Bucher, Heiner, Gibb, Diana, Del Amo, Julia, Thorne, Claire, Mocroft, Amanda, Kirk, Ole, Stephan, Christoph, Pérez-Hoyos, Santiago, Hamouda, Osamah, Bartmeyer, Barbara, Chkhartishvili, Nikoloz, Noguera-Julian, Antoni, Antinori, Andrea, Monforte, Antonella d'Arminio, Prieto, Luis, Conejo, Pablo Rojo, Soriano-Arandes, Antoni, Battegay, Manuel, Kouyos, Roger, Tookey, Pat, Casabona, Jordi, Mirò, Jose M., Castagna, Antonella, Konopnick, Deborah, Goetghebuer, Tessa, Sönnerborg, Anders, Sabin, Caroline, Garrido, Myriam, Haerry, David, Berenguer, Juan, Bohlius, Julia, Bouteloup, Vincent, Cozzi-Lepri, Alessandro, Davies, Mary-Anne, Amo, Julia del, Dunn, David, Egger, Matthias, Furrer, Hansjakob, Guiguet, Marguerite, Grabar, Sophie, Leroy, Valériane, Lodi, Sara, Monge, Susana, Nakagawa, Fumiyo, Paredes, Roger, Phillips, Andrew, Puoti, Massimo, Schomaker, Michael, Smit, Colette, Sterne, Jonathan, van der Valk, Marc, Wyss, Natasha, Epidémiologie et Biostatistique, Institut National de la Santé et de la Recherche Médicale (INSERM), Team MORPH3EUS (INSERM U1219 - UB - ISPED), Bordeaux population health (BPH), Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Infectious Diseases, Hospital Carlos III, Center for Infection and Immunity Amsterdam - CINIMA [Amsterdam, The Netherlands], Homerton University Hospital, Stichting HIV Monitoring [Amsterdam], Universiteit van Amsterdam (UvA), Universität Zürich [Zürich] = University of Zurich (UZH), Université Paris Diderot - Paris 7 (UPD7), Service de Virologie [CHU Bichat], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de recherche en épidémiologie et santé des populations (CESP), 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), Ruhr-Universität Bochum [Bochum], Geneva University Hospital (HUG), CHU de Bordeaux Pellegrin [Bordeaux], Instituto de Salud Carlos III [Madrid] (ISC), CIBER de Epidemiología y Salud Pública (CIBERESP), Istituto Superiore di Sanità (ISS), Hospitais da Universidade de Coimbra (H.U.C.), University of Coimbra [Portugal] (UC), University Hospital of Cologne [Cologne], Innsbruck Medical University = Medizinische Universität Innsbruck (IMU), Hospitalet de Llobregat, University College of London [London] (UCL), National and Kapodistrian University of Athens (NKUA), Service de Médecine Interne et Immunologie clinique [AP-HP Hôpital Bicêtre], Hôpital Bicêtre, Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), FHI 360, Università degli Studi di Modena e Reggio Emilia = University of Modena and Reggio Emilia (UNIMORE), Rigshospitalet [Copenhagen], Copenhagen University Hospital, Université Catholique de Louvain = Catholic University of Louvain (UCL), University Hospital Bonn, Department of Infectious Diseases, Institution of Medicine, Karolinska University Hospital and Karolinska Institutet, Sierrallana Hospital, Università degli Studi 'Magna Graecia' di Catanzaro = University of Catanzaro (UMG), Universidade de Lisboa = University of Lisbon (ULISBOA), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Bordeaux [Bordeaux], AP-HP - Hôpital Bichat - Claude Bernard [Paris], Infectious diseases, Wittkop, L, Arsandaux, J, Trevino, A, van der Loeff, M, Anderson, J, van Sighem, A, Böni, J, Brun-Vezinet, F, Soriano, V, Boufassa, F, Brockmeyer, N, Calmy, A, Dabis, F, Jarrin, I, Dorrucci, M, Duque, V, Fätkenheuer, G, Zangerle, R, Ferrer, E, Porter, K, Judd, A, Sipsas, N, Lambotte, O, Shepherd, L, Leport, C, Morrison, C, Mussini, C, Obel, N, Ruelle, J, Schwarze-Zander, C, Sonnerborg, A, Teira, R, Torti, C, Valadas, E, Colin, C, Friis-Møller, N, Costagliola, D, Thiebaut, R, Chene, G, Matheron, S, Touloumi, G, Warszawski, J, Meyer, L, Krause, M, Ghosn, J, Reiss, P, Wit, F, Prins, M, Bucher, H, Gibb, D, Del Amo, J, Thorne, C, Mocroft, A, Kirk, O, Stephan, C, Pérez-Hoyos, S, Hamouda, O, Bartmeyer, B, Chkhartishvili, N, Noguera-Julian, A, Antinori, A, Monforte, A, Prieto, L, Conejo, P, Soriano-Arandes, A, Battegay, M, Kouyos, R, Tookey, P, Casabona, J, Mirò, J, Castagna, A, Konopnick, D, Goetghebuer, T, Sönnerborg, A, Sabin, C, Garrido, M, Haerry, D, Berenguer, J, Bohlius, J, Bouteloup, V, Cozzi-Lepri, A, Davies, M, Amo, J, Dunn, D, Egger, M, Furrer, H, Guiguet, M, Grabar, S, Leroy, V, Lodi, S, Monge, S, Nakagawa, F, Paredes, R, Phillips, A, Puoti, M, Schomaker, M, Smit, C, Sterne, J, van der Valk, M, Wyss, N, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Istituto Superiore di Sanita [Rome], Gestionnaire, Hal Sorbonne Université, Wittkop, Linda, Arsandaux, Julie, Trevino, Ana, Van Der Loeff V Schim, Maarten, Anderson, Jane, Van Sighem, Ard, Jurg, Boni, Brun-Vezinet, Francoise, Soriano, Vicente, Boufassa, Faroudy, Brockmeyer, Norbert, Calmy, Alexandra, Dabis, Francoi, Jarrin, Inma, Dorrucci, Maria, Duque, Vitor, Fãtkenheuer, Gerd, Zangerle, Robert, Ferrer, Elena, Porter, Kholoud, Judd, Ali, Sipsas, Nikolaos V, Lambotte, Olivier, Shepherd, Leah, Leport, Catherine, Morrison, Charle, Mussini, Cristina, Obel, Niel, Ruelle, Jean, Schwarze-Zander, Carolyne, Sonnerborg, Ander, Teira, Ramon, Torti, Carlo, Valadas, Emilia, Colin, Celine, Friis-Moller, Nina, Costagliola, Dominique, Thiebaut, Rodolphe, Chene, Geneviève, Matheron, Sophie, on behalf of the COHERE in EuroCoord and ACHIeV2e Study, Group, and Castagna, Antonella

Subjects
0301 basic medicine, CD4-Positive T-Lymphocytes, Male, Internationality, [SDV]Life Sciences [q-bio], Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Gastroenterology, Anti-HIV Agents/administration & dosage/adverse effects/therapeutic use, Viral/blood, Cohort Studies, 0302 clinical medicine, CD4 HIV, Pharmacology (medical), 030212 general & internal medicine, Cd4 cell count, ddc:616, Confounding, virus diseases, Middle Aged, Viral Load, 3. Good health, [SDV] Life Sciences [q-bio], Europe, HIV-2/drug effects, Infectious Diseases, HIV-1/drug effects, RNA, Viral, Female, Viral load, Cohort study, Microbiology (medical), Cart, Adult, medicine.medical_specialty, Anti-HIV Agents, 030106 microbiology, 03 medical and health sciences, Internal medicine, medicine, Humans, Pharmacology, business.industry, CD4-Positive T-Lymphocytes/immunology/virology, CD4 Lymphocyte Count, Institutional repository, HIV Infections/blood/drug therapy/immunology/virology, HIV-2, HIV-1, RNA, Panton–Valentine leukocidin, business
Abstract

Background: CD4 cell recovery following first-line combination ART (cART) is poorer in HIV-2+ than in HIV-1+ patients. Only large comparisons may allow adjustments for demographic and pretreatment plasma viral load (pVL). Methods: ART-naive HIV+ adults from two European multicohort collaborations, COHERE (HIV-1 alone) and ACHIeV2e (HIV-2 alone), were included, if they started first-line cART (without NNRTIs or fusion inhibitors) between 1997 and 2011. Patients without at least one CD4 cell count before start of cART, without a pretreatment pVL and with missing a priori-defined covariables were excluded. Evolution of CD4 cell count was studied using adjusted linear mixed models. Results: We included 185 HIV-2+ and 30321 HIV-1+ patients with median age of 46 years (IQR 36-52) and 37 years (IQR 31-44), respectively. Median observed pretreatment CD4 cell counts/mm(3) were 203 (95% CI 100-290) in HIV-2+ patients and 223 (95% CI 100-353) in HIV-1+ patients. Mean observed CD4 cell count changes from start of cART to 12months were + 105 (95% CI 77-134) in HIV-2+ patients and + 202 (95% CI 199-205) in HIV-1+ patients, an observed difference of 97 cells/mm(3) in 1 year. In adjusted analysis, the mean CD4 cell increase was overall 25 CD4 cells/mm(3)/year lower (95% CI 5-44; P=0.0127) in HIV-2+ patients compared with HIV-1+ patients. Conclusions: A poorer CD4 cell increase during first-line cART was observed in HIV-2+ patients, even after adjusting for pretreatment pVL and other potential confounders. Our results underline the need to identify more potent therapeutic regimens or strategies against HIV-2

Published
2017

142. Low-frequency drug-resistant HIV-1 and risk of virological failure to first-line NNRTI-based ART: a multicohort European case–control study using centralized ultrasensitive 454 pyrosequencing

Author

Cozzi-Lepri, Alessandro, Noguera-Julian, Marc, Di Giallonardo, Francesca, Schuurman, Rob, Däumer, Martin, Aitken, Sue, Ceccherini-Silberstein, Francesca, D'Arminio Monforte, Antonella, Geretti, Anna Maria, Booth, Clare L., Kaiser, Rolf, Michalik, Claudia, Jansen, Klaus, Masquelier, Bernard, Bellecave, Pantxika, Kouyos, Roger D., Castro, Erika, Furrer, Hansjakob, Schultze, Anna, Günthard, Huldrych F., Brun-Vezinet, Francoise, Paredes, Roger, Metzner, Karin J., Günthard, Huldrych, Brockmeyer, Norbert, Dabis, F., Bruyand, M., Chêne, G., Lawson-Ayayi, S., Thiébaut, R., Wittkop, L., André, K., Bonnal, F., Bonnet, F., Bernard, N., Caunègre, L., Cazanave, C., Ceccaldi, J., Chossat, I., Courtaud, K., Dauchy, F. A., De Witte, S., Dupon, M., Dupont, A., Duffau, P., Dutronc, H., Farbos, S., Gaborieau, V., Gemain, M. C., Gerard, Y., Greib, C., Hessamfar, M., Lacoste, D., Lataste, P., Lazaro, E., Longy-Boursier, M., Malvy, D., Meraud, J. P., Mercié, P., Monlun, E., Morlat, P., Neau, D., Ochoa, A., Pellegrin, J. L., Pistone, T., Receveur, M. C., Schmeltz, J. Roger, Tchamgoué, S., Vandenhende, M. A., Vareil, M.O., Viallard, J. F., Moreau, J. F., Pellegrin, I., Fleury, H., Lafon, M. E., Masquelier, B., Reigadas, S., Trimoulet, P., Bouchet, S., Breilh, D., Molimard, M., Titier, K., Haramburu, F., Miremont-Salamé., G., Blaizeau, M. J., Decoin, M., Delaune, J., Delveaux, S., D'Ivernois, C., Hanapier, C., Leleux, O., Lenaud, E., Uwamaliya-Nziyumvira, B., Sicard, X., Geffard, S., Le Marec, F., Conte, V., Frosch, A., Leray, J., Palmer, G., Touchard, D., Losso, M., Kundro, M., Ramos Mejia, J. M., Vetter, N., Zangerle, R., Karpov, I., Vassilenko, A., Mitsura, V. M., Suetnov, O., Clumeck, N., De Wit, S., Delforge, M., Florence, E., Vandekerckhove, L., Hadziosmanovic, V., Kostov, K., Begovac, J., Machala, L., Jilich, D., Sedlacek, D., Nielsen, J., Kronborg, G., Benfield, T., Larsen, M., Gerstoft, J., Katzenstein, T., Hansen, A.-B. E., Skinhøj, P., Pedersen, C., Ostergaard, L., Dragsted, U. B., Nielsen, L. N., Zilmer, K., Smidt, Jelena, Ristola, M., Katlama, C., Viard, J. P., Girard, P. M., Vanhems, P., Pradier, C., Duvivier, C., Rockstroh, J., Schmidt, R., van Lunzen, J., Degen, O., Stellbrink, H. J., Bickel, M., Bogner, J., Fätkenheuer, G., Kosmidis, J., Gargalianos, P., Xylomenos, G., Perdios, J., Sambatakou, H., Banhegyi, D., Gottfredsson, M., Mulcahy, F., Yust, I., Turner, D., Burke, M., Pollack, S., HassounRambam, G., Elinav, H., HaouziHadassah, M., EspositoI, R., Mazzotta, F., Vullo, V., Moroni, M., Andreoni, M., Angarano, G., Antinori, A., Castelli, F., Cauda, R., Di Perri, G., Galli, M., Iardino, R., Ippolito, G., Lazzarin, A., Perno, C. F., von Schloesser, F., Viale, P., Monforte, A. D'Arminio, Castagna, A., Ceccherini-Silberstein, F., Cozzi-Lepri, A., Girardi, E., Lo Caputo, S., Mussini, C., Puoti, M., Ammassari, A., Balotta, C., Bonfanti, P., Bonora, S., Borderi, M., Capobianchi, M. R., Cingolani, A., Cinque, P., De Luca, A., Di Biagio, A., Gianotti, N., Gori, A., Guaraldi, G., Lapadula, G., Lichtner, M., Madeddu, G., Maggiolo, F., Marchetti, G., Marcotullio, S., Monno, L., Quiros Roldan, E., Rusconi, S., Cicconi, P., Fanti, I., Formenti, T., Galli, L., Lorenzini, P., Carletti, F., Carrara, S., Castrogiovanni, A., Di Caro, A., Petrone, F., Prota, G., Quartu, S., Giacometti, A., Costantini, A., Mazzoccato, S., Santoro, C., Suardi, C., Vanino, E., Verucchi, G., Minardi, C., Quirino, T., Abeli, C., Manconi, P. E., Piano, P., Vecchiet, J., Falasca, K., Sighinolfi, L., Segala, D., Cassola, G., Viscoli, C., Alessandrini, A., Piscopo, R., Mazzarello, G., Mastroianni, C., Belvisi, V., Caramma, I., Chiodera, A., Castelli, A. P., Rizzardini, G., D'Arminio Monforte, A., Ridolfo, A. L., Piolini, R., Salpietro, S., Carenzi, L., Moioli, M. C., Tincati, C., Puzzolante, C., Abrescia, N., Chirianni, A., Guida, M. G., Gargiulo, M., Baldelli, F., Francisci, D., Parruti, G., Ursini, T., Magnani, G., Ursitti, M. A., d'Avino, A., Gallo, L., Nicastri, E., Acinapura, R., Capozzi, M., Libertone, R., Tebano, G., Cattelan, A., Sasset, L., Mura, M. S., Rossetti, B., Caramello, P., Orofino, G. C., Sciandra, M., Bassetti, M., Londero, A., Pellizzer, G., Manfrin, V., Brockmeyer, N. H., Skaletz-Rorowski, A., Dupke, S., Baumgarten, A., Carganico, A., Köppe, S., Kreckel, P., Lauenroth-Mai, E., Freiwald-Rausch, M., Gölz, J., Moll, A., Zeitz, M., Hower, M., Reuter, S., Jensen, B., Harrer, T., Esser, S., Brodt, H. R., Plettenberg, A., Stöhr, A., Buhk, T., Stoll, M., Kuhlmann, B., Mosthaf, F. A., Rieke, A., Becker, W., Volkert, R., Jäger, H., Hartl, H., Mutz, A., Ulmer, A., Müller, 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., Fux, C. A., Gorgievski, M., Günthard, H., Haerry, D., Hasse, B., Hirsch, H. H., Hösli, I., Kahlert, C., Kaiser, L., Keiser, O., Klimkait, T., Kovari, H., Kouyos, R., 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., Staehelin, C., Tarr, P., Telenti, A., Trkola, A., Vernazza, P., Weber, R., Yerly, S., Universitat de Vic. Càtedra de la Sida i Malalties Relacionades, CHAIN Minority HIV-1 Variants Working Group, Paredes, R., Metzner, KJ., Cozzi-Lepri, A., Schuurman, R., Brun-Vezinet, F., Günthard, H., Ceccherini-Silberstein, F., Kaiser, R., Geretti, AM., Brockmeyer, N., Masquelier, B., University of Zurich, and Metzner, Karin J

Subjects
Male, HIV Infections, Drug resistance, Gastroenterology, 2726 Microbiology (medical), Cohort Studies, 10234 Clinic for Infectious Diseases, chemistry.chemical_compound, 0302 clinical medicine, Antiretroviral Therapy, Highly Active, 2736 Pharmacology (medical), Pharmacology (medical), Treatment Failure, 030212 general & internal medicine, minority drug-resistant HIV-1 variants, CHAIN, antiretroviral therapy, European multicentre study, Original Research, 0303 health sciences, High-Throughput Nucleotide Sequencing, Antiretrovirals, Sida -- Tractament, Settore MED/07 - Microbiologia e Microbiologia Clinica, Virological failure, Antiretroviral therapy, 3. Good health, Europe, Infectious Diseases, 3004 Pharmacology, Reverse Transcriptase Inhibitors, Female, Cohort study, medicine.drug, Adult, Microbiology (medical), medicine.medical_specialty, Efavirenz, Nevirapine, Genotype, minority drug-resistant HIV-1 variants, First line, antiretroviral therapy, 610 Medicine & health, Biology, Risk Assessment, NO, Young Adult, 03 medical and health sciences, European multicentre study, Internal medicine, Drug Resistance, Viral, Minority drug-resistant HIV-1 variants, medicine, VIH (Virus), Humans, CHAIN, 030304 developmental biology, Pharmacology, Case-control study, Computational Biology, Sequence Analysis, DNA, 2725 Infectious Diseases, Virology, chemistry, Case-Control Studies, HIV-1, Pyrosequencing
Abstract

Objectives: It is still debated if pre-existing minority drug-resistant HIV-1 variants (MVs) affect the virological outcomes of first-line NNRTI-containing ART. Methods: This Europe-wide case–control study included ART-naive subjects infected with drug-susceptible HIV-1 as revealed by population sequencing, who achieved virological suppression on first-line ART including one NNRTI. Cases experienced virological failure and controls were subjects from the same cohort whose viraemia remained suppressed at a matched time since initiation of ART. Blinded, centralized 454 pyrosequencing with parallel bioinformatic analysis in two laboratories was used to identify MVs in the 1%–25% frequency range. ORs of virological failure according to MV detection were estimated by logistic regression. Results: Two hundred and sixty samples (76 cases and 184 controls), mostly subtype B (73.5%),were used for the analysis. Identical MVs were detected in the two laboratories. 31.6% of cases and 16.8% of controls harboured pre-existing MVs. Detection of at least one MV versus no MVs was associated with an increased risk of virological failure (OR¼2.75, 95% CI¼1.35–5.60, P¼0.005); similar associations were observed for at least one MV versus no NRTIMVs (OR¼2.27, 95% CI¼0.76–6.77, P¼0.140) and at least oneMV versus no NNRTIMVs (OR¼2.41, 95% CI¼1.12–5.18, P¼0.024). A dose–effect relationship between virological failure and mutational loadwas found. Conclusions: Pre-existing MVs more than double the risk of virological failure to first-line NNRTI-based ART.

Published
2015

143. Hepatitis E antibodies and HIV status.

Author

Bissuel, F, Houhou, N, Leport, C, Brun-Vezinet, F, and Vildé, J L

Subjects
*HIV infection epidemiology, *EPIDEMIOLOGICAL research, *HEPATITIS E, *HEPATITIS viruses, *HOMOSEXUALITY, *VIRAL antibodies, *DISEASE prevalence, *INFECTIOUS disease transmission
Published
1996
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144. Efficacy and safety of three antiretroviral therapy regimens for treatment-naive African adults living with HIV-2 (FIT-2): a pilot, phase 2, non-comparative, open-label, randomised controlled trial.

Author

Eholie SP, Ekouevi DK, Chazallon C, Charpentier C, Messou E, Diallo Z, Zoungrana J, Minga A, Ngom Gueye NF, Hawerlander D, Dembele F, Colin G, Tchounga B, Karcher S, Le Carrou J, Tchabert-Guié A, Toni TD, Ouédraogo AS, Bado G, Toure Kane C, Seydi M, Poda A, Mensah E, Diallo I, Drabo YJ, Anglaret X, and Brun-Vezinet F

Subjects
Humans, Adult, Male, Female, Pilot Projects, CD4 Lymphocyte Count, Treatment Outcome, Lopinavir therapeutic use, Lopinavir adverse effects, Lopinavir administration & dosage, Raltegravir Potassium therapeutic use, Raltegravir Potassium adverse effects, Raltegravir Potassium administration & dosage, Lamivudine therapeutic use, Lamivudine administration & dosage, Lamivudine adverse effects, Viral Load drug effects, Antiretroviral Therapy, Highly Active, Middle Aged, Zidovudine therapeutic use, Zidovudine adverse effects, Zidovudine administration & dosage, Drug Therapy, Combination, HIV-1 drug effects, HIV Infections drug therapy, HIV-2 drug effects, Tenofovir therapeutic use, Tenofovir adverse effects, Emtricitabine therapeutic use, Emtricitabine administration & dosage, Emtricitabine adverse effects, Anti-HIV Agents therapeutic use, Anti-HIV Agents adverse effects, Anti-HIV Agents administration & dosage, Ritonavir therapeutic use, Ritonavir administration & dosage, Ritonavir adverse effects
Abstract

Background: Due to the low number of individuals with HIV-2, no randomised trials of HIV-2 treatment have ever been done. We hypothesised that a non-comparative study describing the outcomes of several antiretroviral therapy (ART) regimens in parallel groups would improve understanding of how differences between HIV-1 and HIV-2 might lead to different therapeutic approaches., Methods: This pilot, phase 2, non-comparative, open-label, randomised controlled trial was done in Burkina Faso, Côte d'Ivoire, Senegal, and Togo. Adults with HIV-2 who were ART naive with CD4 counts of 200 cells per μL or greater were randomly assigned 1:1:1 to one of three treatment groups. A computer-generated sequentially numbered block randomisation list stratified by country was used for online allocation to the next available treatment group. In all groups, tenofovir disoproxil fumarate (henceforth tenofovir) was dosed at 245 mg once daily with either emtricitabine at 200 mg once daily or lamivudine at 300 mg once daily. The triple nucleoside reverse transcriptase inhibitor (NRTI) group received zidovudine at 250 mg twice daily. The ritonavir-boosted lopinavir group received lopinavir at 400 mg twice daily boosted with ritonavir at 100 mg twice daily. The raltegravir group received raltegravir at 400 mg twice daily. The primary outcome was the rate of treatment success at week 96, defined as an absence of serious morbidity event during follow-up, plasma HIV-2 RNA less than 50 copies per mL at week 96, and a substantial increase in CD4 cells between baseline and week 96. This trial is registered at ClinicalTrials.gov, NCT02150993, and is closed to new participants., Findings: Between Jan 26, 2016, and June 29, 2017, 210 participants were randomly assigned to treatment groups. Five participants died during the 96 weeks of follow-up (triple NRTI group, n=2; ritonavir-boosted lopinavir group, n=2; and raltegravir group, n=1), eight had a serious morbidity event (triple NRTI group, n=4; ritonavir-boosted lopinavir group, n=3; and raltegravir group, n=1), 17 had plasma HIV-2 RNA of 50 copies per mL or greater at least once (triple NRTI group, n=11; ritonavir-boosted lopinavir group, n=4; and raltegravir group, n=2), 32 (all in the triple NRTI group) switched to another ART regimen, and 18 permanently discontinued ART (triple NRTI group, n=5; ritonavir-boosted lopinavir group, n=7; and raltegravir group, n=6). The Data Safety Monitoring Board recommended premature termination of the triple NRTI regimen for safety reasons. The overall treatment success rate was 57% (95% CI 47-66) in the ritonavir-boosted lopinavir group and 59% (49-68) in the raltegravir group., Interpretation: The raltegravir and ritonavir-boosted lopinavir regimens were efficient and safe in adults with HIV-2. Both regimens could be compared in future phase 3 trials. The results of this pilot study suggest a trend towards better virological and immunological efficacy in the raltegravir-based regimen., Funding: ANRS MIE., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Published
2024
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145. First-line Raltegravir/Emtricitabine/Tenofovir Combination in Human Immunodeficiency Virus Type 2 (HIV-2) Infection: A Phase 2, Noncomparative Trial (ANRS 159 HIV-2).

Author

Matheron S, Descamps D, Gallien S, Besseghir A, Sellier P, Blum L, Mortier E, Charpentier C, Tubiana R, Damond F, Peytavin G, Ponscarme D, Collin F, Brun-Vezinet F, and Chene G

Subjects
Adult, Aged, CD4 Lymphocyte Count, Cohort Studies, Drug Therapy, Combination, Female, HIV-2, Humans, Integrase Inhibitors therapeutic use, Male, Middle Aged, RNA, Viral blood, Viral Load, Anti-HIV Agents therapeutic use, Emtricitabine therapeutic use, HIV Infections drug therapy, Raltegravir Potassium therapeutic use, Tenofovir therapeutic use
Abstract

Background: New options for first-line treatment of human immunodeficiency virus type 2 (HIV-2) infection are needed. We evaluated an integrase inhibitor (raltegravir)-containing regimen., Methods: Antiretroviral therapy (ART)-naive adults with symptomatic infection by HIV-2 only, CD4 count <500 cells/μL or CD4 decrease >50 cells/μL/year over the past 3 years, or a confirmed plasma HIV-2 RNA (pVL) load ≥100 copies/mL were eligible for this noncomparative trial. The composite primary endpoint was survival at 48 weeks without any of the following: CD4 gain from baseline <100 cells/μL, confirmed pVL ≥40 copies/mL from week 24, raltegravir permanent discontinuation, or incident B or C event. HIV-2 ultrasensitive pVL (uspVL) and total DNA were assessed using in-house polymerase chain reaction (PCR) assays., Results: Baseline median CD4 count of 30 enrolled individuals (67% women) was 436 cells/µL (interquartile range [IQR], 314-507 cells/µL); pVL was ≥40 copies/mL in 67% of them, uspVL was ≥5 copies/mL in 92%, and total DNA was >6 copies by PCR in 32%. At week 48, the composite endpoint of success was reached in 40% [95% confidence interval, 22.7%-59.4%]. Failure was mainly (50%) due to CD4 gain <100 cells/µL; uspVL was <5 copies/mL in 87% and total DNA >6 copies by PCR in 12% of participants. Median CD4 gain was 87 cells/µL (IQR, 38-213 cells/µL; n = 28). No serious adverse reactions were reported., Conclusions: Raltegravir-containing ART is a safe option for first-line treatment of HIV-2 infection, yielding a comparable success rate to protease inhibitors., Clinical Trials Registration: NCT 01605890.

Published
2018
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146. CD4 cell count response to first-line combination ART in HIV-2+ patients compared with HIV-1+ patients: a multinational, multicohort European study.

Author

Wittkop L, Arsandaux J, Trevino A, Schim van der Loeff M, Anderson J, van Sighem A, Böni J, Brun-Vezinet F, Soriano V, Boufassa F, Brockmeyer N, Calmy A, Dabis F, Jarrin I, Dorrucci M, Duque V, Fätkenheuer G, Zangerle R, Ferrer E, Porter K, Judd A, Sipsas NV, Lambotte O, Shepherd L, Leport C, Morrison C, Mussini C, Obel N, Ruelle J, Schwarze-Zander C, Sonnerborg A, Teira R, Torti C, Valadas E, Colin C, Friis-Møller N, Costagliola D, Thiebaut R, Chene G, and Matheron S

Subjects
Adult, Anti-HIV Agents administration & dosage, Anti-HIV Agents adverse effects, CD4-Positive T-Lymphocytes immunology, CD4-Positive T-Lymphocytes virology, Cohort Studies, Europe, Female, HIV Infections blood, HIV Infections drug therapy, Humans, Internationality, Male, Middle Aged, RNA, Viral blood, Viral Load, Anti-HIV Agents therapeutic use, CD4 Lymphocyte Count, HIV Infections immunology, HIV Infections virology, HIV-1 drug effects, HIV-2 drug effects
Abstract

Background: CD4 cell recovery following first-line combination ART (cART) is poorer in HIV-2+ than in HIV-1+ patients. Only large comparisons may allow adjustments for demographic and pretreatment plasma viral load (pVL)., Methods: ART-naive HIV+ adults from two European multicohort collaborations, COHERE (HIV-1 alone) and ACHIeV2e (HIV-2 alone), were included, if they started first-line cART (without NNRTIs or fusion inhibitors) between 1997 and 2011. Patients without at least one CD4 cell count before start of cART, without a pretreatment pVL and with missing a priori-defined covariables were excluded. Evolution of CD4 cell count was studied using adjusted linear mixed models., Results: We included 185 HIV-2+ and 30321 HIV-1+ patients with median age of 46 years (IQR 36-52) and 37 years (IQR 31-44), respectively. Median observed pretreatment CD4 cell counts/mm3 were 203 (95% CI 100-290) in HIV-2+ patients and 223 (95% CI 100-353) in HIV-1+ patients. Mean observed CD4 cell count changes from start of cART to 12 months were +105 (95% CI 77-134) in HIV-2+ patients and +202 (95% CI 199-205) in HIV-1+ patients, an observed difference of 97 cells/mm3 in 1 year. In adjusted analysis, the mean CD4 cell increase was overall 25 CD4 cells/mm3/year lower (95% CI 5-44; P = 0.0127) in HIV-2+ patients compared with HIV-1+ patients., Conclusions: A poorer CD4 cell increase during first-line cART was observed in HIV-2+ patients, even after adjusting for pretreatment pVL and other potential confounders. Our results underline the need to identify more potent therapeutic regimens or strategies against HIV-2., (© The Author 2017. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2017
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147. Low-frequency drug-resistant HIV-1 and risk of virological failure to first-line NNRTI-based ART: a multicohort European case-control study using centralized ultrasensitive 454 pyrosequencing.

Author

Cozzi-Lepri A, Noguera-Julian M, Di Giallonardo F, Schuurman R, Däumer M, Aitken S, Ceccherini-Silberstein F, D'Arminio Monforte A, Geretti AM, Booth CL, Kaiser R, Michalik C, Jansen K, Masquelier B, Bellecave P, Kouyos RD, Castro E, Furrer H, Schultze A, Günthard HF, Brun-Vezinet F, Paredes R, and Metzner KJ

Subjects
Adult, Case-Control Studies, Cohort Studies, Computational Biology, Europe, Female, Genotype, HIV-1 genetics, HIV-1 isolation & purification, High-Throughput Nucleotide Sequencing, Humans, Male, Risk Assessment, Sequence Analysis, DNA, Treatment Failure, Young Adult, Antiretroviral Therapy, Highly Active methods, Drug Resistance, Viral, HIV Infections drug therapy, HIV Infections virology, HIV-1 drug effects, Reverse Transcriptase Inhibitors therapeutic use
Abstract

Objectives: It is still debated if pre-existing minority drug-resistant HIV-1 variants (MVs) affect the virological outcomes of first-line NNRTI-containing ART., Methods: This Europe-wide case-control study included ART-naive subjects infected with drug-susceptible HIV-1 as revealed by population sequencing, who achieved virological suppression on first-line ART including one NNRTI. Cases experienced virological failure and controls were subjects from the same cohort whose viraemia remained suppressed at a matched time since initiation of ART. Blinded, centralized 454 pyrosequencing with parallel bioinformatic analysis in two laboratories was used to identify MVs in the 1%-25% frequency range. ORs of virological failure according to MV detection were estimated by logistic regression., Results: Two hundred and sixty samples (76 cases and 184 controls), mostly subtype B (73.5%), were used for the analysis. Identical MVs were detected in the two laboratories. 31.6% of cases and 16.8% of controls harboured pre-existing MVs. Detection of at least one MV versus no MVs was associated with an increased risk of virological failure (OR = 2.75, 95% CI = 1.35-5.60, P = 0.005); similar associations were observed for at least one MV versus no NRTI MVs (OR = 2.27, 95% CI = 0.76-6.77, P = 0.140) and at least one MV versus no NNRTI MVs (OR = 2.41, 95% CI = 1.12-5.18, P = 0.024). A dose-effect relationship between virological failure and mutational load was found., Conclusions: Pre-existing MVs more than double the risk of virological failure to first-line NNRTI-based ART., (© The Author 2014. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy.)

Published
2015
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148. Lopinavir/r no longer recommended as a first-line regimen: a comparative effectiveness analysis.

Author

Potard V, Rey D, Poizot-Martin I, Mokhtari S, Pradier C, Rozenbaum W, Brun-Vezinet F, and Costagliola D

Subjects
Adenine analogs & derivatives, Adenine therapeutic use, Adult, CD4 Lymphocyte Count, Cohort Studies, Deoxycytidine analogs & derivatives, Deoxycytidine therapeutic use, Emtricitabine, Female, France, Humans, Male, Middle Aged, Organophosphonates therapeutic use, Prospective Studies, Tenofovir, Treatment Failure, Viral Load, Anti-HIV Agents therapeutic use, Antiretroviral Therapy, Highly Active methods, HIV Infections drug therapy, Lopinavir therapeutic use
Abstract

Introduction: We compared the effectiveness of tenofovir/emtricitabine (TDF/FTC) combined with either lopinavir/r (LPV/r) or another recommended third drug in the 2010 French guidelines in antiretroviral-naïve patients starting combination antiretroviral therapy in 2004-2008 in the French Hospital Database on HIV., Methods: The outcomes were stop or switch of the third component, viral load (VL) <500 copies/ml, an increase of at least 100 CD4 cells/mm(3), AIDS-defining event and non-AIDS-defining hospitalization or death. Propensity scores were estimated by logistic regression based on the clinical centre and other confounders. In each clinical centre, each patient initiating LPV/r was matched with a patient initiating another third drug (efavirenz or atazanavir/r) and having a close propensity score. Cox's proportional hazards models were then used, with treatment as covariate. Time was right-censored at four years., Results: 1269 patients started LPV/r plus TDF/FTC, and 890 could be matched to 890 patients receiving another third drug. Baseline characteristics were well balanced between these two groups. LPV/r was associated with a higher risk of third drug stop (hazard ratio (HR): 1.69; 95% confidence interval (CI), 1.42-2.00) and with less rapid viral suppression (HR: 0.83; 95% CI, 0.72-0.95). There was no difference in the time required for a CD4 cell increment of at least 100/mm(3), or to the occurrence of an AIDS-defining event. Non-AIDS-defining hospitalizations or deaths were more frequent with LPV/r (HR: 1.79; 95% CI, 1.33-2.39)., Conclusions: For first-line therapy, in this observational setting, TDF/FTC plus LPV/r were less durable than TDF/FTC plus another recommended third drug, led to a less rapid viral suppression and were associated with a higher risk of non-AIDS morbidity.

Published
2014
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149. Oral antiretroviral drugs as public health tools for HIV prevention: global implications for adherence, drug resistance, and the success of HIV treatment programs.

Author

Gupta RK, Wainberg MA, Brun-Vezinet F, Gatell JM, Albert J, Sönnerborg A, and Nachega JB

Subjects
Adenine administration & dosage, Administration, Oral, Counseling, Deoxycytidine administration & dosage, Drug Therapy, Combination, Emtricitabine, HIV Infections drug therapy, HIV Infections virology, HIV-1 physiology, Humans, Patient Compliance, Public Health, Tenofovir, Adenine analogs & derivatives, Anti-HIV Agents administration & dosage, Deoxycytidine analogs & derivatives, Drug Resistance, Viral, HIV Infections prevention & control, HIV-1 drug effects, Organophosphonates administration & dosage
Abstract

Recent data from studies on treatment as prevention (TasP) and preexposure prophylaxis (PrEP) show that antiretroviral drugs can be used in prevention, as well as in treatment. The movement from first-generation antiretroviral therapy (ART) coformulations based on thymidine analogues to second-generation ART coformulations based on tenofovir may coincide with future prevention strategies that also use tenofovir/emtricitabine, raising concerns regarding drug resistance. In published studies, failure of prophylaxis was associated with poor adherence and low plasma drug levels. Although rates of drug resistance in cases of failed prevention was low, regular human immunodeficiency virus (HIV) testing was undertaken in these clinical trials. Although legitimate concerns exist about ART adherence and drug resistance associated with PrEP and TasP in real-world settings, efforts to curb the continuing HIV epidemic through use of these novel prevention strategies should move forward because the development and approval of newer drugs reserved for prevention might take many more years. Efforts must be made to monitor ART adherence and to intervene through counseling and other means in order to optimize adherence and retention in care, whenever necessary. Finally, further research involving the generalized epidemic is needed to determine when suboptimal drug use may occur and when regular testing and monitoring of the long-term consequences of ART use may not be routine.

Published
2013
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150. Impact of gag genetic determinants on virological outcome to boosted lopinavir-containing regimen in HIV-2-infected patients.

Author

Larrouy L, Vivot A, Charpentier C, Bénard A, Visseaux B, Damond F, Matheron S, Chene G, Brun-Vezinet F, and Descamps D

Subjects
DNA, Viral drug effects, Drug Resistance, Viral drug effects, Drug Resistance, Viral genetics, Female, HIV Infections drug therapy, HIV Protease drug effects, HIV Protease genetics, HIV-2 drug effects, Humans, Male, Molecular Sequence Data, Mutation, Viral Load drug effects, gag Gene Products, Human Immunodeficiency Virus drug effects, pol Gene Products, Human Immunodeficiency Virus drug effects, HIV Infections genetics, HIV Protease Inhibitors pharmacology, HIV-2 genetics, Lopinavir pharmacology, Protease Inhibitors pharmacology, gag Gene Products, Human Immunodeficiency Virus genetics, pol Gene Products, Human Immunodeficiency Virus genetics
Abstract

Objective: This study investigated the impact on virological outcome of the gag cleavage sites and the protease-coding region mutations in protease inhibitor-naive and protease inhibitor-experienced patients infected with HIV-2 receiving lopinavir (LPV) containing regimen., Methods: Baseline gag and protease-coding region were sequenced in 46 HIV-2 group A-infected patients receiving lopinavir. Virological response was defined as plasma viral load less than 100 copies/ml at month 3. Associations between virological response and frequencies of mutations in gag [matrix/capsid (CA), CA/p2, p2/nucleocapsid (NC), NC/p1, p1/p6] and gag-pol (NC/p6) cleavage site and protease-coding region, with respect to the HIV-2ROD strain, were tested using Fisher's exact test., Results: Virological response occurred in 14 of 17 (82%) protease inhibitor-naive and 17 of 29 (59%) protease inhibitor-experienced patients. Virological failure was associated with higher baseline viral load (median: 6765 versus 1098 copies/ml, P = 0.02). More protease-coding region mutations were observed in protease inhibitor-experienced compared with protease inhibitor-naive patients (median: 8 versus 5, P = 0.003). In protease inhibitor-naive patients, T435A (NC/p6), V447M (p1/p6), and Y14H (protease-coding region) were associated with virological failure (P = 0.011, P = 0.033, P = 0.022, respectively). T435A and V447M were associated with Y14H (P = 0.018, P = 0.039, respectively). In protease inhibitor-experienced patients, D427E (NC/p1) was associated with virological response (P = 0.014). A430V (NC/p1) and I82F (protease-coding region) were associated with virological failure (P = 0.046, P = 0.050, respectively). Mutations at position 430 were associated with a higher number of mutations in protease-coding region (median: 10 versus 7, P = 0.008)., Conclusion: We have demonstrated, for the first time, an association between gag, gag-pol cleavage site and protease-coding region mutations, with distinct profiles between protease inhibitor-naive and protease inhibitor-experienced patients. These mutations might impact the virological outcome of HIV-2-infected patients receiving LPV-containing regimen.

Published
2013
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