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1. Global associations of key populations with HIV-1 recombinants: a systematic review, global survey, and individual participant data meta-analysis

Author: Nkazi Nchinda, Ramyiadarsini Elangovan, Jason Yun, Leslie Dickson-Tetteh, Shona Kirtley, Joris Hemelaar, WHO-UNAIDS Network for HIV Isolation and Characterisation, Alash'le G. Abimiku, Simon Agwale, Chris Archibald, Boaz Avidor, Barbás María Gabriela, Francoise Barre-Sinoussi, Banson Barugahare, El Hadj Belabbes, Silvia Bertagnolio, Deborah Birx, Aleksei F. Bobkov, James Brandful, Helba Bredell, Catherine A. Brennan, James Brooks, Marie Bruckova, Luigi Buonaguro, Franco Buonaguro, Stefano Buttò, Anne Buve, Mary Campbell, Jean Carr, Alex Carrera, Manuel Gómez Carrillo, Connie Celum, Beth Chaplin, Macarthur Charles, Dimitrios Chatzidimitriou, Zhiwei Chen, Katsumi Chijiwa, David Cooper, Philip Cunningham, Anoumou Dagnra, Cillian F. de Gascun, Julia Del Amo, Elena Delgado, Ursula Dietrich, Dominic Dwyer, Dennis Ellenberger, Barbara Ensoli, Max Essex, Herve Fleury, Peter N. Fonjungo, Vincent Foulongne, Deepak A. Gadkari, Feng Gao, Federico García, Roger Garsia, Guy Michel Gershy-Damet, Judith R. Glynn, Ruth Goodall, Zehava Grossman, Monick Lindenmeyer Guimarães, Beatrice Hahn, Raph L. Hamers, Osamah Hamouda, Ray Handema, Xiang He, Joshua Herbeck, David D. Ho, Africa Holguin, Mina Hosseinipour, Gillian Hunt, Masahiko Ito, Mohamed Ali Bel Hadj Kacem, Erin Kahle, Pontiano Kaleebu, Marcia Kalish, Adeeba Kamarulzaman, Chun Kang, Phyllis Kanki, Edward Karamov, Jean-Claude Karasi, Kayitesi Kayitenkore, Tony Kelleher, Dwip Kitayaporn, Leondios G. Kostrikis, Claudia Kucherer, Claudia Lara, Thomas Leitner, Kirsi Liitsola, Jai Lingappa, Marek Linka, Ivette Lorenzana de Rivera, Vladimir Lukashov, Shlomo Maayan, Luzia Mayr, Francine McCutchan, Nicolas Meda, Elisabeth Menu, Fred Mhalu, Doreen Mloka, John L. Mokili, Brigitte Montes, Orna Mor, Mariza Morgado, Fausta Mosha, Awatef Moussi, James Mullins, Rafael Najera, Mejda Nasr, Nicaise Ndembi, Joel R. Neilson, Vivek R. Nerurkar, Florian Neuhann, Claudine Nolte, Vlad Novitsky, Philippe Nyambi, Marianna Ofner, Fem J. Paladin, Anna Papa, Jean Pape, Neil Parkin, Chris Parry, Martine Peeters, Alexandra Pelletier, Lucía Pérez-Álvarez, Deenan Pillay, Angie Pinto, Trinh Duy Quang, Cecilia Rademeyer, Filimone Raikanikoda, Mark A. Rayfield, Jean-Marc Reynes, Tobias Rinke de Wit, Kenneth E. Robbins, Morgane Rolland, Christine Rousseau, Jesus Salazar-Gonzales, Hanan Salem, Mika Salminen, Horacio Salomon, Paul Sandstrom, Mario L. Santiago, Abdoulaye D. Sarr, Bryan Schroeder, Michel Segondy, Philippe Selhorst, Sylvester Sempala, Jean Servais, Ansari Shaik, Yiming Shao, Amine Slim, Marcelo A. Soares, Elijah Songok, Debbie Stewart, Julie Stokes, Shambavi Subbarao, Ruengpung Sutthent, Jun Takehisa, Amilcar Tanuri, Kok Keng Tee, Kiran Thapa, Michael Thomson, Tyna Tran, Willy Urassa, Hiroshi Ushijima, Philippe van de Perre, Guido van der Groen, Kristel van Laethem, Joep van Oosterhout, Ard van Sighem, Eric van Wijngaerden, Anne-Mieke Vandamme, Jurgen Vercauteren, Nicole Vidal, Lesley Wallace, Carolyn Williamson, Dawit Wolday, Jianqing Xu, Chunfu Yang, Linqi Zhang, and Rong Zhang
Subjects: HIV, key populations, recombinant, CRF, URF, molecular epidemiology, Public aspects of medicine, RA1-1270
Abstract: IntroductionGlobal HIV infections due to HIV-1 recombinants are increasing and impede prevention and treatment efforts. Key populations suffer most new HIV infections, but their role in the spread of HIV-1 recombinants is unknown. We conducted a global analysis of the associations between key populations and HIV-1 recombinants.MethodsWe searched PubMed, EMBASE, CINAHL, and Global Health for HIV-1 subtyping studies published from 1/1/1990 to 31/12/2015. Unpublished data was collected through a global survey. We included studies with HIV-1 subtyping data of key populations collected during 1990-2015. Key populations assessed were heterosexual people (HET), men who have sex with men (MSM), people who inject drugs (PWID), vertical transmissions (VERT), commercial sex workers (CSW), and transfusion-associated infections (BLOOD). Logistic regression was used to determine associations of key populations with HIV-1 recombinants. Subgroup analyses were performed for circulating recombinant forms (CRFs), unique recombinant forms (URFs), regions, and time periods.ResultsEight hundred and eighty five datasets including 77,284 participants from 83 countries were included. Globally, PWID were associated with the greatest odds of recombinants and CRFs (OR 2.6 [95% CI 2.46–2.74] and 2.99 [2.83–3.16]), compared to HET. CSW were associated with increased odds of recombinants and URFs (1.59 [1.44–1.75] and 3.61 [3.15–4.13]). VERT and BLOOD were associated with decreased odds of recombinants (0.58 [0.54–0.63] and 0.43 [0.33–0.56]). MSM were associated with increased odds of recombinants in 2010–2015 (1.43 [1.35–1.51]). Subgroup analyses supported our main findings.DiscussionAs PWID, CSW, and MSM are associated with HIV-1 recombinants, increased preventative measures and HIV-1 molecular surveillance are crucial within these key populations.Systematic review registrationPROSPERO [CRD42017067164].
Published: 2023
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2. Global and Regional Estimates for Subtype-Specific Therapeutic and Prophylactic HIV-1 Vaccines: A Modeling Study

Author: Ramyiadarsini Elangovan, Michael Jenks, Jason Yun, Leslie Dickson-Tetteh, Shona Kirtley, Joris Hemelaar, WHO-UNAIDS Network for HIV Isolation and Characterisation, Alash’le G Abimiku, Simon Agwale, Chris Archibald, Boaz Avidor, María Gabriela Barbás, Francoise Barre-Sinoussi, Banson Barugahare, El Hadj Belabbes, Silvia Bertagnolio, Deborah Birx, Aleksei F Bobkov, James Brandful, Helba Bredell, Catherine A Brennan, James Brooks, Marie Bruckova, Luigi Buonaguro, Franco Buonaguro, Stefano Buttò, Anne Buvé, Mary Campbell, Jean Carr, Alex Carrera, Manuel Gómez Carrillo, Connie Celum, Beth Chaplin, Macarthur Charles, Dimitrios Chatzidimitriou, Zhiwei Chen, Katsumi Chijiwa, David Cooper, Philip Cunningham, Anoumou Dagnra, Cillian F de Gascun, Julia Del Amo, Elena Delgado, Ursula Dietrich, Dominic Dwyer, Dennis Ellenberger, Barbara Ensoli, Max Essex, Hervé Fleury, Peter N Fonjungo, Vincent Foulongne, Deepak A Gadkari, Feng Gao, Federico García, Roger Garsia, Guy Michel Gershy-Damet, Judith R Glynn, Ruth Goodall, Zehava Grossman, Monick Lindenmeyer Guimarães, Beatrice Hahn, Raph L Hamers, Osamah Hamouda, Ray Handema, Xiang He, Joshua Herbeck, David D Ho, Africa Holguin, Mina Hosseinipour, Gillian Hunt, Masahiko Ito, Mohamed Ali Bel Hadj Kacem, Erin Kahle, Pontiano Kaleebu, Marcia Kalish, Adeeba Kamarulzaman, Chun Kang, Phyllis Kanki, Edward Karamov, Jean-Claude Karasi, Kayitesi Kayitenkore, Tony Kelleher, Dwip Kitayaporn, Leondios G Kostrikis, Claudia Kucherer, Claudia Lara, Thomas Leitner, Kirsi Liitsola, Jai Lingappa, Marek Linka, Ivette Lorenzana de Rivera, Vladimir Lukashov, Shlomo Maayan, Luzia Mayr, Francine McCutchan, Nicolas Meda, Elisabeth Menu, Fred Mhalu, Doreen Mloka, John L Mokili, Brigitte Montes, Orna Mor, Mariza Morgado, Fausta Mosha, Awatef Moussi, James Mullins, Rafael Najera, Mejda Nasr, Nicaise Ndembi, Joel R Neilson, Vivek R Nerurkar, Florian Neuhann, Claudine Nolte, Vlad Novitsky, Philippe Nyambi, Marianna Ofner, Fem J Paladin, Anna Papa, Jean Pape, Neil Parkin, Chris Parry, Martine Peeters, Alexandra Pelletier, Lucía Pérez-Álvarez, Deenan Pillay, Angie Pinto, Trinh Duy Quang, Cecilia Rademeyer, Filimone Raikanikoda, Mark A. Rayfield, Jean-Marc Reynes, Tobias Rinke de Wit, Kenneth E Robbins, Morgane Rolland, Christine Rousseau, Jesus Salazar-Gonzales, Hanan Salem, Mika Salminen, Horacio Salomon, Paul Sandstrom, Mario L Santiago, Abdoulaye D Sarr, Bryan Schroeder, Michel Segondy, Philippe Selhorst, Sylvester Sempala, Jean Servais, Ansari Shaik, Yiming Shao, Amine Slim, Marcelo A Soares, Elijah Songok, Debbie Stewart, Julie Stokes, Shambavi Subbarao, Ruengpung Sutthent, Jun Takehisa, Amilcar Tanuri, Kok Keng Tee, Kiran Thapa, Michael Thomson, Tyna Tran, Willy Urassa, Hiroshi Ushijima, Philippe van de Perre, Guido van der Groen, Kristel van Laethem, Joep van Oosterhout, Ard van Sighem, Eric van Wijngaerden, Anne-Mieke Vandamme, Jurgen Vercauteren, Nicole Vidal, Lesley Wallace, Carolyn Williamson, Dawit Wolday, Jianqing Xu, Chunfu Yang, Linqi Zhang, and Rong Zhang
Subjects: HIV, subtype, recombinant, CRF, URF, vaccine, Microbiology, QR1-502
Abstract: Global HIV-1 genetic diversity forms a major obstacle to the development of an HIV vaccine. It may be necessary to employ subtype-specific HIV-1 vaccines in individual countries according to their HIV-1 subtype distribution. We estimated the global and regional need for subtype-specific HIV-1 vaccines. We took into account the proportions of different HIV-1 variants circulating in each country, the genetic composition of HIV-1 recombinants, and the different genome segments (gag, pol, env) that may be incorporated into vaccines. We modeled different scenarios according to whether countries would employ subtype-specific HIV-1 vaccines against (1) the most common subtype; (2) subtypes contributing more than 5% of HIV infections; or (3) all circulating subtypes. For therapeutic vaccines targeting the most common HIV-1 subtype in each country, 16.5 million doses of subtype C vaccine were estimated globally, followed by subtypes A (14.3 million) and B (4.2 million). A vaccine based on env required 2.6 million subtype E doses, and a vaccine based on pol required 4.8 million subtype G doses. For prophylactic vaccines targeting the most common HIV-1 subtype in each country, 1.9 billion doses of subtype A vaccine were estimated globally, followed by subtype C (1.1 billion) and subtype B (1.0 billion). A vaccine based on env required 1.2 billion subtype E doses, and a vaccine based on pol required 0.3 billion subtype G doses. If subtype-specific HIV-1 vaccines are also directed against less common subtypes in each country, vaccines targeting subtypes D, F, H, and K are also needed and would require up to five times more vaccine doses in total. We conclude that to provide global coverage, subtype-specific HIV-1 vaccines need to be directed against subtypes A, B, and C. Vaccines targeting env also need to include subtype E and those targeting pol need to include subtype G.
Published: 2021
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3. Global and regional epidemiology of HIV-1 recombinants in 1990–2015: a systematic review and global survey

Author: Dawit Wolday, Neil Parkin, Bryan Schroeder, Mary S. Campbell, Barbara Ensoli, Jean-Claude Karasi, Connie Celum, Ard van Sighem, Marcia L. Kalish, Gillian Hunt, Jurgen Vercauteren, Dimitrios Chatzidimitriou, Beth Chaplin, Alex Carrera, Ruth L. Goodall, Guido van der Groen, Martine Peeters, Leondios G. Kostrikis, Edward Karamov, Francine E. McCutchan, Cecilia Rademeyer, Mina C. Hosseinipour, Michael M. Thomson, Fred Mhalu, Christopher M. Parry, Florian Neuhann, Jean-Marc Reynes, James I. Mullins, Vivek R. Nerurkar, Pontiano Kaleebu, Phyllis J. Kanki, Christine Rousseau, Deepak A Gadkari, Luzia Mayr, Kristel Van Laethem, Vincent Foulongne, Guy Michel Gershy-Damet, Lesley Wallace, Mika Salminen, Carolyn Williamson, John L. Mokili, África Holguín, Horacio Salomon, James Brandful, Alexandra Pelletier, Philippe Van de Perre, Xiang He, Tyna Tran, Marie Bruckova, Jianqing Xu, Monick Lindenmeyer-Guimarães, Stefano Buttò, Anoumou Y. Dagnra, Deenan Pillay, Doreen Mloka, Aleksei F Bobkov, Mejda Nasr, Ivette Lorenzana de Rivera, Kenneth E. Robbins, Elisabeth Menu, Ruengpung Sutthent, María Gabriela Barbás, Hervé Fleury, Joep J. van Oosterhout, Rong Zhang, Luigi Buonaguro, Linqi Zhang, David D. Ho, Kayitesi Kayitenkore, Chris P. Archibald, Mario L. Santiago, Dennis Ellenberger, Boaz Avidor, Peter N. Fonjungo, Claudine Nolte, Nicole Vidal, Silvia Bertagnolio, Mohamed Ali Bel Hadj Kacem, Philippe Nyambi, Marianna Ofner, Abdoulaye Dieng Sarr, Rafael Nájera, Chun Kang, Claudia Kücherer, Manuel Gómez Carrillo, El Hadj Belabbes, Simon Agwale, Zhiwei Chen, Zehava Grossman, Dominic M. Dwyer, Eric Van Wijngaerden, Jean W. Pape, Beatrice H. Hahn, Angie N Pinto, Tobias F. Rinke de Wit, Lucía Pérez-Álvarez, Peter D. Ghys, Franco M. Buonaguro, Sylvester Sempala, Vlad Novitsky, Banson Barugahare, Judith R. Glynn, Jason Yun, Macarthur Charles, Katsumi Chijiwa, Kok Keng Tee, Julia del Amo, Adeeba Kamarulzaman, Federico García, Awatef Moussi, Elena Delgado, Hiroshi Ushijima, Shambavi Subbarao, Ray Handema, Catherine A. Brennan, Paul Sandstrom, David A. Cooper, Joel R. Neilson, Ramyiadarsini Elangovan, Dwip Kitayaporn, Claudia Lara, Max Essex, Osamah Hamouda, Anna Papa, Hanan Salem, Elijah M. Songok, Fausta Mosha, Helba Bredell, Shlomo Maayan, Joshua T. Herbeck, Yiming Shao, Ansari Shaik, Kiran Thapa, Jean K. Carr, Raph L. Hamers, Chunfu Yang, Feng Gao, Orna Mor, Filimone Raikanikoda, Jesus Salazar-Gonzales, Nicolas Meda, Erin M. Kahle, Amilcar Tanuri, Tony Kelleher, Masahiko Ito, Fem J Paladin, J.R. Lingappa, Julie Stokes, Shona Kirtley, Vladimir Lukashov, Anne-Mieke Vandamme, Deborah L. Birx, Philip Cunningham, Amine Slim, Nicaise Ndembi, James Brooks, Alash'le Abimiku, Françoise Barré-Sinoussi, Trinh Duy Quang, Eleanor Gouws-Williams, Mariza G. Morgado, Jun Takehisa, Michel Segondy, Joris Hemelaar, Debbie Stewart, Cillian De Gascun, Marcelo A. Soares, Anne Buvé, Mark A. Rayfield, Marek Linka, Ursula Dietrich, Roger Garsia, Thomas Leitner, Philippe Selhorst, Jean Servais, Morgane Rolland, Kirsi Liitsola, Leslie Dickson-Tetteh, Brigitte Montes, Willy Urassa, Global Health, AII - Infectious diseases, Graduate School, Experimental Immunology, APH - Personalized Medicine, APH - Quality of Care, Nuffield Department of Population Health [Oxford], University of Oxford [Oxford], John Radcliffe Hospital [Oxford University Hospital], UNAIDS [Genève, Suisse] (ONUSIDA), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Pathogénèse et contrôle des infections chroniques (PCCI), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre Hospitalier Universitaire de Montpellier (CHU Montpellier )
Subjects: 0301 basic medicine, medicine.medical_specialty, Genotype, Epidemiology, Immunology, HIV Infections, MESH: Global Health, Global Health, MESH: Genotype, MESH: HIV-1, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Virology, Global health, medicine, Humans, MESH: Molecular Epidemiology, 030212 general & internal medicine, MESH: Genetic Variation, HIV vaccine, CRFS, Molecular Epidemiology, MESH: Humans, Molecular epidemiology, business.industry, Genetic Variation, virus diseases, MESH: HIV Infections, 030112 virology, Subtyping, 3. Good health, Infectious Diseases, Systematic review, MESH: Reassortant Viruses, HIV-1, [SDV.IMM]Life Sciences [q-bio]/Immunology, business, Viral load, Reassortant Viruses, Demography
Abstract: International audience; Background: Global HIV-1 genetic diversity and evolution form a major challenge to treatment and prevention efforts. An increasing number of distinct HIV-1 recombinants have been identified worldwide, but their contribution to the global epidemic is unknown. We aimed to estimate the global and regional distribution of HIV-1 recombinant forms during 1990-2015.Methods: We assembled a global HIV-1 molecular epidemiology database through a systematic literature review and a global survey. We searched the PubMed, Embase (Ovid), CINAHL (Ebscohost), and Global Health (Ovid) databases for HIV-1 subtyping studies published from Jan 1, 1990, to Dec 31, 2015. Unpublished original HIV-1 subtyping data were collected through a survey among experts in the field who were members of the WHO-UNAIDS Network for HIV Isolation and Characterisation. We included prevalence studies with HIV-1 subtyping data collected during 1990-2015. Countries were grouped into 14 regions and analyses were done for four time periods (1990-99, 2000-04, 2005-09, and 2010-15). The distribution of circulating recombinant forms (CRFs) and unique recombinant forms (URFs) in individual countries was weighted according to the UNAIDS estimates of the number of people living with HIV in each country to generate regional and global estimates of numbers and proportions of HIV-1 recombinants in each time period. The systematic review is registered with PROSPERO, CRD42017067164.Findings: Our global data collection yielded an HIV-1 molecular epidemiology database of 383 519 samples from 116 countries in 1990-2015. We found that the proportion of recombinants increased over time, both globally and in most regions, reaching 22·8% (7 978 517 of 34 921 639) of global HIV-1 infections in 2010-15. Both the proportion and the number of distinct CRFs detected increased over time to 16·7% and 57 CRFs in 2010-15. The global and regional distribution of HIV-1 recombinants was diverse and evolved over time, and we found large regional variation in the numbers (0-44 CRFs), types (58 distinct CRFs), and proportions (0-80·5%) of HIV-1 recombinants. Globally, CRF02_AG was the most prevalent recombinant, accounting for 33·9% (2 701 364 of 7 978 517) of all recombinant infections in 2010-15. URFs accounted for 26·7% (2 131 450 of 7 978 517), CRF01_AE for 23·0% (1 838 433), and other CRFs for 16·4% (1 307 270) of all recombinant infections in 2010-15. Although other CRFs accounted for small proportions of infections globally (
Published: 2020
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4. Dolutegravir-based dual maintenance regimens combined with lamivudine/emtricitabine or rilpivirine: risk of virological failure in a real-life setting

Author: Caroline Lions, N Biezunski, Sophie Matheron, Romain Guery, Pierre-Marie Roger, Caroline Charlier, Mathieu Dupont, Line Meddeb, Philippe Van de Perre, V Joly, R Lecomte, Matthieu Revest, Claudine Duvivier, B Lefèvre, M Delestan, H Laurichesse, H Marty, F Lemaitre, Martine Valette, Marc-Antoine Valantin, A S Ritleng, A Ménard, Eric Cua, M. Alvarez, A Raoux, M P Bouillon, A Sève, A Brebion, Claire Triffault-Fillit, Sylvie Bregigeon, M Carles, O. Aubry, S Hénard, P. Dellamonica, A Charmillon, E Alidjinou, V Brodard, M Tetart, F Raffi, Paul-Henri Consigny, O Lesens, C Brunet-Cartier, I Lamaury, S Giaché, Amandine Gagneux-Brunon, Jacques Reynes, Karine Sauné, Clotilde Allavena, Q Lepiller, Véronique Reliquet, C Louisin, I Perbost, Jean-Luc Berger, B Prouvost-Keller, Eric Delaporte, Isabelle Lamaury, C Gubavu, L Fagour, Laurent Cotte, G Gaube, Elina Teicher, Faouzi Souala, C Blanc, Dominique Merrien, Isabelle Poizot-Martin, C Drobacheff-Thiébaut, T May, P Richard, M A Trabaud, M Bistoquet, C Klotz, Samira Fafi-Kremer, M Marcel, Charlotte Charpentier, L Lelièvre, K Risso, Sandrine Pierre-François, S Ferrando, S Breaud, S Bevilacqua, A Montoya Ferrer, T Rojas-Rojas, D Boucher, Yazdan Yazdanpanah, Olivier Lortholary, Philippe Colson, Anne-Sophie Brunel, F-Xavier Lescure, Christelle Tomei, M Martin-Degioanni, Eric Rosenthal, Philippe Bossi, Patrick Miailhes, Kevin Bouiller, Lise Cuzin, A Foltzer, F Boulard, Michel Vidal, V Mondain, H Colson, J Pasquier, I Kmiec, F Alby-Laurent, R Agher, A Cabié, Guillaume Martin-Blondel, L Hocqueloux, M Colin, A Madrid, Faiza Ajana, J M Livrozet, V Rio, Karima Amazzough, C Merle de Boever, M Digumber, Thomas Perpoint, A Cheret, Laurence Bocket, Z Julia, Virginie Ferré, M Pradier, M Poisson-Vannier, A Legoff, M J Soavi, Y Quertainmont, Marine Morrier, Christian Chidiac, F Touam, O Zaegel-Faucher, A Marquise, G Benabdelmoumen, Florence Ader, T Guimard, M C Receveur, J C Tardy, P Morineau, K Guitteaud, D. Rey, S Leautez, Catherine Chirouze, Benoit Tressières, A. Ivanova, C Charre, J Reynes, Christian Pradier, Catherine Dhiver, Laurent Boyer, E Frentiu, David Rey, C Allavena, Anne Motte, Tristan Ferry, C Pronier, M. Hentzien, C Rouzaud, O Cabras, K Jidar, F Najioullah, C Clavel, M Orticoni, S Patrat-Delon, M Cavellec, Cécile Herrmann-Storck, V Baclet, Jade Ghosn, M Perry, S Wehrlen-Pugliese, J. M. Chapplain, R Palich, Laurent Hocqueloux, A Maillard, C Deschanvres, O Deradji, F. Lucht, A Grégoire, Veronique Joly, R Ouissa, C Daniel, N Mrozek, D Chirio, O Bollangier, J Bavay, P. Le Turnier, A Maka, C Rioux, Colin Deschanvres, C Brochier, Elisabeth Botelho-Nevers, A Meybeck, C Ceppi, J Lourenco, François Bénézit, Thomas Jovelin, G Zouzou, N Tissot, N. Viget, F Brunel-Dalmas, Brigitte Montes, N Chellum Rungen, K Rome, David Boutoille, B Bigeard, I Fabre, N Oran, M Lefebvre, P Point, C Etienne, Diane Descamps, G Thomas, S Le Gac, Cyrille Delpierre, Pierre Tattevin, M Godinot, P Fischer, C Aumeran, C Boulard, Elisabeth André-Garnier, J Sinteff, V Ronat, F Goehringer, Romain Palich, Luminita Schneider, I Touitou, Eric Billaud, P Thill, Catherine Varache, Olivier Robineau, I Jaquet, Roland Landman, Cédric Arvieux, B. Bonnet, V Rzepecki, Olivier Grossi, Christian Rabaud, L Laine, F Louni, C Cheneau, S Markowicz, Hélène Laroche, A Gervais, C Bernard-Henry, E Goncalvez, N Lerolle, M André, D Lambert, André Boibieux, L. Porte, S Bouchez, E Paredes, E Aïssi, V. Le Moing, S Degroodt, Sylvie Abel, André Cabié, B Lafon-Desmurs, O Babre, M Baldeyrou, C Debreux, A Rodallec, Pierre Delobel, V Icard, Agathe Becker, Edouard Tuaillon, Hervé Tissot-Dupont, M Mokhtari, C Morlat, I Alcaraz, Anne Frésard, O Cannesson, Elodie Curlier, P Chiarello, S. Roux, F Bani-Sadr, François Raffi, Florent Valour, M Piffaut, M Priester, A. Belkhir, J Romaru, Cécile Goujard, A Castro, G Cessot, A Mirand, C Pouderoux, A Brunet, C Michelangeli, Y N’guyen, Patrice Muret, Elisa Demonchy, Christine Jacomet, D Makhloufi, E Jeanmaire, Marialuisa Partisani, Véronique Obry-Roguet, J Turmel, C Mélounou, J. Durant, Christine Katlama, P Parize, O Robineau, S Seang, F. Bozon, S Galie, Alexa Debard, E de Mautort, C Duvivier, Fanny Lanternier, Alain Makinson, A Barrail-Tran, C Aguilar, A Naqvi, Rodolphe Garraffo, N Meftah, C Biron, A de Monte, Pascal Pugliese, V Corbin, S Jaureguiberry, E Lafont, L Hustache Mathieu, R Colarino, Isabelle Ravaux, C Henquell, Benoit Pilmis, M Grégoire, P Lansalot, E Ressiot, T. Huleux, Olivier Baud, S Sécher, R Dupin de Majoubert, J Leporrier, L Cuzin, E Chevalier, M Poinot, R Tubiana, S Lariven, A Boucher, N Atoui, Firouzé Bani-Sadr, T Prazuck, M Ducassou, Gilles Peytavin, A Soria, B J Gaborit, Service des maladies infectieuses et tropicales [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Dat’AIDS Study Group, Département Maladies Infectieuses et Tropicales, Hôpital Universitaire, Montpellier, France, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques et émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), CHU Pointe-à-Pitre/Abymes [Guadeloupe], Les Hôptaux universitaires de Strasbourg (HUS), CHU Strasbourg, CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Universitaire de Reims (CHU Reims), Centre Hospitalier Gustave Dron [Tourcoing], Institut Pasteur [Paris] (IP), Centre Hospitalier Régional d'Orléans (CHRO), Centre d'Epidémiologie et de Recherche en santé des POPulations (CERPOP), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU de la Martinique [Fort de France], AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], CHU Clermont-Ferrand, and Université Clermont Auvergne (UCA)
Subjects: Microbiology (medical), medicine.medical_specialty, Anti-HIV Agents, Pyridones, MESH: Piperazines, HIV Infections, Emtricitabine, Piperazines, law.invention, chemistry.chemical_compound, Randomized controlled trial, law, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Internal medicine, MESH: Pyridones, Oxazines, MESH: Emtricitabine, Humans, Medicine, Pharmacology (medical), MESH: Anti-HIV Agents, Pharmacology, MESH: Heterocyclic Compounds, 3-Ring, MESH: Humans, business.industry, Rilpivirine, Lamivudine, MESH: HIV Infections, Viral Load, [SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences, Virological failure, Regimen, Infectious Diseases, chemistry, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Dolutegravir, Cohort, MESH: Rilpivirine, business, MESH: Viral Load, Heterocyclic Compounds, 3-Ring, MESH: Oxazines, medicine.drug, MESH: Lamivudine
Abstract: Background Maintenance ART with dolutegravir-based dual regimens have proved their efficacy among HIV-1-infected subjects in randomized trials. However, real-life data are scarce, with limited populations and follow-up. Objectives We assessed virological failure (VF) and resistance-associated mutations (RAMs) on dolutegravir maintenance regimens in combination with rilpivirine or with lamivudine or emtricitabine (xTC) and analysed the factors associated with VF. Methods Between 2014 and 2018, all HIV-1-infected adults included in the Dat’AIDS cohort and starting dolutegravir/rilpivirine or dolutegravir/xTC as a maintenance dolutegravir-based dual regimen were selected. VF was defined as two consecutive HIV RNA values >50 copies/mL or a single value >400 copies/mL. We compared cumulative genotypes before initiation of a maintenance dolutegravir-based dual regimen with genotype at VF. Results We analysed 1374 subjects (799 on dolutegravir/rilpivirine and 575 on dolutegravir/xTC) with a median follow-up of 20 months (IQR = 11–31) and 19 months (IQR = 11–31), respectively. VF occurred in 3.8% (n = 30) of dolutegravir/rilpivirine subjects and 2.6% (n = 15) of dolutegravir/xTC subjects. Among subjects receiving dolutegravir/rilpivirine, two genotypes harboured emerging RAMs at VF: E138K on NNRTI (n = 1); and E138K+K101E on NNRTI and N155H on INSTI (n = 1). Among subjects receiving dolutegravir/xTC, no new RAM was detected. The only predictive factor of VF on dolutegravir/rilpivirine was the history of failure on an NNRTI-based regimen (adjusted HR = 2.97, 95% CI = 1.28–6.93). No factor was associated with VF on dolutegravir/xTC. Conclusions In this large real-life cohort, dolutegravir/rilpivirine and dolutegravir/xTC sustained virological suppression and were associated with a low rate of VF and RAM emergence. Careful virological screening is essential before switching to dolutegravir/rilpivirine in virologically suppressed patients with a history of NNRTI therapy.
Published: 2022
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5. Receptor binding domain‐IgG levels correlate with protection in residents facing SARS‐CoV‐2 B.1.1.7 outbreaks

Author: Delphine Muriaux, Amandine Pisoni, Edouard Tuaillon, Brigitte Montes, Sophia Rafasse, Stéphanie Miot, Nejm Si-Mohamed, Clémence Niel, Lucie Gamon, Soraya Groc, Jean Bousquet, Hubert Blain, Anne-Marie Dupuy, Nathalie Gros, Yves Rolland, Valentin Delpui, Marie-Christine Picot, Centre Hospitalier Universitaire de Montpellier (CHU Montpellier ), Institut de Recherche en Infectiologie de Montpellier (IRIM), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)
Subjects: medicine.medical_specialty, COVID-19 Vaccines, Coronavirus disease 2019 (COVID-19), viruses, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), [SDV]Life Sciences [q-bio], efficacy, Immunology, Death risk, nucleocapsid antigenemia, nursing homes, Antibodies, Viral, SARS‐CoV‐2, Disease Outbreaks, 03 medical and health sciences, 0302 clinical medicine, COVID‐19, Internal medicine, Humans, Immunology and Allergy, Medicine, neutralizing antibodies, 030212 general & internal medicine, BNT162 Vaccine, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Vaccines, 0303 health sciences, BNT162b2 vaccine, biology, SARS-CoV-2, business.industry, Incidence (epidemiology), COVID-19, Outbreak, antibody response, Vaccine efficacy, 3. Good health, Immunoglobulin G, residents, biology.protein, symptoms, Original Article, Basic and Translational Allergy Immunology, ORIGINAL ARTICLES, Antibody, business, Nursing homes
Abstract: Background Limited information exists on nursing home (NH) residents regarding BNT162b2 vaccine efficacy in preventing SARS‐CoV‐2 and severe COVID‐19, and its association with post‐vaccine humoral response. Methods 396 residents from seven NHs suffering a SARS‐CoV‐2 B.1.1.7 (VOC‐α) outbreak at least 14 days after a vaccine campaign were repeatedly tested using SARS‐CoV‐2 real‐time reverse‐transcriptase polymerase chain reaction on nasopharyngeal swab test (RT‐qPCR). SARS‐CoV‐2 receptor‐binding domain (RBD) of the S1 subunit (RBD‐IgG) was measured in all residents. Nucleocapsid antigenemia (N‐Ag) was measured in RT‐qPCR‐positive residents and serum neutralizing antibodies in vaccinated residents from one NH. Results The incidence of positive RT‐qPCR was lower in residents vaccinated by two doses (72/317; 22.7%) vs one dose (10/31; 32.3%) or non‐vaccinated residents (21/48; 43.7%; p < .01). COVID‐19–induced deaths were observed in 5 of the 48 non‐vaccinated residents (10.4%), in 2 of the 31 who had received one dose (6.4%), and in 3 of the 317 (0.9%) who had received two doses (p = .0007). Severe symptoms were more common in infected non‐vaccinated residents (10/21; 47.6%) than in infected vaccinated residents (15/72; 21.0%; p = .002). Higher levels of RBD‐IgG (n = 325) were associated with a lower SARS‐CoV‐2 incidence. No in vitro serum neutralization activity was found for RBD‐IgG levels below 1050 AU/ml. RBD‐IgG levels were inversely associated with N‐Ag levels, found as a risk factor of severe COVID‐19. Conclusions Two BNT162b2 doses are associated with a 48% reduction of SARS‐CoV‐2 incidence and a 91.3% reduction of death risk in residents from NHs facing a VOC‐α outbreak. Post‐vaccine RBD‐IgG levels correlate with BNT162b2 protection against SARS‐CoV‐2 B.1.1.7., This study assesses the incidence of positive SARS‐CoV‐2 B.1.1.7 by RT‐qPCR results according to the vaccination status in nursing home residents facing a VOC‐α outbreak. Two BNT162b2 doses are associated with a major reduction of SARS‐CoV‐2 B.1.1.7 incidence and COVID‐19. Post‐vaccine RBD‐IgG levels correlate with protection in this population.
Published: 2021
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6. RBD-IgG levels correlate with protection in Residents Facing SARS-CoV-2 B.1.1.7 Outbreaks

Author: Anne-Marie Dupuy, Amandine Pisoni, Jean Bousquet, Hubert Blain, Edouard Tuaillon, Nejm Si-Mohamed, Sophia Rafasse, Valentin Delpui, Marie-Christine Picot, Stéphanie Miot, Lucie Gamon, Clémence Niel, Yves Rolland, Soraya Groc, Brigitte Montes, Nathalie Gros, and Delphine Muriaux
Subjects: medicine.medical_specialty, biology, Coronavirus disease 2019 (COVID-19), business.industry, Incidence (epidemiology), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Outbreak, Vaccine efficacy, Internal medicine, Neutralization test, medicine, biology.protein, Antibody, Risk factor, business
Abstract: Background Limited information exists on nursing home (NH) residents regarding BNT162b2/Pfizer vaccine efficacy in preventing SARS-CoV-2 and severe Covid-19, and its association with post-vaccine humoral response. Methods 396 residents from seven NHs suffering a SARS-CoV-2 B.1.1.7 (VOC-α) outbreak at least 14 days after a vaccine campaign were repeatedly tested using SARS-CoV-2 real-time reverse-transcriptase polymerase chain reaction on nasopharyngeal swab test (RT-PCR). SARS-CoV-2 Receptor-Binding Domain (RBD) of the S1 subunit (RBD-IgG) was measured in all residents. Nucleocapsid antigenemia (N-Ag) was measured in RT-PCR-positive residents, and serum neutralizing antibodies in vaccinated residents from one NH. Results The incidence of positive RT-PCR was lower in residents vaccinated by two doses (22.7%) vs one dose (32.3%) or non-vaccinated residents (43.7%)(pConclusions Two BNT162b2/Pfizer doses are associated with a 48% reduction of SARS-CoV-2 incidence and a 91.3% reduction of death risk in residents from NHs facing a VOC-α outbreak. BNT162b2/Pfizer efficacy was partly predicted by post-vaccine RBD-IgG levels.
Published: 2021
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7. Spread of SARS-CoV-2 Delta variant infections bearing the S:E484Q and S:T95I mutations in July and August 2021 in France

Author: Brigitte Montes, Mircea T. Sofonea, Gonché Danesh, Laura Verdume, Bénédicte Roquebert, Stéphanie Haim-Boukobza, Edouard Tuaillon, Vincent Foulongne, Samuel Alizon, Sabine Trombert, and Valérie Noël
Subjects: Delta, Whole genome sequencing, Genetics, 2019-20 coronavirus outbreak, Phylogenetic tree, Screening test, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Mutation (genetic algorithm), Biology, Disease cluster
Abstract: Analysing 92,598 variant screening tests performed on SARS-CoV-2 positive samples collected in France between 1 July and 31 August 2021 shows an increase of Kappa-like infections. Full genome sequencing reveals that these correspond to Delta variants bearing the S:E484Q mutation. Most of these sequences belong to a phylogenetic cluster and also bear the S:T95I mutation. Further monitoring is needed to determine if this trend is driven by undocumented superspreading events or an early signal of future viral evolutionary dynamics.
Published: 2021
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8. Diagnosis value of SARS‐CoV‐2 antigen/antibody combined testing using rapid diagnostic tests at hospital admission

Author: Amandine Pisoni, Anne Sophie Bedin, Brigitte Montes, Vincent Le Moing, Michel Segondy, Anne Marie Mondain, Edouard Tuaillon, David Morquin, Nicolas Veyrenche, Karine Bollore, Jacques Ducos, Alain Makinson, Patrick Pastor, Philippe Van de Perre, Vincent Foulongne, Pathogenesis and Control of Chronic and Emerging Infections (PCCEI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Université des Antilles (UA)-Etablissement français du don du sang [Montpellier], CHU de Montpellier, Montpellier, France., CHU de Montpellier, Montpellier, France, Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Département de Maladies Infectieuses et Tropicales, Centre Hospitalier Universitaire de Montpellier, Montpellier, France, and BONIZEC, Sandrine
Subjects: Male, diagnosis, [SDV]Life Sciences [q-bio], Antibodies, Viral, Gastroenterology, Immunoglobulin G, Serology, 0302 clinical medicine, coronavirus disease‐19 (COVID‐19), Nasopharynx, 030212 general & internal medicine, Antigens, Viral, Research Articles, ComputingMilieux_MISCELLANEOUS, Aged, 80 and over, biology, Reverse Transcriptase Polymerase Chain Reaction, Diagnostic test, Middle Aged, Reverse transcription polymerase chain reaction, Hospitalization, [SDV] Life Sciences [q-bio], Infectious Diseases, Hospital admission, 030211 gastroenterology & hepatology, Female, Antibody, Research Article, Adult, medicine.medical_specialty, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Enzyme-Linked Immunosorbent Assay, COVID-19 Serological Testing, 03 medical and health sciences, Antigen, Virology, Internal medicine, parasitic diseases, medicine, Humans, Serologic Tests, rapid diagnostic tests, Aged, Cycle threshold, SARS‐CoV‐2 antibody, SARS-CoV-2, business.industry, COVID-19, Emergency department, Immunoglobulin M, biology.protein, SARS‐CoV‐2 antigen, business
Abstract: The implementation of rapid diagnostic tests (RDTs) may enhance the efficiency of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) testing, as RDTs are widely accessible and easy to use. The aim of this study was to evaluate the performance of a diagnosis strategy based on a combination of antigen and immunoglobulin M (IgM) or immunoglobulin G (IgG) serological RDTs. Plasma and nasopharyngeal samples were collected between 14 March and 11 April 2020 at hospital admission from 45 patients with reverse transcription polymerase chain reaction (RT‐PCR) confirmed COVID‐19 and 20 negative controls. SARS‐CoV‐2 antigen (Ag) was assessed in nasopharyngeal swabs using the Coris Respi‐Strip. For IgM/IgG detection, SureScreen Diagnostics and Szybio Biotech RDTs were used in addition to laboratory assays (Abbott Alinity i SARS‐CoV‐2 IgG and Theradiag COVID‐19 IgM enzyme‐linked immunosorbent assay). Using the Ag RDT, 13 out of 45 (29.0%) specimens tested positive, the sensitivity was 87.0% for cycle threshold (C t) values ≤25% and 0% for C t values greater than 25. IgG detection was associated with high C t values and the amount of time after the onset of symptoms. The profile of isolated IgM on RDTs was more frequently observed during the first and second week after the onset of symptoms. The combination of Ag and IgM/IgG RDTs enabled the detection of up to 84.0% of COVID‐19 confirmed cases at hospital admission. Antigen and antibody‐based RDTs showed suboptimal performances when used alone. However when used in combination, they are able to identify most COVID‐19 patients admitted in an emergency department., Highlights ‐Antigen and antibody‐based RDTs showed suboptimal performances when used alone.‐The Ag RDT showed good sensitivity on samples with CT values below 25.‐IgM/IgG RDTs showed good sensitivity as of the second week after onset of symptoms.‐The combination of Ag and IgM/IgG RDTs identified most patients with COVID‐19.‐RDTs may have a significant place in the global response to the COVID‐19 pandemic.
Published: 2021
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9. Détection de mutations de résistance du VIH aux antirétroviraux : vers un dépistage rapide pré-thérapeutique ?

Author: Jean-Charles Brès, Julien Gomez-Martinez, Nicolas Nagot, Philippe Van de Perre, Chantal Fournier-Wirth, Brigitte Montes, Jean-Pierre Molès, Didier Laureillard, Jean-François Cantaloube, and Vincent Foulongne
Subjects: Biochemistry (medical), Clinical Biochemistry, Hematology
Published: 2021
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10. Factors associated with the emergence of integrase resistance mutations in patients failing dual or triple integrase inhibitor-based regimens in a French national survey

Author: Anne-Genevieve, Marcelin, Charlotte, Charpentier, Pantxika, Bellecave, Basma, Abdi, Marie-Laure, Chaix, Virginie, Ferre, Stephanie, Raymond, Djeneba, Fofana, Laurence, Bocket, Audrey, Mirand, Helene, Le Guillou-Guillemette, Brigitte, Montes, Corinne, Amiel, Coralie, Pallier, Samira, Fafi-Kremer, Anne, De Monte, Elodie, Alessandri-Gradt, Caroline, Scholtes, Anne, Maillard, Helene, Jeulin, Magali, Bouvier-Alias, Catherine, Roussel, Georges, Dos Santos, Anne, Signori-Schmuck, Julia, Dina, Sophie, Vallet, Karl, Stefic, Cathia, Soulié, Vincent, Calvez, Diane, Descamps, Philippe, Flandre, S, Marque Juillet, Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Bordeaux [Bordeaux], Génomes, biologie cellulaire et thérapeutiques (GenCellDi (U944 / UMR7212)), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre hospitalier universitaire de Nantes (CHU Nantes), Pathogenèse virale du diabète de type 1 - ULR 3610 (Laboratoire de Virologie), Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), CHU Clermont-Ferrand, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), CHU Montpellier, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Hôpital Paul Brousse, CHU Strasbourg, Centre Hospitalier Universitaire de Nice (CHU Nice), CHU Rouen, Normandie Université (NU), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Rennes] = Virology [Rennes], CHU Pontchaillou [Rennes], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Service de bactériologie, virologie, hygiène [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CHU Amiens-Picardie, CHU de la Martinique [Fort de France], Centre Hospitalier Universitaire [Grenoble] (CHU), Université de Caen Normandie (UNICAEN), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Service de virologie et unité de surveillance biologique [Bordeaux], Gestionnaire, HAL Sorbonne Université 5, Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génomes, biologie cellulaire et thérapeutiques (GenCellDi (UMR_S_944)), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier Régional Universitaire de Tours (CHRU TOURS), and Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Subjects: 0301 basic medicine, Oncology, genotype, Integrase inhibitor, hiv, HIV Infections, gerstmann-straussler-scheinker, HIV Integrase, viral load result, chemistry.chemical_compound, 0302 clinical medicine, Genotype, Pharmacology (medical), 030212 general & internal medicine, Univariate analysis, biology, 3. Good health, Integrase, univariate analysis, integrase inhibitors, Infectious Diseases, Tolerability, Dolutegravir, Heterocyclic Compounds, 3-Ring, medicine.drug, Microbiology (medical), medicine.medical_specialty, Pyridones, 030106 microbiology, 03 medical and health sciences, Internal medicine, Raltegravir Potassium, Drug Resistance, Viral, medicine, Humans, HIV Integrase Inhibitors, plasma, Pharmacology, disease, business.industry, genetics raltegravir dolutegravir, Raltegravir, Regimen, chemistry, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Mutation, biology.protein, HIV-1, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, hiv-1 integrase, business
Abstract: Background Successful 2-drug regimens (2DRs) for HIV were made possible by the availability of drugs combining potency and tolerability with a high genetic barrier to resistance. How these deal with resistance development/re-emergence, compared with 3DRs, is thus of paramount importance. Materials and methods A national survey including patients who were either naive or experienced with any 2DR or 3DR but failing integrase strand transfer inhibitor (INSTI)-containing regimens [two consecutive plasma viral load (VL) values >50 copies/mL] was conducted between 2014 and 2019. Genotypic resistance tests were interpreted with the v28 ANRS algorithm. Results Overall, 1104 patients failing any INSTI-containing regimen (2DRs, n = 207; 3DRs, n = 897) were analysed. Five hundred and seventy-seven (52.3%) patients were infected with a B subtype and 527 (47.3%) with non-B subtypes. Overall, 644 (58%) patients showed no known integrase resistance mutations at failure. In multivariate analysis, factors associated with the emergence of at least one integrase mutation were: high VL at failure (OR = 1.24 per 1 log10 copies/mL increase); non-B versus B subtype (OR = 1.75); low genotypic sensitivity score (GSS) (OR = 0.10 for GSS = 2 versus GSS = 0–0.5); and dolutegravir versus raltegravir (OR = 0.46). Although 3DRs versus 2DRs reached statistical significance in univariate analysis (OR = 0.59, P = 0.007), the variable is not retained in the final model. Conclusions This study is one of the largest studies characterizing integrase resistance in patients failing any INSTI-containing 2DR or 3DR in routine clinical care and reveals factors associated with emergence of integrase resistance that should be taken into consideration in clinical management. No difference was evidenced between patients receiving a 2DR or a 3DR.
Published: 2021
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11. Near-point-of-care assay with a visual readout for detection of HIV-1 drug resistance mutations: A proof-of-concept study

Author: Brigitte Montes, Didier Laureillard, Jean-Charles Brès, Chantal Fournier-Wirth, Nicolas Nagot, Vincent Foulongne, Jean-Pierre Molès, Philippe Van de Perre, Julien Gomez-Martinez, Jean-François Cantaloube, Pathogenesis and Control of Chronic and Emerging Infections (PCCEI), Université des Antilles (UA)-Etablissement français du don du sang [Montpellier]-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Laboratoire de Virologie, Centre Hospitalier Universitaire de Montpellier, Montpellier, France.
Subjects: Genotype, Anti-HIV Agents, [SDV]Life Sciences [q-bio], Point-of-Care Systems, HIV Infections, 02 engineering and technology, Drug resistance, 01 natural sciences, Analytical Chemistry, Lateral flow test, symbols.namesake, Drug Resistance, Viral, medicine, Humans, Multiplex, ComputingMilieux_MISCELLANEOUS, Sanger sequencing, Reverse-transcriptase inhibitor, Chemistry, Transmission (medicine), 010401 analytical chemistry, 021001 nanoscience & nanotechnology, Virology, 0104 chemical sciences, 3. Good health, Mutation, symbols, HIV-1, DNA microarray, 0210 nano-technology, HIV drug resistance, medicine.drug
Abstract: Human immunodeficiency virus (HIV) infection is a chronic disease that can be treated with antiretroviral (ARV) therapy. However, the success of this treatment has been jeopardized by the emergence of HIV infections resistant to ARV drugs. In low-to middle-income countries (LMICs), where transmission of resistant viruses has increased over the past decade, there is an urgent need to improve access to HIV drug resistance testing. Here, we present a proof-of-concept study of a rapid and simple molecular method to detect two major mutations (K103 N, Y181C) conferring resistance to first-line nonnucleoside reverse transcriptase inhibitor regimens. Our near-point-of-care (near-POC) diagnostic test, combining a sequence-specific primer extension and a lateral flow DNA microarray strip, allows visual detection of HIV drug resistance mutations (DRM) in a short turnaround time (4 h 30). The assay has a limit of detection of 100 copies of plasmid DNA and has a higher sensitivity than standard Sanger sequencing. The analytical performance was assessed by use of 16 plasma samples from individuals living with HIV-1 and results demonstrated the specificity and the sensitivity of this approach for multiplex detection of the two DRMs in a single test. Furthermore, this near-POC assay could be easily taylored to detect either new DRMs or DRM of from various HIV clades and might be useful for pre-therapy screening in LMICs with high levels of transmitted drug resistance.
Published: 2021
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12. Incidence of diabetes in HIV-infected patients treated with first-line integrase strand transfer inhibitors: a French multicentre retrospective study

Author: P Fischer, C Aumeran, V Ronat, L Laine, S Bouchez, André Cabié, D Lambert, Eric Cua, J Pasquier, F Touam, Laurent Hocqueloux, A Maillard, O Deradji, Charlotte Charpentier, Véronique Avettand-Fenoel, Catherine Tamalet, Anne Frésard, Elodie Curlier, M Batard, S Ferrando, S Breaud, Philippe Bossi, C Pronier, C Gubavu, M Martin-Degiovani, Samira Fafi-Kremer, A. Duréault, Christian Pradier, A Montoya Ferrer, M Piffaut, Faiza Ajana, V Rio, A Maka, C Biron, Pierre Delobel, A de Monte, P Choisy, L Lelièvre, K Risso, N. Viget, Q Lepiller, Véronique Reliquet, I Perbost, Laurence Bocket, C Rioux, G Thomas, O. Aubry, L. Porte, Cédric Arvieux, Thomas Jovelin, Elisabeth Botelho-Nevers, Pierre-Marie Roger, C Etienne, David Boutoille, S Le Gac, Caroline Charlier, Virginie Ferré, M Pradier, M C Receveur, Isabelle Ravaux, Philippe Colson, K Rome, O Lesens, C Brunet-Cartier, A Meybeck, Romain Palich, P Martinet, V. Le Moing, C Ceppi, Hélène Laroche, I Lamaury, V Brodard, N Oran, M Lefebvre, P Morineau, K Guitteaud, M Bistoquet, Diane Descamps, O Cabras, Amandine Gagneux-Brunon, Brigitte Montes, Olivier Robineau, I Jaquet, Roland Landman, C Cheneau, V Mondain, Caroline Lions, Olivier Grossi, Laurent Boyer, C Debreux, M André, A Rodallec, Philippe Van de Perre, Jade Ghosn, Clotilde Allavena, Sylvie Abel, Karine Sauné, F Louni, F Boulard, Luminita Schneider, Dominique Merrien, D Chirio, S Pillet, Mathieu Dupont, A Motte, F Lemaitre, C Guennoun, Benoît Henry, S Sausse, Michel Vidal, M Mokhtari, O Zaegel-Faucher, Eric Rosenthal, Isabelle Poizot-Martin, Faouzi Souala, Matthieu Revest, M Baldeyrou, S Patrat-Delon, Jacques Reynes, M Cavellec, Laurent Cotte, C Michelangeli, François Danion, M Priester, Axel Ursenbach, C Mackoumbou-Nkouka, Thomas Perpoint, A Cheret, P Geneau de Lamarlière, Christian Rabaud, Agathe Becker, Tristan Ferry, A. Ivanova, Elina Teicher, T Bonijoly, F-Xavier Lescure, O Bollangier, A S Ritleng, Patrick Miailhes, A Gervais, Y N’guyen, Patrice Muret, Elisa Demonchy, Vincent Max, I Alcaraz, N Meftah, M P Bouillon, S Degroodt, A Foltzer, Laurent Hustache-Mathieu, Jean-Luc Berger, A Ménard, J Prouteau, B. Bonnet, Kevin Bouiller, Lise Cuzin, Christian Chidiac, R Agher, S Leautez, Catherine Chirouze, M Poinot, R Tubiana, E Aïssi, O Babre, J Lourenco, Benoit Tressières, C Clavel, Cécile Goujard, A Brunet, Claire Triffault-Fillit, F Raffi, E Sidani, Anne-Sophie Brunel, A Madrid, B Prouvost-Keller, Eric Delaporte, M J Soavi, J. M. Chapplain, M Orticoni, Pascal Pugliese, V Corbin, Pierre Tattevin, C Boulard, Véronique Obry-Roguet, P. Loubet, Paul-Henri Consigny, Elisabeth André-Garnier, J Sinteff, S Lariven, A Boucher, N Lerolle, C Blanc, Y Quertainmont, Sylvie Bregigeon, Bruno Hoen, André Boibieux, S Casanova, N Atoui, C Dhiver, N Biezunski, R Ouissa, M. Hentzien, C Bernard-Henry, Sophie Matheron, Cécile Herrmann-Storck, Firouzé Bani-Sadr, I Touitou, Eric Billaud, I Kmiec, Benoit Pilmis, T Prazuck, Romain Guery, Karima Amazzough, C Merle de Boever, Marine Morrier, T Guimard, M Poisson-Vanier, H Laurichesse, Catherine Varache, J Goesch, Guillaume Martin-Blondel, Z Julia, M Ducassou, F. Lucht, B Lafon-Desmurs, Martine Valette, A Sève, Marc-Antoine Valantin, G Zouzou, A Barrail-Tran, M Delestan, M. Alvarez, A Naqvi, Colin Deschanvres, A Raoux, L Meddeb, Rodolphe Garraffo, C Daniel, T May, A. Galinier, François Bénézit, Yazdan Yazdanpanah, Veronique Joly, Olivier Lortholary, C Louisin, K Jidar, I Fabre, Cyrille Delpierre, Christine Katlama, P Parize, S Galie, Claudine Duvivier, P. Dellamonica, L Osei, C Drobacheff-Thiébaut, Sandrine Pierre-François, G Cessot, C. Tomei, F. Biron, Christine Jacomet, G Benabdelmoumen, Florence Ader, David Rey, Marialuisa Partisani, J Turmel, J. Durant, S Seang, F. Bozon, M Illiaquer, N Hall, Edouard Tuaillon, S. Roux, Florent Valour, A. Belkhir, Marine Maurel, V Baclet, N Mrozek, Olivier Baud, S Sécher, P Letertre-Gibert, Alexa Debard, E de Mautort, Fanny Lanternier, Alain Makinson, H. Tissot Dupont, P Lansalot, E Ressiot, T. Huleux, S Wehrlen-Pugliese, M Landon, C Brochier, C Bernaud, Gilles Peytavin, A Soria, Institut Hospitalier Universitaire Méditerranée Infection (IHU Marseille), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Université Montpellier 1 (UM1), Département Maladies Infectieuses et Tropicales, Hôpital Universitaire, Montpellier, France, Pathogénèse et contrôle des infections chroniques (PCCI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre Hospitalier Universitaire de Montpellier (CHU Montpellier ), Service de pharmacologie, Hôpital Pasteur [Nice] (CHU)-Centre Hospitalier Universitaire de Nice (CHU Nice), Centre Hospitalier Universitaire de Reims (CHU Reims), Laboratoire de Virologie Médicale et Moléculaire - EA 4684 (CardioVir), Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre Hospitalier Universitaire de Reims (CHU Reims), Groupe Immunité des Muqueuses et Agents Pathogènes (GIMAP), Université Jean Monnet [Saint-Étienne] (UJM), School of Civil and Environmental Engineering [Sydney], University of New South Wales [Sydney] (UNSW), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Laboratoire Chrono-environnement - CNRS - UFC (UMR 6249) (LCE), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon), Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 (P3CELL), and Université de Reims Champagne-Ardenne (URCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Subjects: 0301 basic medicine, Microbiology (medical), Adult, medicine.medical_specialty, [SDV]Life Sciences [q-bio], Integrase inhibitor, HIV Infections, HIV Integrase, Diabetes Therapy, Cohort Studies, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Internal medicine, Diabetes mellitus, medicine, Diabetes Mellitus, Humans, Pharmacology (medical), 030212 general & internal medicine, HIV Integrase Inhibitors, ComputingMilieux_MISCELLANEOUS, Retrospective Studies, Pharmacology, Integrases, business.industry, Incidence, Retrospective cohort study, Raltegravir, medicine.disease, Comorbidity, 3. Good health, 030104 developmental biology, Infectious Diseases, chemistry, Dolutegravir, business, medicine.drug, Cohort study
Abstract: BackgroundIntegrase strand transfer inhibitors (INSTIs) are increasingly used in patients living with HIV due to their safety, effectiveness and high genetic barrier. However, an association with weight gain has recently been suggested and several cases of diabetes mellitus have been reported with raltegravir and dolutegravir. The long-time metabolic impact of these recent molecules remains unclear.ObjectivesTo assess if an INSTI as a third agent is statistically associated with new-onset diabetes mellitus compared with an NNRTI or a PI.Patients and methodsPatients undergoing first-line combined ART (cART) without diabetes at baseline were retrospectively included from the Dat’AIDS French cohort study (ClinicalTrials.gov NCT02898987). Incident diabetes mellitus was defined as a notification of new diabetes in the medical history, a glycated haemoglobin (HbA1c) level superior to 7.5% or the start of a diabetes therapy following the initiation of ART.ResultsFrom 2009 to 2017, 19 462 patients were included, among which 265 cases of diabetes mellitus occurred. Multivariate and survival analyses did not highlight an increase in new-onset diabetes in patients undergoing cART with an INSTI as a third agent compared with an NNRTI or a PI. BMI >30 kg/m2, age >37 years old (in survival analysis), black race or Hispanic ethnicity, arterial hypertension and AIDS were associated with a higher proportion of incident diabetes.ConclusionsINSTIs were not statistically associated with new-onset diabetes. However, clinicians should remain aware of this possible metabolic comorbidity, particularly in patients with a high BMI and older patients.
Published: 2020
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13. Sexual transmission of an extensively drug-resistant HIV-1 strain

Author: Guillaume Martin-Blondel, Jonathan Bigot, Pierre Delobel, Jacques Izopet, Marie Piffaut, Brigitte Montes, Kevin Bertrand, Stéphanie Raymond, Michelle Cazabat, Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Toulouse], CHU Toulouse [Toulouse], Service des maladies infectieuses et tropicales [Toulouse], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Hôpital Purpan [Toulouse], Laboratoire de Virologie [CHRU Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Service des Maladies Infectieuses et Tropicales, Centre Hospitalier de Perpignan, PINIER, CHRISTINE, Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Service Maladies infectieuses et tropicales [CHU Toulouse], Pôle Inflammation, infection, immunologie et loco-moteur [CHU Toulouse] (Pôle I3LM Toulouse), and Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)
Subjects: Sexual transmission, Strain (chemistry), Epidemiology, business.industry, Immunology, MESH: Anti HIV Agents therapeutic use, Drug Resistance, Multiple, Viral, Founder Effect , HIV Infections transmission, HIV Infections virology, HIV-1 drug effects, Humans, Male, Middle Aged, Young Adult, Human immunodeficiency virus (HIV), Drug resistance, 030204 cardiovascular system & hematology, medicine.disease_cause, Virology, 03 medical and health sciences, 0302 clinical medicine, Infectious Diseases, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, medicine, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, 030212 general & internal medicine, business, ComputingMilieux_MISCELLANEOUS
Abstract: International audience
Published: 2020
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14. Reaching the Second and Third Joint United Nations Programme on Human Immunodeficiency Virus (HIV)/AIDS 90-90-90 Targets Is Accompanied by a Dramatic Reduction in Primary HIV Infection and in Recent HIV Infections in a Large French Nationwide HIV Cohort

Author: Claudine Duvivier, Clotilde Allavena, J Lippmann, P. Dellamonica, A Soria, Sandrine Pierre-François, B J Gaborit, Isabelle Poizot-Martin, Anne Frésard, Elodie Curlier, F. Biron, Eric Cua, M Saadia Mokhtari, I Luquet Besson, C Gubavu, Caroline Lions, Laurent Cotte, C. Tomei, Elina Teicher, Faouzi Souala, Karima Amazzough, C Merle de Boever, Romain Palich, C Brochier, Véronique Reliquet, Patrick Miailhes, M Priester, Samira Fafi-Kremer, Mathieu Dupont, M Piffaut, I. Schlienger, C Bernaud, A S Ritleng, F-Xavier Lescure, C Cheneau, L Lelièvre, C Biron, Adrien Le Guillou, Alexa Debard, Marc-Antoine Valantin, Gilles Peytavin, S Lariven, G Benabdelmoumen, Florence Ader, I Kmiec, I Fabre, Cyrille Delpierre, C. Longuet, François Raffi, A de Monte, M. Alvarez, David Rey, A Boucher, M. Valette, E de Mautort, Jean-Luc Berger, H Bertone, Bruno Hoen, M Poisson-Vanier, Pascal Pugliese, Virginie Ferré, M Pradier, Z Julia, Nathalie Dournon, M Baldeyrou, N Biezunski, Caroline Charlier, J Goesch, J Pasquier, M P Bouillon, Cécile Goujard, Sophie Matheron, V. Le Moing, Romain Guery, N. Viget, N Atoui, C Dhiver, A Meybeck, Fanny Lanternier, F Touam, Tristan Ferry, M Carta Padovani, G Thomas, C Ceppi, A Brunet, Alain Makinson, Isabelle Ravaux, Laurent Hocqueloux, A Maillard, Firouzé Bani-Sadr, P. Loubet, Laurent Boyer, O Deradji, I Alcaraz, T Prazuck, A Rodallec, F Lemaitre, B Lafon-Desmurs, J Turmel, A Sève, Benoit Pilmis, A Gervais, C. Augustin-Normand, D Chirio, Brigitte Montes, Cédric Arvieux, V Brodard, M Delestan, E Aïssi, C Louisin, Christian Chidiac, M Ducassou, S Leautez, Catherine Chirouze, M André, Dominique Merrien, Q Gardiennet, P Fischer, Sylvie Abel, Guillaume Martin-Blondel, Benoît Henry, H. Tissot Dupont, S Patrat-Delon, A Ménard, E. Billaud, Malikhone Chansombat, K Jidar, Karine Sauné, Colin Deschanvres, V. Gueripel, M Cavellec, K. Schepers, C Pronier, R Ouissa, P Choisy, A Cheret, A. Belkhir, P Parize, A Barrail-Tran, B. Bonnet, C Mackoumbou-Nkouka, A. Galinier, M Monclar, P Lansalot, S Bouchez, C Guennoun, N Meftah, C Brunet-Cartier, Pierre Tattevin, J. Durant, E Ressiot, T. Huleux, François Bénézit, C Boulard, M Poinot, Elisabeth André-Garnier, J Sinteff, André Cabié, Charlotte Charpentier, L Meddeb, Rodolphe Garraffo, M Batard, D. Lebrun, R Tubiana, M J Soavi, I Lamaury, Philippe Bossi, Y Quertainmont, S Galie, C Michelangeli, François Danion, N Lerolle, Y N’guyen, Amandine Gagneux-Brunon, Elisa Demonchy, Christine Katlama, C Bernard-Henry, V Mondain, S Seang, David Boutoille, P. Le Turnier, Faiza Ajana, André Boibieux, J Koffi, L. Porte, Laurence Bocket, O Bollangier, A Maka, S Sécher, Marine Morrier, T Guimard, Matthieu Revest, C Godard, C Rioux, C Etienne, M Illiaquer, O. Aubry, N Hall, Paul-Henri Consigny, C Blanc, P Morineau, K Guitteaud, T. Perpoint, G Cessot, V Baclet, Lise Cuzin, T May, E Braun, Marialuisa Partisani, Veronique Joly, Jacques Reynes, Olivier Lortholary, C Blanco-Betancourt, Philippe Van de Perre, D Lambert, Moustapha Dramé, S Ferrando, S Breaud, A Montoya Ferrer, Yazdan Yazdanpanah, M. Hentzien, Cécile Herrmann-Storck, A. Duréault, A. Ivanova, F. Lucht, Pierre Delobel, Thomas Jovelin, J. M. Chapplain, Olivier Robineau, Roland Landman, Olivier Grossi, F Louni, Elisabeth Botelho-Nevers, J Lourenco, M Lefebvre, Diane Descamps, Luminita Schneider, R Agher, M Orticoni, D Rahli, S Degroodt, CHU de la Martinique [Fort de France], Centre Hospitalier Universitaire de Nice (CHU Nice), Service de maladies infectieuses et tropicales [Nantes], Université de Nantes (UN)-Hôtel-Dieu-Centre hospitalier universitaire de Nantes (CHU Nantes), Department of Infectious Diseases [Nantes], Hôtel-Dieu de Nantes, Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Infectious Diseases and Tropical Medicine Unit [Fort-de-France, Martinique], Centre Hospitalier Universitaire de Reims (CHU Reims), Laboratoire de Virologie Médicale et Moléculaire - EA 4684 (CardioVir), Université de Reims Champagne-Ardenne (URCA)-Centre Hospitalier Universitaire de Reims (CHU Reims)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV), Département de maladies infectieuses, and Hospices Civils de Lyon (HCL)
Subjects: 0301 basic medicine, Microbiology (medical), Cart, medicine.medical_specialty, Longitudinal study, business.industry, Public health, Incidence (epidemiology), medicine.disease, 030112 virology, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, Infectious Diseases, Acquired immunodeficiency syndrome (AIDS), Interquartile range, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Internal medicine, Epidemiology, Cohort, Medicine, 030212 general & internal medicine, business
Abstract: Background In late 2013, France was one of the first countries to recommend initiation of combination antiretroviral therapy (cART) irrespective of CD4 cell count. Methods To assess the impact of achieving the second and third Joint United Nations Programme on HIV/AIDS 90-90-90 targets (ie, 90% of diagnosed people on sustained cART, and, of those, 90% virologically controlled) on human immunodeficiency virus (HIV) incidence, we conducted a longitudinal study to describe the epidemiology of primary HIV infection (PHI) and/or recent HIV infection (patients with CD4 cell count ≥500/mm3 at HIV diagnosis; (PRHI) between 2007 and 2017 in a large French multicenter cohort. To identify changes in trends in PHI and PRHI, we used single breakpoint linear segmented regression analysis. Results During the study period, 61 822 patients were followed in the Dat’AIDS cohort; 2027 (10.0%) had PHI and 7314 (36.1%) had PRHI. The second and third targets were reached in 2014 and 2013, respectively. The median delay between HIV diagnosis and cART initiation decreased from 9.07 (interquartile range [IQR], 1.39–33.47) months in 2007 to 0.77 (IQR, 0.37–1.60) months in 2017. A decrease in PHI (−35.1%) and PRHI (−25.4%) was observed starting in 2013. The breakpoints for PHI and PRHI were 2012.6 (95% confidence interval [CI], 2010.8–2014.4) and 2013.1 (95% CI, 2011.3–2014.8), respectively. Conclusions Our findings show that the achievements of 2 public health targets in France and the early initiation of cART were accompanied by a reduction of about one-third in PHI and PRHI between 2013 and 2017. Clinical Trials Registration NCT02898987.
Published: 2020
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15. Characterization of viral rebounds on dual etravirine/raltegravir maintenance therapy (ANRS-163 ETRAL trial)

Author: Cathia, Soulie, Lambert, Assoumou, Basma, Abdi, Sophie, Sayon, Thuy, Nguyen, Marc-Antoine, Valantin, Lydie, Beniguel, Virginie, Ferre, Chakib, Alloui, Brigitte, Montes, Véronique, Avettand-Fenoel, Constance, Delaugerre, Diane, Descamps, Esteban, Martinez, Jacques, Reynes, Gilles, Peytavin, Dominique, Costagliola, Christine, Katlama, Vincent, Calvez, Anne-Geneviève, Marcelin, and Yazdan, Yazdanpanah
Subjects: 0301 basic medicine, Microbiology (medical), medicine.medical_specialty, Anti-HIV Agents, 030106 microbiology, Etravirine, HIV Infections, Drug resistance, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Maintenance therapy, Internal medicine, Raltegravir Potassium, Drug Resistance, Viral, Nitriles, medicine, Humans, Pharmacology (medical), 030212 general & internal medicine, Pharmacology, biology, business.industry, Viral Load, Raltegravir, Reverse transcriptase, 3. Good health, Integrase, Pyridazines, Regimen, Infectious Diseases, Pyrimidines, biology.protein, HIV-1, business, Viral load, medicine.drug
Abstract: Background The ANRS-163 ETRAL trial, a switch study to an etravirine 200 mg/raltegravir 400 mg twice-daily regimen in 165 patients with HIV-1 infection, showed durable efficacy until Week 96. The aim of this work was to investigate in detail the virological rebounds (VRs), defined as at least one plasma HIV viral load (VL) >50 copies/mL. Methods Quantification of HIV-DNA level was assessed at baseline, Week 48 and Week 96 (n = 157). VLs were measured in seminal plasma at Week 48 (n = 26). Genotypic resistance testing by ultra-deep sequencing (UDS) for reverse transcriptase (RT) and integrase regions was performed at baseline and at the time of VR. Results In this study, 19 patients experienced VR, with 2 patients having virological failure (VF; two consecutive VLs >50 copies/mL). For the first patient with VF, UDS detected minority resistant variants only in RT (K103N, 9.6%; Y181C, 4.9%) at baseline. Some RT variants became dominant at VF (K101E, 86.3%; Y181C, 100.0%; G190A, 100.0%) and others emerged in integrase (Y143C, 2.4%; Q148R, 6.2%; N155H, 18.8%). For the second patient with VF, neither RT nor integrase mutations were detected at baseline and VF. Median HIV-DNA level was similar at baseline, Week 48 and Week 96 (2.17, 2.06 and 2.11 log10 copies/106 cells, respectively). Only one patient had a detectable seminal HIV VL (505 copies/mL). Conclusions The dual etravirine/raltegravir regimen as maintenance therapy was effective and the emergence of mutations in cases of VF was similar to that seen in other dual-regimen studies. No HIV-DNA level modification was evidenced by Week 96.
Published: 2020

16. Resistance to integrase inhibitors: a national study in HIV-1-infected treatment-naive and -experienced patients

Author: Constance Delaugerre, Virginie Ferré, Anne Maillard, Vincent Calvez, Audrey Mirand, Anne-Geneviève Marcelin, Corinne Amiel, Julia Dina, Coralie Pallier, Hélène Le Guillou-Guillemette, Stéphanie Raymond, D. B. Fofana, Thomas Mourez, Hélène Jeulin, Samira Fafi-Kremer, Brigitte Montes, Pantxika Bellecave, Sophie Vallet, Thuy Van Nguyen, Diane Descamps, Catherine Roussel, Maxime Grude, Mary-Anne Trabaud, Charlotte Charpentier, Laurence Bocket, Philippe Flandre, Laura Le Guen, Anne Signori-Schmuck, Epidémiologie, stratégies thérapeutiques et virologie cliniques dans l'infection à VIH, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Laboratoire Bordelais de Recherche en Informatique (LaBRI), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB), Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Centre hospitalier universitaire de Nantes (CHU Nantes), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CHU Toulouse [Toulouse], Laboratoire Microorganismes : Génome et Environnement (LMGE), Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), CIC CHU ( Lille)/inserm, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Laboratoire de Virologie [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Simulation et Traitement de l'information pour l'Exploitation des systèmes de Production (EDF R&D STEP), EDF R&D (EDF R&D), EDF (EDF)-EDF (EDF), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Groupe de Recherche sur l'Adaptation Microbienne (GRAM 2.0), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université de Caen Normandie (UNICAEN), Normandie Université (NU), Laboratoire de virologie [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Interaction virus-hôte et maladies du foie, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Amiens-Picardie, Service de Virologie [CHU Caen], CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Laboratoire Universitaire de Biodiversité et Ecologie Microbienne (LUBEM), Université de Brest (UBO), Institut de biologie structurale (IBS - UMR 5075 ), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Rennes] = Virology [Rennes], CHU Pontchaillou [Rennes], AP-HP - Hôpital Bichat - Claude Bernard [Paris], Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Microbiologie Fondamentale et Pathogénicité (MFP), Service de virologie et unité de surveillance biologique [Bordeaux], CHU Bordeaux [Bordeaux], Hôpital Paul Brousse, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse, Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), CHU Clermont-Ferrand, CHU Lille, CHU Saint-Antoine [AP-HP], Laboratoire de Virologie [CHU Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Hôpital Saint Eloi (CHRU Montpellier), Service de Virologie [CHRU Nancy], CHU Strasbourg, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Hôpital de la Cavale Blanche - CHRU Brest (CHU - BREST ), Centre Hospitalier Universitaire [Grenoble] (CHU), Centre d’Investigation Clinique de Nantes (CIC Nantes), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre hospitalier universitaire de Nantes (CHU Nantes), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Centre National de la Recherche Scientifique (CNRS)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020]), Université de Caen Normandie (UNICAEN), Service de Virologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPC)-Université Sorbonne Paris Nord, Hôpital Paul Brousse-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Toulouse], CHU Saint-Eloi, Mzembaba, Sandy, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
Subjects: Male, 0301 basic medicine, MESH: Sequence Analysis, DNA, MESH: Treatment Failure, Aucun, Integrase inhibitor, HIV Infections, Drug resistance, MESH: HIV Seropositivity / drug therapy, MESH: Genotype, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, MESH: Risk Factors, HIV Seropositivity, Pharmacology (medical), Treatment Failure, 030212 general & internal medicine, ComputingMilieux_MISCELLANEOUS, [SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, MESH: Middle Aged, biology, Elvitegravir, Middle Aged, Viral Load, 3. Good health, Integrase, MESH: HIV-1 / genetics, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Dolutegravir, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Female, Viral load, medicine.drug, Adult, Microbiology (medical), medicine.medical_specialty, MESH: Mutation, Genotype, MESH: HIV Integrase Inhibitors / therapeutic use, 030106 microbiology, MESH: HIV Infections / drug therapy, MESH: Drug Resistance, Multiple, Viral / genetics, MESH: HIV-1 / drug effects, 03 medical and health sciences, Drug Resistance, Multiple, Viral, Internal medicine, medicine, Humans, HIV Integrase Inhibitors, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Pharmacology, MESH: Viral Load / drug effects, MESH: Humans, business.industry, MESH: Adult, Sequence Analysis, DNA, Raltegravir, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Male, Regimen, chemistry, Mutation, HIV-1, biology.protein, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, business, MESH: Female
Abstract: International audience; Objectives: To describe integrase strand transfer inhibitor (INSTI) resistance profiles and factors associated with resistance in antiretroviral-naive and -experienced patients failing an INSTI-based regimen in clinical practice.Methods: Data were collected from patients failing an INSTI-containing regimen in a multicentre French study between 2014 and 2017. Failure was defined as two consecutive plasma viral loads (VL) >50 copies/mL. Reverse transcriptase, protease and integrase coding regions were sequenced at baseline and failure. INSTI resistance-associated mutations (RAMs) included in the Agence Nationale de Recherches sur le SIDA genotypic algorithm were investigated.Results: Among the 674 patients, 359 were failing on raltegravir, 154 on elvitegravir and 161 on dolutegravir therapy. Overall, 90% were experienced patients and 389 (58%) patients showed no INSTI RAMs at failure. The strongest factors associated with emergence of at least one INSTI mutation were high VL at failure (OR = 1.2 per 1 log10 copies/mL increase) and low genotypic sensitivity score (GSS) (OR = 0.08 for GSS ≥3 versus GSS = 0-0.5). Patients failing dolutegravir also had significantly fewer INSTI RAMs at failure than patients failing raltegravir (OR = 0.57, P = 0.02) or elvitegravir (OR = 0.45, P = 0.005). Among the 68 patients failing a first-line regimen, 11/41 (27%) patients on raltegravir, 7/18 (39%) on elvitegravir and 0/9 on dolutegravir had viruses with emergent INSTI RAMs at failure.Conclusions: These results confirmed the robustness of dolutegravir regarding resistance selection in integrase in the case of virological failure in routine clinical care.
Published: 2019
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17. Stable prevalence of transmitted drug resistance mutations and increased circulation of non-B subtypes in antiretroviral-naive chronically HIV-infected patients in 2015/2016 in France

Author: Gilles Peytavin, Mary-Anne Trabaud, Anne Signori-Schmuck, Charlotte Charpentier, Marc Wirden, Cécile Henquell, Laurence Bocket, Catherine Delamare, Samira Fafi-Kremer, Jacques Izopet, Chakib Allaoui, Georges Dos Santos, A. Beby-Defaux, Benoit Visseaux, Virginie Ferré, Coralie Pallier, Diane Descamps, Stéphanie Marque-Juillet, Lambert Assoumou, Magali Bouvier-Alias, Sophie Vallet, Alexis de Rougemont, Hélène Le Guillou-Guillemette, Vincent Calvez, Stéphanie Raymond, Corinne Amiel, Honorine Fenaux, Anne De Monte, Francis Barin, Anne Krivine, Véronique Avettand-Fenoel, Annick Allardet-Servent, Jean-Christophe Plantier, Rachid Ait-Namane, Laurence Morand-Joubert, Marie-Laure Chaix, Camille Tumiotto, Maxime Grude, Anne Maillard, Laurence Courdavault, Brigitte Montes, Epidémiologie, stratégies thérapeutiques et virologie cliniques dans l'infection à VIH, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CIC CHU ( Lille)/inserm, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire Bordelais de Recherche en Informatique (LaBRI), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB), 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), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Hôpital Avicenne [AP-HP], CHU Clermont-Ferrand, Service de Virologie [CHU Cochin], Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU de la Martinique [Fort de France], Centre hospitalier régional Metz-Thionville (CHR Metz-Thionville), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre hospitalier universitaire de Nantes (CHU Nantes), CHU Nice [Cimiez], Hôpital Cimiez [Nice] (CHU), Institut de biologie structurale (IBS - UMR 5075 ), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Rennes] = Virology [Rennes], CHU Pontchaillou [Rennes], Services des Maladies Infectieuses et Tropicales [CHU Saint-Antoine], CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), CHU Bordeaux [Bordeaux], Interaction virus-hôte et maladies du foie, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Trousseau [Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Centre Hospitalier de Versailles André Mignot (CHV), Centre Hospitalier Victor Dupouy, Laboratoire Universitaire de Biodiversité et Ecologie Microbienne (LUBEM), Université de Brest (UBO), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Procédés Alimentaires et Microbiologiques [Dijon] (PAM), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Service de Virologie [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Université Sorbonne Paris Cité (USPC), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Groupe de Recherche sur l'Adaptation Microbienne (GRAM 2.0), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université de Caen Normandie (UNICAEN), Normandie Université (NU), Laboratoire de virologie [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Laboratoire de Virologie [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université de Caen Normandie (UNICAEN), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Mzembaba, Sandy, Epidémiologie, Systèmes d'Information, Modélisation, Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Service de Virologie [Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Hôpital Paul Brousse, Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Service de Virologie [CHU Pitié-Salpêtrière], CHU Pitié-Salpêtrière [AP-HP], Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Service de Virologie Médicale et Moléculaire [CHU Clermont-Ferrand], CHU Gabriel Montpied [Clermont-Ferrand], CHU Clermont-Ferrand-CHU Clermont-Ferrand-CHU Estaing [Clermont-Ferrand], Laboratoire de Virologie-Immunologie [Fort de France, Martinique] (EA 4537), Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], CHU Henri Mondor, Centre Hospitalier Universitaire [Grenoble] (CHU), Laboratoire de Virologie [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Sorbonne Université (SU), Service de virologie et unité de surveillance biologique [Bordeaux], CHU Strasbourg, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre hospitalier Argenteuil (CH Argenteuil), CHU Dijon, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université Paris Descartes, Sorbonne Paris Cité, Groupe de Recherche sur les Antimicrobiens et les Micro-Organismes (GRAM 1.0), Normandie Université (NU)-Normandie Université (NU), Pathologie cellulaire : aspects moléculaires et viraux / Pathologie et Virologie Moléculaire, Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS), and ANRS – France REcherche Nord&Sud Sida-hiv Hépatites
Subjects: 0301 basic medicine, Male, MESH: CD4 Lymphocyte Count, [SDV]Life Sciences [q-bio], Integrase inhibitor, hiv, HIV Infections, Drug resistance, MESH: HIV-1 / genetics, MESH: Genotype, MESH: HIV Infections / epidemiology, 0302 clinical medicine, Genotype, Blood plasma, HIV Seropositivity, rna-directed dna polymerase, Prevalence, rna, Pharmacology (medical), 030212 general & internal medicine, MESH: Chronic Disease / epidemiology, ComputingMilieux_MISCELLANEOUS, cd4 count determination procedure, [SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, anti-retroviral agents, MESH: France / epidemiology, Antiinfective agent, MESH: Middle Aged, Incidence (epidemiology), Middle Aged, MESH: Drug Resistance, Viral / genetics, 3. Good health, endopeptidases, [SDV] Life Sciences [q-bio], integrase inhibitors, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, RNA, Viral, MESH: RNA, Viral / blood, Female, France, MESH: HIV Seropositivity / epidemiology, Microbiology (medical), Adult, medicine.medical_specialty, peptide hydrolases, MESH: Mutation, Anti-HIV Agents, 030106 microbiology, MESH: HIV Infections / drug therapy, MESH: HIV-1 / classification, MESH: HIV-1 / drug effects, Virus, MESH: HIV Infections / transmission, 03 medical and health sciences, Pharmacotherapy, Internal medicine, Drug Resistance, Viral, medicine, Humans, viruses, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, plasma, safe sex, MESH: Prevalence, Pharmacology, drug resistance, MESH: Humans, business.industry, MESH: Adult, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Male, CD4 Lymphocyte Count, MESH: Anti-HIV Agents / therapeutic use, Chronic Disease, Mutation, HIV-1, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, business, MESH: Female
Abstract: International audience; Objectives: We estimated the prevalence of transmitted-drug-resistance-associated mutations (TDRAMs) in antiretroviral-naive chronically HIV-1-infected patients.Patients and methods: TDRAMs were sought in samples from 660 diagnosed HIV-1-infected individuals in 2015/2016 in 33 HIV clinical centres. Weighted analyses, considering the number of patients followed in each centre, were used to derive representative estimates of the percentage of individuals with TDRAMs. Results were compared with those of the 2010/2011 survey (n = 661) using the same methodology.Results: At inclusion, median CD4 cell counts and plasma HIV-1 RNA were 394 and 350/mm3 (P = 0.056) and 4.6 and 4.6 log10 copies/mL (P = 0.360) in the 2010/2011 survey and the 2015/2016 survey, respectively. The frequency of non-B subtypes increased from 42.9% in 2010/2011 to 54.8% in 2015/2016 (P < 0.001), including 23.4% and 30.6% of CRF02_AG (P = 0.004). The prevalence of virus with protease or reverse-transcriptase TDRAMs was 9.0% (95% CI = 6.8-11.2) in 2010/2011 and 10.8% (95% CI = 8.4-13.2) in 2015/2016 (P = 0.269). No significant increase was observed in integrase inhibitor TDRAMs (6.7% versus 9.2%, P = 0.146). Multivariable analysis showed that men infected with the B subtype were the group with the highest risk of being infected with a resistant virus compared with others (adjusted OR = 2.2, 95% CI = 1.3-3.9).Conclusions: In France in 2015/2016, the overall prevalence of TDRAMs was 10.8% and stable compared with 9.0% in the 2010/2011 survey. Non-B subtypes dramatically increased after 2010. Men infected with B subtype were the group with the highest risk of being infected with a resistant virus, highlighting the need to re-emphasize safe sex messages.
Published: 2018
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18. Phenotypic analysis of HIV-1 E157Q integrase polymorphism and impact on virological outcome in patients initiating an integrase inhibitor-based regimen

Author: Alexandre Storto, Diane Descamps, Anne Maillard, Audrey Mirand, Corinne Amiel, Charlotte Charpentier, Vincent Calvez, Thuy Van Nguyen, Laurence Bocket, Coralie Pallier, Audrey Rodallec, Elisabeth André-Garnier, Marie Leoz, Laurence Morand-Joubert, Isabelle Malet, Stéphanie Raymond, Véronique Schneider, Catherine Roussel, Camille Tumiotto, Constance Delaugerre, Anne-Geneviève Marcelin, Julia Dina, Jean-Christophe Plantier, Brigitte Montes, Anne Signori-Schmuck, Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Université Paris Diderot - Paris 7 (UPD7), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôtel-Dieu de Nantes, Service de Virologie [Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service de bactériologie-virologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Service de virologie [Hôpital Tenon], CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Ecophysiologie Végétale, Agronomie et Nutritions (EVA), Institut National de la Recherche Agronomique (INRA)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU), Service de virologie [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Laboratoire de virologie [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Service de Virologie [CHU Caen], CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Service de Virologie [Villejuif], Hôpital Paul Brousse, Laboratoire Microorganismes : Génome et Environnement (LMGE), Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Service de bactériologie-virologie [Tours], Hôpital Bretonneau-Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Institut de biologie structurale (IBS - UMR 5075 ), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie [Toulouse], CHU Toulouse [Toulouse], Génétique et Ecologie des Virus, Génétique des Virus et Pathogénèse des Maladies Virales, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), 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), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Saint-Antoine [APHP], CHU Tenon [APHP], Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Recherche Agronomique (INRA), Laboratoire Microorganismes : Génome et Environnement - Clermont Auvergne (LMGE), Université Clermont Auvergne (UCA)-Centre National de la Recherche Scientifique (CNRS), Unit for Virus Host-Cell Interactions [Grenoble] (UVHCI), Université Joseph Fourier - Grenoble 1 (UJF)-European Molecular Biology Laboratory [Grenoble] (EMBL)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], 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), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-Hôpital Bretonneau, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], and Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)
Subjects: 0301 basic medicine, Microbiology (medical), Genotype, 030106 microbiology, Mutation, Missense, Integrase inhibitor, HIV Infections, HIV Integrase, [SDV.MP.PRO]Life Sciences [q-bio]/Microbiology and Parasitology/Protistology, Virus, 03 medical and health sciences, chemistry.chemical_compound, Gene Frequency, medicine, Prevalence, Humans, Pharmacology (medical), HIV Integrase Inhibitors, Pharmacology, biology, Elvitegravir, business.industry, Viral Load, Raltegravir, Virology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, Integrase, Regimen, Infectious Diseases, Treatment Outcome, chemistry, Dolutegravir, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, biology.protein, HIV-1, France, business, Viral load, medicine.drug
Abstract: International audience; ObjectivesTo assess the phenotypic susceptibility of the E157Q polymorphism in HIV-1 integrase (IN) and the virological outcome of patients infected with E157Q-mutated virus initiating an IN inhibitor (INI)-based regimen.MethodsThis was a multicentre study assessing IN sequences from INI-naive patients among 17 French HIV clinical centres. E157Q site-directed mutants in pNL4.3 and pCRF02_AG contexts were assessed in a recombinant phenotypic assay.ResultsPrevalence of the E157Q polymorphism was 2.7% among 8528 IN sequences from INI-naive patients and its distribution was 1.7%, 5.6% and 2.2% in B, CRF02_AG and various non-B subtypes, respectively. Thirty-nine INI-naive patients with E157Q-mutated virus initiated an INI-based regimen. Among them, 15 had a viral load (VL) 50 copies/mL at the time of INI-based regimen initiation. Among them eight were receiving a first-line regimen and the only two patients who did not reach VL
Published: 2018
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19. Performance of genotypic algorithms for predicting tropism for HIV-1 CRF01_AE recombinant

Author: Samira Fafi-Kremer, Laurence Morand-Joubert, Audrey Mirand, Vincent Calvez, Cathia Soulié, Mary-Anne Trabaud, A G Marcelin, Jacqueline Cottalorda, Anne Signori-Schmuck, S. Berger, Julia Dina, Coralie Pallier, Véronique Avettand-Fenoel, Brigitte Montes, Pantxika Bellecave, Karen Zafilaza, Charlotte Charpentier, L. Le Guen, Sabine Yerly, Catherine Roussel, Corinne Amiel, Sophie Sayon, Service de Virologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Pitié-Salpêtrière [APHP], 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), Service de chirurgie pédiatrique [Hôpital Lapeyronie-Arnaud de Villeneuve], Hôpital Lapeyronie [Montpellier] (CHU), Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), CHU Montpellier, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Laboratoire de Virologie [Strasbourg], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Equipe de Recherche en Physico-Chimie et Biotechnologie (ERPCB), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU), UR 0420 - Station de pathologie végétale, Laboratoire de pathologie forestière, Institut National de la Recherche Agronomique (INRA)-Institut National de la Recherche Agronomique (INRA), Neuroimagerie cognitive (LCogn), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de biologie structurale des interactions entre virus et cellule hôte, Université Joseph Fourier - Grenoble 1 (UJF)-Centre National de la Recherche Scientifique (CNRS), CHU Clermont-Ferrand, Laboratoire Microorganismes : Génome et Environnement - Clermont Auvergne (LMGE), Université Clermont Auvergne (UCA)-Centre National de la Recherche Scientifique (CNRS), Saint-Gobain Recherche (SGR), SAINT-GOBAIN, CHU Pitié-Salpêtrière [APHP], Service de virologie [CHU Pitié-Salpêtrière], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Biologie structurale des interactions entre virus et cellule hôte (UVHCI), European Molecular Biology Laboratory [Grenoble] (EMBL)-Centre National de la Recherche Scientifique (CNRS)-Université Joseph Fourier - Grenoble 1 (UJF), Laboratoire Microorganismes : Génome et Environnement (LMGE), Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Microbiologie Fondamentale et Pathogénicité (MFP), Université Joseph Fourier - Grenoble 1 (UJF)-European Molecular Biology Laboratory [Grenoble] (EMBL)-Centre National de la Recherche Scientifique (CNRS), Saint-Gobain, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)
Subjects: 0301 basic medicine, Genotype, Genotyping Techniques, viruses, Concordance, 030106 microbiology, Human immunodeficiency virus (HIV), HIV Infections, ddc:616.07, HIV Envelope Protein gp120, Biology, medicine.disease_cause, [SDV.MP.PRO]Life Sciences [q-bio]/Microbiology and Parasitology/Protistology, law.invention, 03 medical and health sciences, 0302 clinical medicine, law, Virology, HIV tropism, medicine, Humans, False Positive Reactions, 030212 general & internal medicine, Tropism, ComputingMilieux_MISCELLANEOUS, virus diseases, Viral Load, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, CD4 Lymphocyte Count, 3. Good health, Viral Tropism, Infectious Diseases, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, HIV-1, Recombinant DNA, RNA, Viral, France, False positive rate, Viral load, Algorithm, Algorithms, Switzerland, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: Objectives There is no consensus about the performances of genotypic rules for predicting HIV-1 non-B subtype tropism. Three genotypic methods were compared for CRF01_AE HIV-1 tropism determination. Methods The V3 env region of 207 HIV-1 CRF01_AE and 178 B subtypes from 17 centers in France and 1 center in Switzerland was sequenced. Tropism was determined by Geno2Pheno algorithm with false positive rate (FPR) 5% or 10%, the 11/25 rule or the combined criteria of the 11/25, net charge rule and NXT/S mutations. Results Overall, 72.5%, 59.4%, 86.0%, 90.8% of the 207 HIV-1 CRF01_AE were R5-tropic viruses determined by Geno2pheno FPR5%, Geno2pheno FPR10%, the combined criteria and the 11/25 rule, respectively. A concordance of 82.6% was observed between Geno2pheno FPR5% and the combined criteria for CRF01_AE. The results were nearly similar for the comparison between Geno2pheno FPR5% and the 11/25 rule. More mismatches were observed when Geno2pheno was used with the FPR10%. Neither HIV viral load, nor current or nadir CD4 was associated with the discordance rate between the different algorithms. Conclusion Geno2pheno predicted more X4-tropic viruses for this set of CRF01_AE sequences than the combined criteria or the 11/25 rule alone. For a conservative approach, Geno2pheno FPR5% seems to be a good compromise to predict CRF01_AE tropism.
Published: 2018

20. HIV-1-infected patients from the French National Observatory experiencing virological failure while receiving enfuvirtide

Author: Virginie Ferré, Jacqueline Cottalorda, Anne-Geneviève Marcelin, Véronique Schneider, Laurence Morand-Joubert, Jacques Izopet, Diane Descamps, Lambert Assoumou, Coralie Pallier, Souhila Saidi, Bernard Masquelier, Marie-Laure Chaix, Annick Ruffault, Constance Delaugerre, Vincent Calvez, Sabine Yerly, Françoise Brun-Vézinet, Jean-Christophe Plantier, Gilles Peytavin, Brigitte Montes, Dominique Costagliola, and Catherine Tamalet
Subjects: Microbiology (medical), Adult, Male, Enfuvirtide, Mutation, Missense, Salvage therapy, Gp41, HIV Fusion Inhibitors, Immunopathology, Medicine, Humans, Pharmacology (medical), Sida, Pharmacology, Salvage Therapy, Acquired Immunodeficiency Syndrome, biology, business.industry, Sequence Analysis, DNA, Middle Aged, Viral Load, biology.organism_classification, Virology, HIV Envelope Protein gp41, Peptide Fragments, CD4 Lymphocyte Count, Infectious Diseases, Treatment Outcome, Amino Acid Substitution, Lentivirus, HIV-1, RNA, Viral, Female, Viral disease, France, business, HIV drug resistance, medicine.drug
Abstract: Objectives: We studied gp41 mutations associated with failing enfuvirtide salvage therapy. Methods: This multicentre study involved patients with HIV-1 plasma viral load (pVL) > 5000 copies/mL after at least 3 months of uninterrupted enfuvirtide therapy and with plasma samples available at inclusion (TO), at initial enfuvirtide failure (T1) and at last follow-up visit during continued failing enfuvirtide therapy (T2). The HR-1 and HR-2 domains of the gp41 gene were sequenced at TO, T1 and T2. Results: Ninety-nine patients were enrolled. At baseline, the median pVL and CD4 cell count were 5.1 log copies/mL and 72 cells/mm 3 , respectively. Based on the ANRS Resistance Group algorithm, the proportion of patients harbouring viruses with enfuvirtide resistance mutations increased significantly between TO and T1. In the HR-1 domain, the V38A/M, Q40H, N42T, N43D and L45M mutations were selected (P< 0.02). In the HR-2 domain, no mutations were significantly selected during the follow-up. None of the mutations was associated with a CD4 cell count increment. Conclusions: Mutations selected during failing enfuvirtide salvage therapy are mainly located in the HR-1 domain of the gp41 gene, between codons 38 and 45. No mutations were associated with an increase in the CD4 cell count.
Published: 2017

21. Antiretroviral-treated HIV-1 patients can harbour resistant viruses in CSF despite an undetectable viral load in plasma

Author: Sabine Yerly, Maxime Grude, Audrey Mirand, Philippe Flandre, Anne Maillard, Aurélie Guigon, Sandrine Reigadas, Corinne Amiel, Chakib Alloui, Samira Fafi-Kremer, Stéphanie Haim-Boukobza, Stéphanie Raymond, Anne Signori-Schmuck, Hélène Jeulin, Laurence Morand-Joubert, Virginie Ferré, Catherine Roussel, Brigitte Montes, Pantxika Bellecave, Anne-Geneviève Marcelin, Sophie Vallet, Diane Descamps, Lambert Assoumou, Mary-Anne Trabaud, Vincent Calvez, Cathia Soulié, Francis Barin, Constance Delaugerre, Coralie Pallier, 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 Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), 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), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, CHU Tenon [AP-HP], CHU Saint-Antoine [AP-HP], Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Service de Virologie [Hôpital Paul-Brousse - APHP] (World Health Organization Rubella National Reference Laboratory), Hôpital Paul Brousse, CHU Bordeaux [Bordeaux], Service de virologie et unité de surveillance biologique [Bordeaux], Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Laboratoire de Virologie [CHU Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Department of Infectious Diseases [Paris], Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Laboratoire de Virologie [CHRU Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Service de virologie [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Laboratoire de virologie CHU de NANCY BRADOIS, Service de bactériologie-Virologie-Hygiène [Avicenne], Université Paris 13 (UP13)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Avicenne [AP-HP], Geneva University Hospital (HUG), Département de virologie [Grenoble], Centre Hospitalier Universitaire [Grenoble] (CHU), CHU Orléans, Laboratoire de Virologie [Strasbourg], CHU Clermont-Ferrand, CHU Pontchaillou [Rennes], CHU-BREST-Service de Virologie, and CHU Amiens-Picardie
Subjects: Adult, Male, Microbiology (medical), Genotype, Genotyping Techniques, Population, Human immunodeficiency virus (HIV), HIV Infections, Microbial Sensitivity Tests, Drug resistance, Biology, medicine.disease_cause, Plasma, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Drug Resistance, Viral, HIV encephalitis, medicine, Humans, Pharmacology (medical), 030212 general & internal medicine, Sida, education, Cognitive impairment, Cerebrospinal Fluid, Retrospective Studies, Pharmacology, education.field_of_study, Middle Aged, Viral Load, biology.organism_classification, Virology, Infectious Diseases, Anti-Retroviral Agents, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Immunology, HIV-1, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, Female, France, Viral load, Switzerland, 030217 neurology & neurosurgery
Abstract: International audience; Background: HIV therapy reduces the CSF HIV RNA viral load (VL) and prevents disorders related to HIV encephalitis. However, these brain disorders may persist in some cases. A large population of antiretroviral-treated patients who had a VL > 1.7 log10 copies/mL in CSF with detectable or undetectable VL in plasma associated with cognitive impairment was studied, in order to characterize discriminatory factors of these two patient populations.Methods: Blood and CSF samples were collected at the time of neurological disorders for 227 patients in 22 centres in France and 1 centre in Switzerland. Genotypic HIV resistance tests were performed on CSF. The genotypic susceptibility score was calculated according to the last Agence Nationale de Recherche sur le Sida et les hépatites virales Action Coordonnée 11 (ANRS AC11) genotype interpretation algorithm.Results: Among the 227 studied patients with VL > 1.7 log10 copies/mL in CSF, 195 had VL detectable in plasma [median (IQR) HIV RNA was 3.7 (2.7–4.7) log10 copies/mL] and 32 had discordant VL in plasma (VL 1.7 log10 copies/mL. Resistance to antiretrovirals was observed in CSF for the two groups of patients.Conclusions: Fourteen percent of this population of patients with cognitive impairment and detectable VL in CSF had well controlled VL in plasma. Thus, it is important to explore CSF HIV (VL and genotype) even if the HIV VL is controlled in plasma because HIV resistance may be observed.
Published: 2017
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22. HIV-1 DNA ultra-deep sequencing analysis at initiation of the dual therapy dolutegravir + lamivudine in the maintenance DOLULAM pilot study

Author: Nadia Meftah, Marine Perrier, Brigitte Montes, Charlotte Charpentier, Jacques Reynes, Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), and Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Université Montpellier 1 (UM1)
Subjects: 0301 basic medicine, Male, [SDV]Life Sciences [q-bio], HIV Infections, Pilot Projects, HIV Integrase, dna, medicine.disease_cause, Piperazines, chemistry.chemical_compound, Genotype, Pharmacology (medical), rna, Mutation, viral genome, Lamivudine, High-Throughput Nucleotide Sequencing, Resistance mutation, Stop codon, HIV Reverse Transcriptase, 3. Good health, Integrase, virology, dolutegravir, Infectious Diseases, Dolutegravir, Drug Therapy, Combination, Female, Heterocyclic Compounds, 3-Ring, medicine.drug, Microbiology (medical), Adult, Anti-HIV Agents, Pyridones, 030106 microbiology, Genome, Viral, Biology, 03 medical and health sciences, massively-parallel genome sequencing, Drug Resistance, Viral, Oxazines, medicine, Humans, Pharmacology, Genetic Variation, Virology, chemistry, DNA, Viral, biology.protein, HIV-1, integrase, DNA
Abstract: International audience; Background: The DOLULAM study assessed the efficacy of dolutegravir + lamivudine dual therapy to maintain virological suppression in heavily treatment-experienced HIV-1-infected adults. No virological failure occurred during the first year of the dual therapy. Objectives: A virological substudy was conducted to assess the prevalence of M184I/V mutations at dual therapy initiation using historical DNA/RNA genotypes and baseline DNA genotype obtained by next-generation sequencing (NGS). Methods: HIV-1 RT sequences were obtained from DNA and/or historical RNA using Sanger technology. HIV-1 DNA RT and integrase NGS was performed using Illumina\textregistered technology. Results: Among the 27 patients enrolled in the DOLULAM study, historical HIV DNA and RNA Sanger sequences were available in 14 and 18 patients, respectively. At the initiation of DOLULAM, DNA NGS genotypes showed that 45% and 21% of the patients harboured minority resistant variants (MRV) in RT and integrase, respectively. Combining all available genotype data, an M184I/V was observed in 17 of 27 (63%) of the patients. Most M184V were detected in historical RNA genotypes (n = 8 of 11), whereas M184I were exclusively detected in DNA genotypes (n = 10, including 7 as MRV). Ten patients displayed defective viral genomes in cellular reservoirs, all including M184I and stop codons. At the time of DOLULAM initiation, M184V was observed in DNA NGS in five patients, including one as MRV. Conclusions: These first NGS data on HIV DNA at initiation of a switch study showed (i) a high proportion of patients harbouring defective viral genomes, whose mutation M184I is a marker, and (ii) a low number of patients in whom M184V remained as a major viral variant in PBMCs.
Published: 2017
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23. Increasing prevalence of transmitted drug resistance mutations and non-B subtype circulation in antiretroviral-naive chronically HIV-infected patients from 2001 to 2006/2007 in France

Author: Jacques Izopet, Jacqueline Cottalorda, Vincent Calvez, Charlotte Charpentier, Henia Saoudin, Georges Dos Santos, Mary-Anne Trabaud, Francis Barin, V. Calvez, Cécile Henquell, Delphine Desbois, C. Delaugerre, Slim Fourati, D. Bettinger, Thomas Bourlet, Anne Krivine, Bernard Masquelier, S. Vallet, M. Bouvier-Alias, Catherine Tamalet, B. Masquelier, S. Rogez, Coralie Pallier, J. C. Plantier, C. Charpentier, F. Barin, J. Cottalorda, A. Maillard, Alexandre Storto, G. DosSantos, Chakib Alloui, B. Montes, Marie-Laure Chaix, A. G. Marcelin, Anne Signori-Schmuck, D. Desbois, Anne-Geneviève Marcelin, Marie Laure Chaix, C. Tamalet, F. Brun-Vézinet, Françoise Brun-Vézinet, J. Izopet, Philippe Flandre, G. Anies, Anne Maillard, Diane Descamps, Patrice Andre, Jean-Claude Tardy, Dominique Costagliola, Brigitte Montes, Laurence Morand-Joubert, Annick Ruffault, Jean-Christophe Plantier, Sophie Pakianather, L. Morand-Joubert, and Constance Delaugerre
Subjects: Male, Microbiology (medical), Anti-HIV Agents, HIV Infections, Drug resistance, Nucleoside Reverse Transcriptase Inhibitor, 03 medical and health sciences, 0302 clinical medicine, HIV Protease, Drug Resistance, Viral, HIV Seropositivity, Prevalence, medicine, Humans, Pharmacology (medical), 030212 general & internal medicine, Pharmacology, 0303 health sciences, Reverse-transcriptase inhibitor, biology, 030306 microbiology, Proteolytic enzymes, biology.organism_classification, Virology, HIV Reverse Transcriptase, Reverse transcriptase, 3. Good health, Infectious Diseases, Chronic Disease, Mutation, Immunology, Lentivirus, HIV-1, Reverse Transcriptase Inhibitors, Female, France, Viral disease, Viral load, medicine.drug
Abstract: Objectives: To estimate the prevalence of transmitted drug resistance mutations and non-B subtype circulation in antiretroviral-naive chronically HIV-1-infected patients in France. Methods: Resistance mutations were sought in samples from 530 newly diagnosed HIV-1-infected patients from October 2006 to March 2007. Protease and reverse transcriptase mutations were identified from the 2007 Stanford Resistance Surveillance list. Results: Reverse transcriptase and protease resistance mutations were determined in 466 patients with duration of seropositivity
Published: 2010
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24. Evaluation of Different RNA Extraction Methods and Storage Conditions of Dried Plasma or Blood Spots for Human Immunodeficiency Virus Type 1 RNA Quantification and PCR Amplification for Drug Resistance Testing

Author: François Boillot, Marjorie Monleau, Brigitte Montes, Christian Laurent, Martine Peeters, Celine Montavon, Michel Segondy, and Eric Delaporte
Subjects: Microbiology (medical), Time Factors, HIV Infections, Biology, Polymerase Chain Reaction, Virus, Specimen Handling, law.invention, Plasma, law, Virology, Drug Resistance, Viral, Blood plasma, Humans, Sample preparation, Desiccation, Polymerase chain reaction, Temperature, RNA, Viral Load, Blood, Molecular Diagnostic Techniques, Specimen collection, HIV-1, RNA, Viral, Reagent Kits, Diagnostic, RNA extraction, Viral load
Abstract: The development and validation of dried sample spots as a method of specimen collection are urgently needed in developing countries for monitoring of human immunodeficiency virus (HIV) infection. Our aim was to test some crucial steps in the use of dried spots, i.e., viral recovery and storage over time. Moreover, we investigated whether dried plasma and blood spots (DPS and DBS, respectively) give comparable viral load (VL) results. Four manual RNA extraction methods from commercial HIV type 1 (HIV-1) VL assays—a QIAamp minikit (Qiagen), the Abbott Molecular sample preparation system, the Nuclisens assay (bioMarieux), and High Pure viral nucleic acid kit (Roche Applied Science)—were compared for VL quantification and PCR amplification for genotypic drug resistance testing on dried spots from spiked plasma and residual samples from HIV-1 patients (n= 47; median VL, 4.13 log10copies/ml). RNA recovery from DPS was efficient using Nuclisens extraction (median difference, 0.03 log10copies/ml) and slightly underestimated using the Abbott Molecular sample preparation system (median difference, 0.35 log10copies/ml). PCR amplification results were in concordance. Measurements from DBS overestimated VL for plasma, with VL results showing 10copies/ml. VL was stable for up to 3 months in spiked DPS stored at 20°C but for only 1 month at 37°C. A faster decline was observed in PCR efficiency: DPS could be stored for 1 week at 37°C and for 1 month at 20°C. In conclusion, the RNA extraction method is an important factor in obtaining reliable RNA quantification and PCR amplification of HIV-1 on DPS/DBS. DBS could be used as an alternative for DPS depending on HIV RNA cutoffs for virological failure. VL measurements remain stable over a longer period than do PCR amplification results.
Published: 2009
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25. Tipranavir-Ritonavir Genotypic Resistance Score in Protease Inhibitor-Experienced Patients

Author: Jacques Izopet, Gilles Peytavin, Chakib Alloui, Marie-Laure Chaix, Francis Barin, Diane Descamps, Bernard Masquelier, Georges Dos Santos, Anne Signori-Schmuck, Marc Lavignon, Annick Ruffault, Brigitte Montes, Vincent Calvez, Magali Bouvier-Alias, Corinne Amiel, Anne-Geneviève Marcelin, Charlotte Charpentier, and Philippe Flandre
Subjects: Male, Genotype, Anti-HIV Agents, Pyridines, medicine.medical_treatment, HIV Infections, Biology, medicine.disease_cause, Antiviral Agents, HIV Protease, Drug Resistance, Viral, medicine, Humans, HIV Protease Inhibitor, Pharmacology (medical), Protease inhibitor (pharmacology), Pharmacology, Sulfonamides, Mutation, Ritonavir, Protease, HIV Protease Inhibitors, Virology, Infectious Diseases, Pyrones, Enzyme inhibitor, HIV-1, biology.protein, Reverse Transcriptase Inhibitors, Drug Therapy, Combination, Female, Tipranavir, medicine.drug
Abstract: To identify mutations associated with the virological response (VR) to a tipranavir-ritonavir (TPV/r)-based regimen, 143 patients previously treated with protease inhibitor (PI) were studied. VR was defined by a decrease of at least 1 log10in, or undetectable, human immunodeficiency virus (HIV) RNA at month 3. The effect of each mutation in the protease, considering all variants at a residue as a single variable, on the VR to TPV/r was investigated. Mutations at six residues were associated with a lower VR (E35D/G/K/N, M36I/L/V, Q58E, Q61D/E/G/H/N/R, H69I/K/N/Q/R/Y, and L89I/M/R/T/V), and one mutation was associated with a higher VR (F53L/W/Y). The genotypic score M36I/L/V − F53L/W/Y + Q58E + H69I/K/N/Q/R/Y + L89I/M/R/T/V was selected as providing a strong association with VR. For the seven patients with a genotypic score of −1 (viruses with only mutation at codon 53), the percentage of responders was 100% and the percentages were 79%, 56%, 33%, 21%, and 0% for those with scores of 0, 1, 2, 3, and 4, respectively. The percentage of patients showing a response to TPV/r was lower for patients infected with non-clade B viruses (n= 16, all non-B subtypes considered together) than for those infected with clade B viruses (n= 127) (25% and 59%, respectively;P= 0.015). Most mutations associated with VR to TPV/r had not previously been associated with PI resistance. This is consistent with phenotypic analysis showing that TPV has a unique resistance profile. Mutations at five positions (35, 36, 61, 69, and 89) were observed significantly more frequently in patients infected with a non-B subtype than in those infected with the B subtype, probably explaining the lower VR observed in these patients.
Published: 2008
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26. Mutations Associated with Failure of Raltegravir Treatment Affect Integrase Sensitivity to the Inhibitor In Vitro

Author: Brigitte Montes, Jacques Reynes, Vincent Calvez, Cathia Soulié, Gilles Peytavin, Jean-François Mouscadet, Anne-Geneviève Marcelin, Marc-Antoine Valantin, Luba Tchertanov, Marc Wirden, Isabelle Malet, Olivier Delelis, and Christine Katlama
Subjects: Mutant, Integrase inhibitor, HIV Infections, HIV Integrase, Microbial Sensitivity Tests, Drug resistance, Biology, medicine.disease_cause, Antiviral Agents, Raltegravir Potassium, Drug Resistance, Viral, medicine, Humans, Pharmacology (medical), Amino Acid Sequence, HIV Integrase Inhibitors, Treatment Failure, Organic Chemicals, Gene, Pharmacology, Mutation, Viral Load, Raltegravir, Virology, Pyrrolidinones, Integrase, Infectious Diseases, Amino Acid Substitution, HIV-1, biology.protein, medicine.drug
Abstract: Raltegravir (MK-0518) is a potent inhibitor of human immunodeficiency virus (HIV) integrase and is clinically effective against viruses resistant to other classes of antiretroviral agents. However, it can select mutations in the HIV integrase gene. Nine heavily pretreated patients who received salvage therapy including raltegravir and who subsequently developed virological failure under raltegravir therapy were studied. For each patient, the sequences of the integrase-coding region were determined and compared to that at the beginning of the treatment. Four different mutation profiles were identified in these nine patients: E92Q, G140S Q148H, N155H, and E157Q mutations. For four patients, each harboring a different profile, the wild-type and mutated integrases were produced, purified, and assayed in vitro. All the mutations identified altered the activities of integrase protein: both 3′ processing and strand transfer activities were moderately affected in the E92Q mutant; strand transfer was markedly impaired in the N155H mutant; both activities were strongly impaired in the G140S Q148H mutant; and the E157Q mutant was almost completely inactive. The sensitivities of wild-type and mutant integrases to raltegravir were compared. The E92Q and G140S Q148H profiles were each associated with a 7- to 8-fold decrease in sensitivity, and the N155H mutant was more than 14-fold less sensitive to raltegravir. At least four genetic profiles (E92Q, G140S Q148H, N155H, and E157Q) can be associated with in vivo treatment failure and resistance to raltegravir. These mutations led to strong impairment of enzymes in vitro in the absence of raltegravir: strand transfer activity was affected, and in some cases 3′ processing was also impaired.
Published: 2008
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27. Comparison of the LCx Human Immunodeficiency Virus (HIV) RNA Quantitative, RealTime HIV, and COBAS AmpliPrep-COBAS TaqMan Assays for Quantitation of HIV Type 1 RNA in Plasma

Author: Marie-Noelle Didelot-Rousseau, Brigitte Montes, Michel Segondy, and Vincent Foulongne
Subjects: Microbiology (medical), Cobas taqman, Human immunodeficiency virus (HIV), HIV Infections, Biology, medicine.disease_cause, Polymerase Chain Reaction, Virus, law.invention, law, Virology, medicine, TaqMan, Humans, Polymerase chain reaction, virus diseases, RNA, Viral Load, biology.organism_classification, Molecular biology, Lentivirus, HIV-1, RNA, Viral, Reagent Kits, Diagnostic, Viral load
Abstract: The LCx human immunodeficiency virus (HIV) RNA Quantitative, RealTime HIV, and COBAS AmpliPrep-COBAS TaqMan assays for HIV type 1 (HIV-1) were compared for their abilities to quantitate HIV-1 RNA in plasma. High degrees of correlation and agreement were observed between the assays. Differences in HIV-1 RNA levels according to HIV-1 subtypes did not reach statistical significance.
Published: 2006
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28. Thalidomide for steroid-dependent immune reconstitution inflammatory syndromes during AIDS

Author: A. S. Brunel, Olivier Lortholary, Alain Makinson, Jacques Reynes, Edouard Tuaillon, Pierre-Alain Rubbo, Brigitte Montes, and Vincent Le Moing
Subjects: Adult, Male, medicine.drug_class, Immunology, Meningitis, Cryptococcal, Immune system, Acquired immunodeficiency syndrome (AIDS), Refractory, Immune reconstitution inflammatory syndrome, Immune Reconstitution Inflammatory Syndrome, Recurrence, Antiretroviral Therapy, Highly Active, medicine, Humans, Tuberculosis, Immunology and Allergy, Acquired Immunodeficiency Syndrome, AIDS-Related Opportunistic Infections, business.industry, Middle Aged, medicine.disease, Thalidomide, Steroid dependency, Treatment Outcome, Infectious Diseases, Corticosteroid, Female, Steroids, business, Meningitis, Immunosuppressive Agents, medicine.drug
Abstract: Management of relapsing or refractory immune reconstitution inflammatory syndromes (IRISs) despite corticosteroid therapy is yet to be defined. We describe three HIV-infected patients with corticosteroid-dependent and life-threatening paradoxical immune reconstitution inflammatory syndrome for whom thalidomide treatment induced rapid clinical remission and permitted complete corticosteroid withdrawal without clinical relapse.
Published: 2012
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29. Emergence of zidovudine and multidrug-resistance mutations in the HIV-1 reverse transcriptase gene in therapy-naive patients receiving stavudine plus didanosine combination therapy

Author: J. Puel, Jacques Reynes, Jacques Izopet, Isabelle Pellegrin, Michel Segondy, Hervé Fleury, Denayrolles M, Brigitte Montes, Patrice Massip, and Jean-Luc Pellegrin
Subjects: Adult, Combination therapy, Anti-HIV Agents, Immunology, Salvage therapy, HIV Infections, Biology, medicine.disease_cause, Zidovudine, medicine, Humans, Immunology and Allergy, Didanosine, Mutation, Stavudine, Viral Load, Virology, Drug Resistance, Multiple, HIV Reverse Transcriptase, Reverse transcriptase, Multiple drug resistance, Infectious Diseases, Reverse Transcriptase Inhibitors, Drug Therapy, Combination, medicine.drug
Abstract: Objective: Assessment of genotypic changes in the reverse transcriptase gene of HIV-1 occurring in antiretroviral naive patients treated by stavudine plus didanosine combination therapy. Methods: Sequence analysis (codons 1-230) was performed after amplification of the reverse transcriptase gene from plasma samples collected at baseline and at the end of treatment from 39 previously treatment-naive patients treated for 24-48 weeks. Results: At baseline, mutations associated with zidovudine resistance were detected in plasma from two patients: Asp67Asn/Lys219Gln and Leu210Trp. Among the 39 subjects, 18 (46%) developed mutations: one developed the Val75Thr/Ala mutation, four (10%) developed a Gln151Met multidrug-resistance mutation (MDR), associated in one of them with the Phe77Leu and the Phe116Tyr MDR mutations and 14 (36%) developed one or more zidovudine-specific mutations (Met41Leu, Asp67Asn, Lys70Arg, Leu210Trp, Thr215Tyr/Phe). The development of a Met41Leu zidovudine-specific mutation was associated with the development of a Gln151Met mutation in one patient. Other reverse transcriptase mutations known to confer resistance to nucleoside analogues were not detected. At inclusion, there was no statistical difference in HIV-1 load between patients who developed resistance mutations and those who did not. RNA HIV-1 load decrease was higher (P = 0.05) in patients who maintained a wild-type reverse transcriptase genotype (-2.22 log 10 copies/ml) than in patients who developed resistance mutations (-1.14 log 10 copies/ml). Conclusion: Stavudine/didanosine combination therapy is associated with emergence of zidovudine-related resistance or MDR mutations in naive patients. These findings should be considered when optimizing salvage therapy for patients who have received a treatment including stavudine/didanosine combination.
Published: 1999
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30. Significance of cytomegalovirus (CMV)‐pp65 antigenemia in the diagnosis of CMV disease in human immunodeficiency virus‐infected patients

Author: Nadine Atoui, Brigitte Montes, Jacques Reynes, and Michel Segondy
Subjects: Adult, Male, Neutrophils, viruses, Congenital cytomegalovirus infection, Cytomegalovirus, Retinitis, medicine.disease_cause, Virus, Herpesviridae, Viral Matrix Proteins, Betaherpesvirinae, Virology, Immunopathology, medicine, Humans, Sida, Antigens, Viral, AIDS-Related Opportunistic Infections, biology, business.industry, virus diseases, Middle Aged, Phosphoproteins, biology.organism_classification, medicine.disease, CD4 Lymphocyte Count, surgical procedures, operative, Infectious Diseases, Cytomegalovirus Infections, Immunology, HIV-1, Female, Viral disease, business, Follow-Up Studies
Abstract: To establish the diagnostic value of the cytomegalovirus (CMV)-pp65 antigenemia in CMV disease occurring in human immunodeficiency (HIV)-infected patients, CMV-pp65 antigen in polymorphonuclear leukocytes (PMNLs) was assayed in 373 samples from 138 randomly included patients followed up for symptomatic HIV-1 infection and the correlation between CMV-pp65 antigenemia and diagnosis of CMV disease was investigated. Thirty-seven CMV disease episodes were observed in 30 patients and 89.2% of these episodes were associated with a positive CMV-pp65 antigenemia. In contrast, 94% of the patients negative for CMV-pp65 antigenemia remained free of CMV disease. Patients with CMV disease had significantly higher levels of CMV-pp65 antigenemia than CMV disease-free patients (695 positive cells/2 x 10(5) PMNLs vs. 28 positive cells/2 x 10(5) PMNLs). The positive and negative predictive values of the test were 45% and 94%, respectively, but were 93% and 80%, respectively, when a CMV-pp65 antigenemia level of > 100 positive cells/2 x 10(5) PMNLs was taken into consideration. These results indicate that the CMV-pp65 antigenemia assay is useful for the diagnosis and monitoring of CMV disease in HIV-infected patients.
Published: 1996
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31. Impact of lopinavir/ritonavir use on antiretroviral resistance in recent clinical practice

Author: Sidonie, Lambert-Niclot, Bernard, Masquelier, Isabelle, Cohen Codar, Cathia, Soulie, Constance, Delaugerre, Laurence, Morand-Joubert, Charlotte, Charpentier, Virginie, Ferre, Jean-Christophe, Plantier, Brigitte, Montes, Sophie, Carret, Valerie, Perrot, Gilles, Peytavin, Dominique, Costagliola, Vincent, Calvez, Anne-Geneviève, Marcelin, A, Si-Mohamed, Epidémiologie, stratégies thérapeutiques et virologie cliniques dans l'infection à VIH, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de microbiologie [Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Laboratoire de Virologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Impacts de la puissance antivirale des antirétroviraux et de la résistance virale sur les stratégies thérapeutiques des infections par les virus de l'immunodéficience humaine, Université Paris Diderot - Paris 7 (UPD7), Centre hospitalier universitaire de Nantes (CHU Nantes), CHU Rouen, Normandie Université (NU), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Club Rhumatismes et Inflammation, Micro-Environnement et Régulation Cellulaire Intégrée (MERCI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Service de pharmacie, Unité de Mathématiques Pures et Appliquées (UMPA-ENSL), École normale supérieure de Lyon (ENS de Lyon)-Centre National de la Recherche Scientifique (CNRS), Numerical Medicine (NUMED), École normale supérieure de Lyon (ENS de Lyon)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Centre National de la Recherche Scientifique (CNRS)-Inria Grenoble - Rhône-Alpes, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Service de virologie et d'immunologie biologique, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service de bactériologie-virologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon), and Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Inria Grenoble - Rhône-Alpes
Subjects: Microbiology (medical), Adult, Male, medicine.medical_specialty, Genotype, Anti-HIV Agents, [SDV]Life Sciences [q-bio], protease inhibitors, Lopinavir/ritonavir, Fosamprenavir, HIV Infections, Microbial Sensitivity Tests, Gastroenterology, Lopinavir, 03 medical and health sciences, immune system diseases, Internal medicine, Drug Resistance, Viral, medicine, Humans, Pharmacology (medical), Protease inhibitor (pharmacology), Treatment Failure, Darunavir, 030304 developmental biology, Pharmacology, 0303 health sciences, Ritonavir, 030306 microbiology, business.industry, Proteolytic enzymes, virus diseases, Middle Aged, Viral Load, Virology, 3. Good health, Atazanavir, Infectious Diseases, Cross-Sectional Studies, resistance mutations, HIV-1, Female, France, business, medicine.drug
Abstract: International audience; Objectives This observational study was requested by French health authorities to determine the impact of lopinavir/ritonavir (Kaletra®) on antiretroviral resistance in clinical practice. Virological failures of lopinavir/ritonavir and their effects on the resistance to protease inhibitors and reverse transcriptase inhibitors were evaluated in protease inhibitor-experienced patients.Patients and methods Virological failure was defined as an HIV-1 plasma viral load >50 copies/mL after at least 3 months of lopinavir/ritonavir-containing antiretroviral therapy. For all patients, a resistance genotypic test was available at failure and before lopinavir/ritonavir treatment. Data from 72 patients with inclusion criteria were studied. Results The mean viral load at baseline was 4 log10 copies/mL (1.6–6.5). Mutations in the protease gene significantly selected between baseline and failure were L10V, K20R, L33F, M36I, I47V, I54V, A71V and I85V (P < 0.05). Patients who had more than seven protease inhibitor mutations at baseline showed a significantly increased risk of occurrence of protease inhibitor mutations. The proportion of viruses susceptible to atazanavir, fosamprenavir and darunavir decreased significantly between baseline and failure (P < 0.05). Among patients with a virus susceptible to atazanavir at day 0, 26% (n = 14) exhibited a virus resistant or possibly resistant at the time of failure. This proportion was 32% (n = 16) for fosamprenavir and 16% (n = 7) for darunavir. Conclusions A darunavir-based regimen appears to be a sequential option in the case of lopinavir/ritonavir failure. To compare and determine the best treatment sequencing, similar studies should be performed for darunavir/ritonavir and atazanavir/ritonavir.
Published: 2012
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32. Improved V3 genotyping with duplicate PCR amplification for determining HIV-1 tropism

Author: Hervé Fleury, Bernard Masquelier, P. André, Anne Maillard, Florence Nicot, Stéphanie Raymond, Jacques Izopet, Ali Si-Mohammed, Anne-Geneviève Marcelin, B. Masquelier, Françoise Brun-Vézinet, Michel Segondy, Diane Descamps, Jean-Claude Tardy, Muriel Macé, P. Recordon-Pinson, F. Nicot, V. Calvez, Mary-Anne Trabaud, A G Marcelin, Corinne Amiel, Adrien Saliou, Véronique Schneider, Catherine Tamalet, Pierre Delobel, Brigitte Montes, Mouna Lazrek, Laurence Morand-Joubert, Astrid Vabret, Coralie Pallier, Annick Ruffault, Patricia Recordon-Pinson, C Charpentier, Vincent Calvez, Cathia Soulié, Delphine Desbois, Virginie Ferré, Jacqueline Cottalorda, F. Flandre, S. Raymond, P. Delobel, E. Dussaix, Philippe Flandre, J. Izopet, Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT), Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Microbiologie Fondamentale et Pathogénicité (MFP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Service Maladies infectieuses et tropicales [CHU Toulouse], Pôle Inflammation, infection, immunologie et loco-moteur [CHU Toulouse] (Pôle I3LM Toulouse), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Virology Laboratory, Hospital, Service de microbiologie, 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), Epidémiologie, stratégies thérapeutiques et virologie cliniques dans l'infection à VIH, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Unité de Mathématiques Pures et Appliquées (UMPA-ENSL), École normale supérieure de Lyon (ENS de Lyon)-Centre National de la Recherche Scientifique (CNRS), Service de virologie et d'immunologie biologique, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Fédérale Toulouse Midi-Pyrénées, Laboratoire de Virologie, CHU Toulouse [Toulouse]-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Service des Maladies Infectieuses et Tropicales, École normale supérieure - Lyon (ENS Lyon)-Centre National de la Recherche Scientifique (CNRS), and VIROLOGIE
Subjects: Microbiology (medical), Adult, Male, Receptors, CXCR4, Genotype, education, HIV Infections, Biology, MESH: Phenotype, MESH: Receptors, CXCR4, law.invention, MESH: Genotype, MESH: HIV-1, 03 medical and health sciences, 0302 clinical medicine, law, MESH: Reverse Transcriptase Polymerase Chain Reaction, HIV tropism, Humans, Pharmacology (medical), 030212 general & internal medicine, Genotyping, Tropism, Polymerase chain reaction, Pharmacology, 0303 health sciences, MESH: Humans, MESH: Middle Aged, 030306 microbiology, Reverse Transcriptase Polymerase Chain Reaction, MESH: Adult, MESH: HIV Infections, Amplicon, Middle Aged, Virology, Molecular biology, MESH: Male, 3. Good health, Viral Tropism, Infectious Diseases, Phenotype, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Tissue tropism, HIV-1, Female, MESH: Female, MESH: Viral Tropism, Trofile assay
Abstract: International audience; OBJECTIVES: To determine whether genotyping of HIV-1 by duplicate PCR amplification of the region encoding the V3 loop is more sensitive than single PCR for detecting CXCR4-using viruses. PATIENTS AND METHODS: The V3 genotypes of the HIV-1 infecting 152 patients enrolled in the multicentre GenoTropism ANRS study were determined by all the participating laboratories using a single PCR and V3 bulk sequencing. In parallel, one laboratory determined the V3 genotype using duplicate PCR and bulk sequencing of pooled amplicons. HIV tropism was predicted with the geno2pheno10 algorithm. The phenotypes of all samples were determined with the Trofile assay and the Toulouse tropism test (TTT) recombinant virus assay. RESULTS: Geno2pheno10 was 56.8% sensitive and 75.9% specific when compared with the Trofile assay for detecting CXCR4-using viruses after a single PCR. Duplicate amplification and bulk sequencing of the pooled PCR amplicons increased the sensitivity to 68.2% and specificity to 79.6%. Geno2pheno10 was 64.1% sensitive and 77.0% specific when compared with the TTT assay for detecting CXCR4-using viruses after a single PCR. Duplicate amplification and sequencing of the pooled PCR amplicons increased sensitivity to 76.9% and specificity to 80.5%. CONCLUSIONS: The genotypic determination of HIV-1 tropism can be improved by duplicate amplifications and sequencing the pooled PCR products. This is a good compromise between improved sensitivity and reasonable cost for the genotype-based determination of tropism.
Published: 2011
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33. CXCR4 overexpression during the course of HIV-1 infection correlates with the emergence of X4 strains

Author: Yea-Lih, Lin, Pierre, Portales, Michel, Segondy, Vincent, Baillat, Corinne Merle, de Boever, Vincent, Le Moing, Brigitte, Réant, Brigitte, Montes, Jacques, Clot, Jacques, Reynes, and Pierre, Corbeau
Subjects: Adult, CD4-Positive T-Lymphocytes, Male, Receptors, CXCR4, Adolescent, Interleukin-7, Gene Expression, HIV Infections, Middle Aged, Viral Load, Virus Replication, CD4 Lymphocyte Count, Phenotype, HIV-1, Humans, Female, Chemokine CCL5, Aged
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, P0.001). 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

34. Comparison of drug resistance mutations and their interpretation in patients infected with non-B HIV-1 variants and matched patients infected with HIV-1 subtype B

Author: Jacques Reynes, Laurence Vergne, Martine Peeters, Brigitte Montes, Eric Delaporte, and Michel Segondy
Subjects: Male, AMPRENAVIR, ZIDOVUDINE, HIV Infections, Drug resistance, NEVIRAPINE, HIV Protease, Indinavir, Genotype, ABACAVIR, PHYLOGENIE, Pharmacology (medical), STAVUDINE, MUTATION, SIDA, SAQUINAVIR, NELFINAVIR, Middle Aged, TRANSCRIPTASE REVERSE, HIV Reverse Transcriptase, PREVALENCE, Infectious Diseases, SENSIBILITE RESISTANCE, VIRUS, DIDANOSINE, Female, medicine.drug, Adult, PROTEASE, Anti-HIV Agents, RITONAVIR, Biology, LAMIVUDINE, EFAVIRENZ, Zidovudine, Amprenavir, Drug Resistance, Viral, ETUDE COMPARATIVE, medicine, Humans, ZALCITABINE, LOPINAVIR, Genetic Variation, MEDICAMENT, DIVERSITE GENETIQUE, Virology, Reverse transcriptase, INDINAVIR, Immunology, Mutation, HIV-1, Ritonavir, Saquinavir
Abstract: Objective: To compare the prevalence of mutations associated with resistance to antiretroviral drugs and their interpretation in patients infected with non-B HIV-1 variants versus HIV-1subtype B–infected patients with similar treatment regimens. Methods: The reverse transcriptase (RT) and protease genes of HIV-1 were sequenced, and subtypes were determined by phylogenetic analysis. Each sequence belonging to a non-B variant was matched with a sequence belonging to subtype B. Patterns of resistance mutations were interpreted in terms of drug resistance using the HIV db algorithm. Results: RT mutations M41L, L210W, and, to a lesser extent, T215Y were less prevalent in patients infected with non-B variants. This lower prevalence was associated with subtypes A (A1/A2), C, F (F1/F2), and CRF06_cpx. A lower prevalence of high-level resistance to zidovudine was also observed in patients infected with these HIV-1 variants. In the protease gene, differences between patients infected with B or non-B strains were mainly observed for mutations playing a minor role in drug resistance and known to occur mainly as a natural polymorphism in non-B strains: K20R/M/I, M36I, L63P, A71V/T, and V77I. Interpretation of genotypes using the HIV db algorithm indicated that resistance to saquinavir, ritonavir, indinavir, and amprenavir was more frequently a high-level resistance for subtype B and an intermediate-level resistance for non-B variants, but this difference was only significant for amprenavir. Conclusion: Our results suggest that the genetic diversity of HIV-1 does not play a major role in the development of resistance to antiretroviral drugs.
Published: 2004

35. Prevalence of the mutational pattern E44D/A and/or V118I in the reverse transcriptase (RT) gene of HIV-1 in relation to treatment with nucleoside analogue RT inhibitors

Author: Michel Segondy and Brigitte Montes
Subjects: Nucleoside analogue, Reverse-transcriptase inhibitor, Genes, Viral, Anti-HIV Agents, Stavudine, Lamivudine, Deoxyribonucleosides, HIV Infections, Biology, Resistance mutation, Virology, Molecular biology, Reverse transcriptase, HIV Reverse Transcriptase, Nucleoside Reverse Transcriptase Inhibitor, Infectious Diseases, Mutagenesis, medicine, HIV-1, Prevalence, Humans, Reverse Transcriptase Inhibitors, Didanosine, medicine.drug
Abstract: It has been reported that a new pattern of mutations, E44D/A and/or V118I, in the reverse transcriptase (RT) gene of HIV-1 confers a moderate level of resistance to lamivudine in the absence of the M184V mutation. The prevalence of this mutational pattern was studied in HIV-1 isolates obtained from 280 patients. These mutations were not identified in the RT sequences from 23 antiretroviral-naive patients but were detected in 82 (31.9%) of the 257 RT sequences obtained from nucleoside reverse transcriptase inhibitors (NRTI)-experienced patients. Mutation at codon 44 was identified in 41 patients (7 mutations E44A and 34 mutations E44D), mutation V118I was identified in 73 patients and a combination of mutations at codons 44 and 118 was found in 32 patients. Multivariate analysis showed an association between the E44D/A and/or V118I mutational pattern and the RT mutations D67N, T69D, L210W, and T215Y/F. No relationship was observed between this mutational pattern and the lamivudine-specific resistance mutation M184V. The prevalence of these mutations increased significantly with the number of drug regimens experienced and a prevalence of 42.4% was observed in patients who had received >or= 4 antiretroviral regimens. A relationship was found between the E44D/A and/or V118I mutational pattern and experience with didanosine or stavudine but not with lamivudine. The results suggest that the development of the E44D/A and/or V118I mutational pattern is frequent in patients treated with NRTIs. Thymidine analogues and didanosine, but not lamivudine, could promote the development of these mutations.
Published: 2002

36. Phenotypic resistance pattern of HIV-1 isolates with zidovudine and/or multidrug resistance mutations after didanosine-stavudine combination therapy

Author: Patrice Massip, Jacques Izopet, Jean-Luc Pellegrin, Isabelle Pellegrin, Brigitte Montes, Jacques Reynes, Jacqueline Puel, Isabelle Garrigue, Michel Segondy, and Hervé Fleury
Subjects: Combination therapy, Anti-HIV Agents, HIV Infections, Zidovudine, Zalcitabine, Abacavir, medicine, Humans, Pharmacology (medical), Didanosine, business.industry, Stavudine, Lamivudine, Drug Resistance, Microbial, Viral Load, Virology, Drug Resistance, Multiple, HIV Reverse Transcriptase, Multiple drug resistance, Infectious Diseases, Phenotype, Mutation, HIV-1, Reverse Transcriptase Inhibitors, Drug Therapy, Combination, business, medicine.drug
Published: 2001

37. Patterns of resistance mutations to antiretroviral drugs in extensively treated HIV-1-infected patients with failure of highly active antiretroviral therapy

Author: Marie‐Noelle Didelot Rousseau, Martine Peeters, Michel Segondy, Eric Delaporte, Brigitte Montes, Jacques Reynes, and Laurence Vergne
Subjects: Time Factors, AMPRENAVIR, DNA Mutational Analysis, HIV Infections, Gene Frequency, HIV Protease, Indinavir, Abacavir, Antiretroviral Therapy, Highly Active, TECHNIQUE PCR, ABACAVIR, Pharmacology (medical), Treatment Failure, MUTATION, METHODE D'ANALYSE, Reverse-transcriptase inhibitor, SIDA, Stavudine, SAQUINAVIR, virus diseases, Drug Resistance, Microbial, NELFINAVIR, Viral Load, HIV Reverse Transcriptase, TRANSCRIPTASE REVERSE, Infectious Diseases, Phenotype, Algorithms, DDC, medicine.drug, ENZYME, Genotype, PROTEASE, Anti-HIV Agents, DDI, RITONAVIR, Biology, Zidovudine, Viral Proteins, medicine, ETUDE COMPARATIVE, Humans, Protease inhibitor (pharmacology), 3TC, D4T, ZDV, MEDICAMENT, ABT-378, Virology, GENE, INDINAVIR, Mutation, HIV-1, ETUDE EXPERIMENTALE, Ritonavir, Saquinavir, RESISTANCE
Abstract: Summary: Resistance-mutation pattems in the reverse transcriptase (RT) and protease ' genes of HIV-1 were analyzed in 22 patients who had been extensively prekeated and who failed to respond to highly active antiretroviral therapy (HAART). The number of mutations ranged from 8 to 19 (median, 13): 4 to 12 (median, 6) mutations in the RT gene, and 4 to 8 (median, 7) mutations in the protease gene. In the RT gene, the most frequent resistance mutations were found at codons 215 (loo%), 41 (95%), 67 (91%), and 210 (77%). Multidrug-resistant mutation pattems including QI5 1M and insertion mutations at codon 69, which confer cross-resistance to the different nucleoside ana- Iogue RT inhibitors were detected in l and 3 patients, respectively; l patient with insertion mutation displayed a NGQCV sequence at codons 67 to 70. In the protease gene, the most frequent mutations were found at codons 63 (95%), 10 (86%), 90(86%), 71(77%), 46 @O%), 36 (45%), and 84 (45%). Genotypic resistance to zidovudine, saquinavir, and indinavir was found in 100% of the patients. All patients showed also resistance or possible resistance to stavudine, abacavir, ritonavir, and nelfiavir. Mu- tations conferring genotypic resistance to nonnucleoside analogue RT inhibitors ("RTIs) were found in 12 (80%) of the "RTI-experienced patients and 1 of 7 NNRTI-naive patients. Our results indicate that failure of HAART in the patients extensively pretreated results from the multiplicity of RT and protease mutations that confer genotypic resistance to almost all available antiretroviral drugs. In these pa- tients, genotypic resistance tests confirm the lack of altemative salvage therapy strat- egies based on the currently available antiretroviral drugs. Key Words: Mutations- Genotypic resistance-Highly active antiretroviral therapy-Treatment fdure.
Published: 2001

38. Comparison of the QUANTIPLEX HIV-1 RNA 2.0 Assay with the AMPLICOR HIV-1 MONITOR 1.0 Assay for Quantitation of Levels of Human Immunodeficiency Virus Type 1 RNA in Plasma of Patients Receiving Stavudine-Didanosine Combination Therapy

Author: Jacques Reynes, Christophe Pasquier, Martine Peeters, Isabelle Pellegrin, Béatrice Dumon, Michel Segondy, J. Puel, Hervé Fleury, Brigitte Montes, and Jacques Izopet
Subjects: Microbiology (medical), Combination therapy, Anti-HIV Agents, Viremia, HIV Infections, Virus, Virology, medicine, Humans, Didanosine, biology, Stavudine, RNA, virus diseases, medicine.disease, biology.organism_classification, Molecular biology, Evaluation Studies as Topic, Lentivirus, HIV-1, RNA, Viral, Drug Therapy, Combination, Viral load, medicine.drug
Abstract: We compared the QUANTIPLEX HIV-1 RNA 2.0 assay with the AMPLICOR HIV-1 MONITOR 1.0 assay for quantitation of human immunodeficiency virus type 1 (HIV-1) RNA in plasma in the Stadi trail, which evaluated a stavudine plus didanosine combination therapy in 52 patients. HIV-1 RNA baseline values measured with AMPLICOR HIV-1 MONITOR 1.0 were significantly higher than those measured with QUANTIPLEX HIV-1 RNA 2.0, and decreases in HIV-1 RNA levels from baseline were also found to be significantly higher when measured with the AMPLICOR HIV-1 MONITOR 1.0 assay. The frequency of HIV-1 RNA levels below the lower limit of quantitation was significantly higher with QUANTIPLEX HIV-1 RNA 2.0 than with AMPLICOR HIV-1 MONITOR 1.0. Reanalysis of these results by an ultrasensitive procedure of AMPLICOR HIV-1 MONITOR 1.0 or by a modified version of the test that included additional primers adapted for non-B HIV-1 clades yielded greater differences between the QUANTIPLEX HIV-1 RNA 2.0 assay and the AMPLICOR HIV-1 MONITOR 1.0 assay. Our results indicate that a valid comparison of the virological efficacies obtained with different antiretroviral drug regimens requires the use of the same viral load quantitation procedure; further standardization between the different HIV-1 RNA quantitation kits is therefore needed.
Published: 1998

39. Evaluation of the Nuclisens HIV-1 QT assay for quantitation of human immunodeficiency virus type 1 RNA levels in plasma

Author: Brigitte Montes, Michel Segondy, Thoai-Duong Ly, and Martine Lapeyre
Subjects: Microbiology (medical), Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Sensitivity and Specificity, Virus, Lower limit, Virology, medicine, Humans, Viremia, biology, RNA, virus diseases, Reproducibility of Results, Nucleic acid amplification technique, biology.organism_classification, Molecular biology, NASBA, Evaluation Studies as Topic, Lentivirus, HIV-1, RNA, Viral, Viral load, Nucleic Acid Amplification Techniques
Abstract: Nuclisens HIV-1 QT is a new version of the NASBA HIV-1 QT assay for quantitation of human immunodeficiency virus type 1 (HIV-1) RNA in plasma. The specificity of this assay was 100% in one laboratory and 99%—with nonrepeatability of the initial false positive—in another. The test was linear between 2.0 and 6.0 log RNA copies per ml. According to the input HIV-1 RNA concentration, accuracy varied from −0.11 to +0.10 log RNA copy per ml and precision varied from 0.66 to 0.14 log RNA copy per ml. Reproducibility decreased when the HIV-1 RNA level was near the lower limit of quantitation of the test. HIV-1 RNA could be quantitated by Nuclisens HIV-1 QT in 36% (laboratory 1) and 24% (laboratory 2) of clinical samples with HIV-1 RNA levels lower than the lower limit of quantitation by NASBA HIV-1 QT. Nuclisens HIV-1 QT was not suitable for measurement of RNA from clade G and group O HIV-1 strains.
Published: 1998

40. Effect of HIV-1 genetic diversity on HIV-1 RNA quantification in plasma: comparative evaluation of three commercial assays

Author: Jacques Reynes, Eric Delaporte, Michel Segondy, Christiane Segarra, Martine Peeters, Joliette Coste, and Brigitte Montes
Subjects: Immunology, Human immunodeficiency virus (HIV), HIV Infections, Biology, medicine.disease_cause, Polymerase Chain Reaction, Hiv 1 rna, Comparative evaluation, Virology, ETUDE COMPARATIVE, medicine, Immunology and Allergy, Humans, VARIABILITE GENETIQUE, Cells, Cultured, DOSAGE, Genetics, Genetic diversity, PLASMA, SIDA, Genetic Variation, ARN, Evaluation Studies as Topic, HIV-1, RNA, Viral, Reagent Kits, Diagnostic
Published: 1997

41. Prevalence and Conditions of Selection of the K65R Mutation in the Reverse Transcriptase Gene of HIV-1

Author: Brigitte Montes and Michel Segondy
Subjects: Genes, Viral, Anti-HIV Agents, Organophosphonates, Human immunodeficiency virus (HIV), HIV Infections, Biology, Reverse transcriptase gene, medicine.disease_cause, Text mining, Gene Frequency, Drug Resistance, Viral, medicine, Humans, Point Mutation, Pharmacology (medical), Selection, Genetic, Tenofovir, Selection (genetic algorithm), Genetics, business.industry, Adenine, K65r mutation, HIV Reverse Transcriptase, Infectious Diseases, Amino Acid Substitution, HIV-1, Reverse Transcriptase Inhibitors, business
Published: 2005
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42. Comparative evaluation of three assays for the quantitation of human immunodeficiency virus type 1 RNA in plasma

Author: Joliette Coste, Christiane Segarra, Martine Peeters, Jacques Reynes, Michel Segondy, Brigitte Montes, Jean-Pierre Vendrell, and Eric Delaporte
Subjects: HIV Core Protein p24, HIV Infections, Biology, Polymerase Chain Reaction, Sensitivity and Specificity, Virus, law.invention, chemistry.chemical_compound, law, Virology, BDNA test, ETUDE COMPARATIVE, Humans, Viremia, Polymerase chain reaction, METHODE D'ANALYSE, SIDA, Nucleic acid sequence, RNA, virus diseases, Nucleic Acid Hybridization, Reproducibility of Results, NASBA, Molecular biology, CD4 Lymphocyte Count, ARN, Infectious Diseases, chemistry, Genetic Techniques, Evaluation Studies as Topic, HIV-1, VIRUS, RNA, Viral, VIH-1, Viral load, Nucleic Acid Amplification Techniques, DNA
Abstract: Reverse transcriptase-coupled polymerase chain reaction (Amplicor HIV-1 Monitor), the branched DNA (bDNA) method (Quantiplex HIV-1 RNA) and the nucleic acid sequence-based assay (NASBA HIV-1 RNA QT) were comparatively evaluated for the quantitation of human immunodeficiency virus type 1 (HIV-1) RNA in plasma. Among 60 plasma specimens from HIV-1 infected patients, HIV-1 RNA was detected in 56 by Amplicor (sensitivity, 93.3 %), in 41 by bDNA (sensitivity, 68.3 %), and in 60 by NASBA (sensitivity, 100 %). HIV-1 RNA was not detected by any of these methods in 34/34 plasma specimens from HIV-1-seronegative blood donors (specificity, 100 %). The HIV-1 RNA levels as determined by the different methods were correlated significantly. The frequency of concordant results (log difference less than 0.50) was 80.4 % between Amplicor and NASBA, 77.5 % between Amplicor and bDNA, and 58.6 % between bDNA and NASBA. After initiation of antiviral therapy, HIV-1 RNA level variations observed with the three methods were similar. HIV-1 RNA levels were inversely correlated with the CD4+ T cell counts, whereas no correlation was found with HIV-1 p24-antigen levels. When the methods were evaluated for reproducibility, coefficients of variation ranged from 11 % to 40 % for Amplicor, from 6 % to 35 % for bDNA, and from 13 % to 62 % for NASBA. Quantitation of HIV-1 RNA in culture supernatants from HIV-1 subtype A to H strains showed that bDNA can be used to quantitate RNA from all HIV-1 subtypes, whereas Amplicor failed to detect RNA from subtype A strains and NASBA subtype G strains. (Résumé d'auteur)
Published: 1996

43. Amino Acid Substitutions at Position 69 of the Reverse Transcriptase of Human Immunodeficiency Virus Type 1 Are Frequent in Zalcitabine-Naive Antiretroviral-Drug-Experienced Patients

Author: Michel Segondy and Brigitte Montes
Subjects: Genotype, HIV Infections, Biology, medicine.disease_cause, Zidovudine, Zalcitabine, medicine, Humans, Pharmacology (medical), Codon, Letter to the Editor, Didanosine, Pharmacology, chemistry.chemical_classification, Mutation, Stavudine, Genetic Variation, Drug Resistance, Microbial, Virology, HIV Reverse Transcriptase, Reverse transcriptase, Amino acid, Infectious Diseases, chemistry, HIV-1, Reverse Transcriptase Inhibitors, medicine.drug
Abstract: Winters and Merigan recently reported interesting results showing that several amino acid substitutions encoded by codon 69 of the human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT) gene affect susceptibility to nucleoside-nucleotide analog RT inhibitors (NRTIs) (5). While it is classically considered that the T69D/N mutation confers resistance to zalcitabine (dideoxycytidine [ddC]) (1), we have demonstrated, and Winters and Merigan have confirmed, that this mutation can be identified in ddC-naive individuals (4). On the basis of this observation, we have further analyzed the amino acid substitutions at position 69 in the RT sequences obtained routinely in our laboratory; amino acid insertions or deletions at this position have not been considered in this study. After exclusion of the patients tested after treatment interruption, 789 RT sequences were available for analysis: 34 from antiretroviral-naive patients and 755 from antiretroviral-experienced patients. Among the antiretroviral-experienced patients, 50 (6.6%) had received one antiretroviral regimen, 444 (58.8%) had received two or three antiretroviral regimens, and 261 (34.6%) had received four or more antiretroviral regimens; 3 (0.4%) had received one NRTI, 58 (7.7%) had received two NRTIs, 89 (11.8%) had received three NRTIs, 221 (29.3%) had received four NRTIs, 235 (31.1%) had received five NRTIs, 145 (19.2%) had received six NRTIs, and 4 (0.5%) had received seven NRTIs. Amino acid substitutions at position 69 were not found in sequences from the NRTI-naive patients but were found in those from 116 (15.4%) NRTI-experienced patients: 71 patient sequences (61.2%) had T69D mutations, 28 (24.1%) had T69N mutations, 7 (6.0%) had T69S mutations, 4 (3.4%) had T69A mutations, 3 (2.6%) had T69E mutations, and 1 each (0.9%) had T69G, T69I, and T69L mutations. The prevalence of amino acid substitutions at position 69 increased significantly with the number of drug regimens that a patient received (P = 0.0002), since a prevalence of 8.0% was observed in patients who had received one treatment regimen and a prevalence of 21.8% was observed in patients who had received four or more treatment regimens. A significant relationship (P = 0.01) between the prevalence of amino acid substitutions at position 69 and the number of NRTIs that a patient received was also observed. A multivariate logistic-regression analysis showed that the number of antiretroviral drug regimens that a patient received was the sole factor independently related to amino acid substitutions at position 69. However, when only the D and N substitutions were considered, a significant relationship (P = 0.03) between the T69D/N mutation and experience with didanosine (ddI) was observed (data not shown). There was no significant relationship between D/N (P = 0.26) or other amino acid substitutions (P = 0.13) at position 69 and experience with ddC. By univariate analysis, amino acid substitutions at position 69 were significantly associated with mutations at positions 44, 67, 70, 118, 210, 215, and 219, whereas a borderline significance was observed for the association with the L74V mutation (Table (Table1).1). By multivariate analysis, however, only E44D/A (P = 0.02), D67N (P < 0.0001), and V118I (P = 0.0001) remained significantly associated with amino acid substitutions at position 69. By focusing on the D and N substitutions, a significant association was observed with the T69D/N mutation and the Q151M mutation (P = 0.004). TABLE 1. Association of the amino acid substitutions at position 69 with other NRTI resistance mutations in 789 sequences These results indicate that amino acid substitutions (mainly T→D and T→N) are common in multi-NRTI-experienced patients, that the prevalence of these mutations increases with the number of NRTI combination regimens received, and that previous ddI rather than ddC experience could be a factor of selection of the T69D/N mutations in multi-NRTI-treated pa-tients. These conditions of selection are also supported by the association observed between amino acid substitutions at position 69 and the E44A/D, V118I, and Q151M mutations, which are also known to be associated with multiple NRTI experience, including experience with ddI (2, 3). Amino acid substitutions were also closely associated with the D67N mutation, which is located in the same β3-β4 hairpin loop (positions 67 to 70) region of the RT; this association suggests that interactions exist between these mutations. Our results, in agreement with those reported by Winters and Merigan (5), indicate that amino acid substitutions at position 69 may be selected for by ddC-free antiretroviral regimens. These mutations could therefore be involved in resistance to NRTIs other than ddC. This is supported by the findings of Winters and Merigan that show that different substitutions at position 69 confer reduced susceptibility to zidovudine, ddI, and stavudine. The T69D/N mutation is currently taken into consideration for interpreting resistance to ddI (low-level resistance) and stavudine (potential low-level resistance) by using the Stanford HIV RT and protease sequence database algorithm (http://hivdb.stanford.edu). However, more effort is needed to accurately interpret HIV-1 genotypes that encode amino acid sub-stitutions at position 69. In particular, the effect of the different amino acid substitutions at this position and the interactions of these substitutions with the other NRTI resistance-associated mutations remain poorly documented.
Published: 2002
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44. Changes in HIV-1 RNA Plasma Level in Patients Treated with Foscarnet

Author: Christine Leclercq, Benedicte Delmas, Brigitte Montes, Jacques Reynes, Michel Segondy, and François Janbon
Subjects: Foscarnet, Anti-HIV Agents, business.industry, Immunology, HIV Infections, Plasma levels, Virology, Hiv 1 rna, Cytomegalovirus Retinitis, HIV-1, Humans, RNA, Viral, Immunology and Allergy, Medicine, In patient, business, medicine.drug
Published: 1997
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45. HIV-1-infected patients from the French National Observatory experiencing virological failure while receiving enfuvirtide.

Author: Diane Descamps, Lambert Assoumou, Bernard Masquelier, Anne-Geneviève Marcelin, Souhila Saidi, Catherine Tamalet, Jacqueline Cottalorda, Jean-Christophe Plantier, Brigitte Montes, Jacques Izopet, Gilles Peytavin, Sabine Yerly, Véronique Schneider, Constance Delaugerre, Virginie Ferré, Annick Ruffault, Coralie Pallier, Laurence Morand-Joubert, Marie-Laure Chaix, and Vincent Calvez
Subjects: HIV-positive persons, PATIENTS, HIV infections, AIDS patients
Abstract: : Objectives We studied gp41 mutations associated with failing enfuvirtide salvage therapy. : Methods This multicentre study involved patients with HIV-1 plasma viral load (pVL) > 5000 copies/mL after at least 3 months of uninterrupted enfuvirtide therapy and with plasma samples available at inclusion (T0), at initial enfuvirtide failure (T1) and at last follow-up visit during continued failing enfuvirtide therapy (T2). The HR-1 and HR-2 domains of the gp41 gene were sequenced at T0, T1 and T2. : Results Ninety-nine patients were enrolled. At baseline, the median pVL and CD4 cell count were 5.1 log copies/mL and 72 cells/mm3, respectively. Based on the ANRS Resistance Group algorithm, the proportion of patients harbouring viruses with enfuvirtide resistance mutations increased significantly between T0 and T1. In the HR-1 domain, the V38A/M, Q40H, N42T, N43D and L45M mutations wereselected (P < 0.02). In the HR-2 domain, no mutations were significantly selected during the follow-up. None of the mutations was associated with a CD4 cell count increment. : Conclusions Mutations selected during failing enfuvirtide salvage therapy are mainly located in the HR-1 domain of the gp41 gene, between codons 38 and 45. No mutations were associated with an increase in the CD4 cell count. [ABSTRACT FROM AUTHOR]
Published: 2008

46. Nasopharyngeal and serological anti SARS-CoV-2 IgG/IgA responses in COVID-19 patients

Author: Sylvie van der Werf, Caroline Demeret, Bernadette Crescenzo-Chaigne, Lila Bouadma, Jade Ghosn, Vincent Enouf, Sarah Tubiana, Stéphane Petres, Marie Noelle Ungeheuer, Sylvie Behillil, Nicolas Escriou, Génétique Moléculaire des Virus à ARN - Molecular Genetics of RNA Viruses (GMV-ARN (UMR_3569 / U-Pasteur_2)), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPC), Centre National de Référence des virus des infections respiratoires (dont la grippe) - National Reference Center Virus Influenzae [Paris] (CNR), Institut Pasteur [Paris], Plateforme de Microbiologie Mutualisée (PIBnet) - Mutualized Platform for Microbiology (P2M), Laboratoire d’innovation : vaccins – Innovation lab : vaccines, Plateforme technologique Production et purification de protéines recombinantes – Production and Purification of Recombinant Proteins Technological Platform (PPR), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Investigation Clinique et d’Accès aux Ressources Biologiques (Plate-forme) - Clinical Investigation and Access to BioResources (ICAReB), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPC)-Université Sorbonne Paris Nord, Services de Maladies Infectieuses et Tropicales [CHU Bichat], AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre d'Investigations Cliniques [CHU Bichat] (CIC plurithématique), This work was supported by the « URGENCE COVID-19 » fundraising campaign of Institut Pasteur, by REACTING (Research & Action Emerging Infectious Diseases) and by the H2020 project 101003589 (RECOVER). The French Covid Cohort is funded through the Ministry of Health and Social Affairs (PHRC n°20-0424) and Ministry of Higher Education and Research dedicated COVID19 fund., List of the membership of the French COVID cohort study group : Mélanie RORIZ, Patrick RISPAL, Sarah REDL (CHG d'Agen), Laurent LEFEBVRE, Pascal GRANIER, Laurence MAULIN (CH du Pays d'Aix, Aix en Provence), Cédric JOSEPH, Julien MOYET, Sylvie LION-DAOLIO (CHU Amiens Nord), Rafael MAHIEU, Alexandra DU-CANCELLE, Vincent DUBEE (CHU d'Angers), Stéphane SALLA-BERRY, Aldric MANUEL, Gabriel MACHEDA, Mylène MAILLET, Bruno CHANZY (CH d'Annecy Genevois), Jean-Charles GAGNARD (Hôpital privé d'Antony), Guillermo GIORDANO, Clara MOUTON PERROT, Vincent PESTRE (CH Henri Duffaut, Avignon), Cécile FICKO, Marie GOMINET, Aurore BOUSQUET (Hôpital d'instruction des armées Begin), Charline VAUCHY, Kévin BOUILLER, Maïder PAGADOY, Solène MARTY-QUINTERNET, Quentin LEPILLER (CHU Jean Minjoz, Besançon), Cyril LE BRIS, Benoit THILL, Marie-Laure CASANOVA, Georges LE FALHER, Eric OZIOL (CH de Béziers), Hugues CORDEL, Nathalie DOURNON, Olivier BOUCHAUD, Ségolène BRICHLER (Hôpital Avicenne, Bobigny), Duc NGUYEN, Pantxika BELLECAVE, Camille CICCONE, Marie-Edith LAFON (CHU Pellegrin, Bordeaux), Ségolène GREFFE (CHU Ambroise Paré, Boulogne Billancourt), Camille BOUISSE, Nicholas SEDILLOT, Damien BOUHOUR (CH Fleyriat, Bourg en Bresse), Camille CHASSIN (CH Pierre Oudot, Bourgoin-Jallieu), Erwan L'HER, Séverine ANSART, Cécile TROMEUR, Dewi GUELLEC (CHRU de Brest), Antoine MERCKX (CH de Cahors), Felix DJOSSOU (CH Andrée Rosemon, Cayenne), Vincent PEIGNE, Carola PIEROBON, Marie-Christine CARRET, Florence JEGO, Margaux ISNARD (CHMS Chambéry NH), Johann AUCHABIE, Roxane COURTOIS (CH de Cholet), Olivier LESENS (CHU Gabriel Montpied, Clermont-Ferrand), Martin MARTINOT (Hôpital Pasteur, Colmar), Olivier PICONE (Hôpital Louis Mourier, Colombes), Marie LACOSTE (CH Alpes Leman Contamine sur Arve), Brigitte ELHAR-RAR, Valérie GARRAIT, Isabelle DELACROIX, Thomas MAITRE, Jean Baptiste ASSIE (Centre Hospitalier Intercommunal de Créteil), Elsa NYAMANKOLLY (CH de Dax), François Xavier CATHERINE, Ma-thieu BLOT, Sophie MAHY, Marielle BUISSON, Lionel PIROTH, Florence GUILLOTIN, Alexis DE ROUGEMONT (CHU de Dijon Bourgogne), Valentine CAMPANA, Jérémie PASQUIER, André CABIE (CHU de Martinique, Fort de France), Simon BESSIS (Hôpital Raymond Poincaré, Garches), Olivier EPAULARD, Nicolas TERZI, Jean-François PAYEN, Laurence BOUILLET, Rebecca HAMIDFAR, Marion Le MARECHAL (CHU de Grenoble), Moïse MACHADO, Audrey BARRELET, Alexandra BEDOSSA (Grand Hôpital de l'Est Francilien site Marne-la-Vallée, Jossigny), Gwenhaël COLIN, Romain DECOURS, Thomas GUIMARD (CHD Les Oudairies, La Roche Sur Yon), Cécile GOUJARD, Stéphane JAUREGUIBERRY, Antoine CHERET (Hôpital Universitaire Bicêtre, Le Kremlin-Bicêtre), Anne Sophie RESSEGUIER (CH Emile Roux, Le Puy en Velay), Julien POISSY, Daniel MATHIEU, Saad NSEIR, Ilka ENGELMANN, Martine REMY (CHRU de Lille, Hôpital Salengro), Fanny VUOTTO, Benoit GACHET, Karine FAURE, Marielle BOYER-BESSEYRE, Kazali Enagnon (CHRU de Lille, Hôpital Fourrier), Marc LAMBERT, Arnaud SCHERPEREEL, Dominique DEPLANQUE, Stéphanie FRY, Cécile YELNIK (CHRU de Lille, Hôpital Albert Calmette), Laurent BITKER, Mehdi MEZIDI, Hodane YONIS, Nicolas BENECH, Thomas PERPOINT, Anne CONRAD, Vinca ICARD, Martine VALETTE (Hôpital de la Croix Rousse, Lyon), Simon-Djamel THIBERVILLE (Hôpital Louis Raffalli, Manosque), Stanislas REBAUDET (Hôpital Européen de Marseille), Bertrand DUSSOL (Hôpital Conception, Marseille), Sylvain DIAMANTIS, Catherine CHAKVEATZE, Clara FLATEAU (Groupe Hospitalier Sud Ile De France, hôpital de Melun), Vincent DINOT, Rostane GACI, Nadia OUAMARA (Hôpital de Mercy, CHR Metz-Thionville, Ars laquenexy), Hajnal-Gabriela ILLES, Louis GER-BAUD MORLAES, Jérôme DIMET (CH de Mont Marsan), Vincent LE MOING, Nathalie PANSU, Clément LE BIHAN, Brigitte MONTES (CHU de Montpellier), Anne Sophie BOUREAU, Clotilde ALLAVENA, Sabelline BOUCHEZ, Romain GUERY, Paul LE TURNIER, Cécile MEAR-PASSARD, Virginie FERRE (CHU de Nantes), Christophe RAPP (Hôpital Américain de Paris, Neuilly sur Seine), Elisa DE-MONCHY, Céline MICHELANGELLI, Karine RISSO (CHU de Nice), Paul LOUBET, Jean-Phillippe LAVIGNE (CHU Caremeau, Nîmes), Etienne DE MONTMOLLIN, Juliette PATRIER, Paul Henri WICKY, Lucie LE FEVRE, Pierre JACQUET, Raphael BORIE, Antoine DOSSIER, Dominique LUTON, Valentina ISERNIA, Sylvie LE GAC (Hôpital Bichat, Paris), Cécile AZOULAY, Nicolas CARLIER, Liem LUONG, Marie LACHATRE, Odile LAUNAY (Hôpital Cochin, Paris), Younes KERROUMI, Vanina MEYSSONNIER (Groupe Hospitalier Diaconesses Croix Saint-Simon, Paris), Jean-Luc DIEHL, Jean-Sébastien HULOT, Bernard CHOLLEY, Jean-Benoît ARLET, Olivier SANCHEZ (Hôpital Européen Georges Pompidou, Paris), Victoria MANDA, Laurène AZEMAR, Guylaine CASTOR-ALEXANDRE (Hôpital Lariboisière, Paris), Karine LACOMBE, Thibault CHIARABINI, Bénédicte LEFEBVRE, Laurence MORAND-JOUBERT, Djeneba FOFANA, Aurélie SCHNURIGER (Hôpital Saint Antoine, Paris), Nathalie DE CASTRO, Constance DELAUGERRE, Marie-Laure CHAIX (Hôpital Saint Louis, Paris), Julie CHAS (Hôpital Tenon, Paris), Valérie GABORIEAU, Eve LE COUSTUMIER, Walter PICARD (CH de Pau), Jean-Benoît ZABBE, Florent PEELMAN, Edouard SOUM (CH de Périgueux), Hugues AUMAÎTRE (CH de Perpignan), Elodie CURLIER, Rachida OUISSA, Isabelle FABRE (CHU de Pointe à Pitre, Guadeloupe), Blandine RAMMAERT (CHU de Poitiers), Nadia SAIDANI (CH Quimper), Firouzé BANI-SADR, Maxime HENTZIEN, Yohan N 'GUYEN, Juliette ROMARU, Kévin DIDIER (CHU Reims), Isabelle ENDERLE, Vincent THIBAULT, Fabrice LAINE, Matthieu LESOU-HAITIER, Matthieu REVEST, Pierre TATTEVIN (CHU Rennes), Jean-Christophe PLANTIER, Manuel ETIENNE, Véronique LEMEE, Eglantine FERRAND DEVOUGE, Kévin ALEXANDRE, Elise ARTAUD-MACCARI (CHU Rouen), Nathalie ALLOU, Marie LAGRANGE, Julien JABOT (CH Saint Denis et Saint Pierre, La réunion), Benoît ROZE, Delphine BREGEAUD, Younes AIT TAMLIHAT (CH Saintes), Ali HACHEMI (CH Soisson), Hélène SALVATOR, Erwan FOURN, David ZUCMAN (Hôpital Foch, Suresnes), Eric DELAVEUVE, Coline JAUD-FISCHER, Paul DUNAND (Hôpital Bel Air, Thionville), François BISSUEL (CH Thonon les Bains), Karen DELAVIGNE, Marie PIEL-JULIAN, Pierre DELOBEL, Benjamine SARTON, Marie RAFIQ, Guillaume MARTIN-BLONDEL, Laurent GUILLEMINAULT, Marlène MURRIS, Agnès SOMMET (CHU de Toulouse), Eric SENNEVILLE, Olivier ROBINEAU, Agnès MEYBECK (CH Tourcoing), Denis GAROT, Laurent PLANTIER, Valérie GISSOT, Julien MARLET, Karl STEFIC, Catherine GAUDY-GRAFFIN, Francis BARIN, Adrien LEMAIGNEN (CHU Bretonneau, Tours), Grégory CORVAISIER, Delphine LARIVIERE, Marie LANGELOT-RICHARD (CH Vannes), Elisabeth BOTELHO-NEVERS , Amandine GAGNEUX-BRUNON, Tiffany TROUILLON, Thomas BOURLET, Thomas BOURLET, Sylvie PILLET, Bruno POZZETTO (CHU de St Etienne), Antoine KIMMOUM, Bruno LEVY, Mathieu MATTEI, François GOEHRINGER, Christian RABAUD, Sibylle BEVILACQUA, Benjamin LEFEVRE, Anne GUILLAUMOT, Véronique VENARD, Hélène JEULIN, Evelyne SCHVOERER, Cédric HARTARD (CHU de Nancy, Vandoeuvre les Nancy), Pauline CARAUX PAZ, Laurent RICHIER, Mohamed EL SANHARAWI (CH Villeneuve St Georges)., European Project: 101003589, H2020-SC1-PHE-CORONAVIRUS-2020,RECOVER(2020), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre National de Référence des virus des infections respiratoires (dont la grippe) - National Reference Center Virus Influenzae [Paris] (CNR - laboratoire coordonnateur), Institut Pasteur [Paris] (IP), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Université Sorbonne Paris Nord
Subjects: Coronavirus disease 2019 (COVID-19), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), [SDV]Life Sciences [q-bio], Severe disease, Infectious and parasitic diseases, RC109-216, Article, Serology, 03 medical and health sciences, 0302 clinical medicine, Medicine, Mucosal Immunity, 030304 developmental biology, 0303 health sciences, biology, 030306 microbiology, business.industry, Epithelium, 3. Good health, Nucleoprotein, medicine.anatomical_structure, Antibody response, SARS CoV, 030220 oncology & carcinogenesis, Immunology, biology.protein, Antibody, business
Abstract: BackgroundThe systemic antibody responses to SARS-CoV-2 in COVID-19 patients has been extensively studied. However, much less is known about the mucosal responses in the upper airways at the site of initial SARS-CoV-2 replication. Local antibody responses in the nasopharyngeal epithelium, that are likely to determine the course of infection, have not been analysed so far nor their correlation with antibody responses in serum.MethodsThe IgG and IgA antibody responses were analysed in the plasma as well as in nasopharyngeal swabs (NPS) from the first four COVID-19 patients confirmed by RT-qPCR in France. Two were pauci-symptomatic while two developed severe disease. Taking advantage of a comprehensive series of plasma and nasopharyngeal samples, we characterized their antibody profiles from the second week post symptoms onset, by using an in-house ELISA to detect anti-SARS-CoV-2 Nucleoprotein (N) IgG and IgA.ResultsAnti-N IgG and IgA antibodies were detected in the NPS of severe patients. Overall, the levels of IgA and IgG antibodies in plasma and NPS appeared specific to each patient.ConclusionsAnti-N IgG and IgA antibodies are detected in NPS, and their levels are related to antibody levels in plasma. The two patients with severe disease exhibited different antibody profiles that may reflect different disease outcome. For the pauci-symptomatic patients, one showed a low anti-N IgG and IgA response in the plasma only, while the other one did not exhibit overt serological response.
Published: 2021
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47. Global and regional molecular epidemiology of HIV-1, 1990–2015: a systematic review, global survey, and trend analysis

Author: Hemelaar, Joris, Elangovan, Ramyiadarsini, Yun, Jason, Dickson-Tetteh, Leslie, Fleminger, Isabella, Kirtley, Shona, Williams, Brian, Gouws-Williams, Eleanor, Ghys, Peter D, Abimiku, Alash'le G, Agwale, Simon, Archibald, Chris, Avidor, Boaz, Barbás, María Gabriela, Barre-Sinoussi, Francoise, Barugahare, Banson, Belabbes, El Hadj, Bertagnolio, Silvia, Birx, Deborah, Bobkov, Aleksei F, Brandful, James, Bredell, Helba, Brennan, Catherine A, Brooks, James, Bruckova, Marie, Buonaguro, Luigi, Buonaguro, Franco, Buttò, Stefano, Buve, Anne, Campbell, Mary, Carr, Jean, Carrera, Alex, Carrillo, Manuel Gómez, Celum, Connie, Chaplin, Beth, Charles, Macarthur, Chatzidimitriou, Dimitrios, Chen, Zhiwei, Chijiwa, Katsumi, Cooper, David, Cunningham, Philip, Dagnra, Anoumou, de Gascun, Cillian F, Del Amo, Julia, Delgado, Elena, Dietrich, Ursula, Dwyer, Dominic, Ellenberger, Dennis, Ensoli, Barbara, Essex, Max, Gao, Feng, Fleury, Herve, Fonjungo, Peter N, Foulongne, Vincent, Gadkari, Deepak A, García, Federico, Garsia, Roger, Gershy-Damet, Guy Michel, Glynn, Judith R, Goodall, Ruth, Grossman, Zehava, Lindenmeyer-Guimarães, Monick, Hahn, Beatrice, Hamers, Raph L, Hamouda, Osamah, Handema, Ray, He, Xiang, Herbeck, Joshua, Ho, David D, Holguin, Africa, Hosseinipour, Mina, Hunt, Gillian, Ito, Masahiko, Bel Hadj Kacem, Mohamed Ali, Kahle, Erin, Kaleebu, Pontiano Kaleebu, Kalish, Marcia, Kamarulzaman, Adeeba, Kang, Chun, Kanki, Phyllis, Karamov, Edward, Karasi, Jean-Claude, Kayitenkore, Kayitesi, Kelleher, Tony, Kitayaporn, Dwip, Kostrikis, Leondios G, Kucherer, Claudia, Lara, Claudia, Leitner, Thomas, Liitsola, Kirsi, Lingappa, Jai, Linka, Marek, Lorenzana de Rivera, Ivette, Lukashov, Vladimir, Maayan, Shlomo, Mayr, Luzia, McCutchan, Francine, Meda, Nicolas, Menu, Elisabeth, Mhalu, Fred, Mloka, Doreen, Mokili, John L, Montes, Brigitte, Mor, Orna, Morgado, Mariza, Mosha, Fausta, Moussi, Awatef, Mullins, James, Najera, Rafael, Nasr, Mejda, Ndembi, Nicaise, Neilson, Joel R, Nerurkar, Vivek R, Neuhann, Florian, Nolte, Claudine, Novitsky, Vlad, Nyambi, Philippe, Ofner, Marianna, Paladin, Fem J, Papa, Anna, Pape, Jean, Parkin, Neil, Parry, Chris, Peeters, Martine, Pelletier, Alexandra, Pérez-Álvarez, Lucía, Pillay, Deenan, Pinto, Angie, Quang, Trinh Duy, Rademeyer, Cecilia, Raikanikoda, Filimone, Rayfield, Mark A, Reynes, Jean-Marc, Rinke de Wit, Tobias, Robbins, Kenneth E, Rolland, Morgane, Rousseau, Christine, Salazar-Gonzales, Jesus, Salem, Hanan, Salminen, Mika, Salomon, Horacio, Sandstrom, Paul, Santiago, Mario L, Sarr, Abdoulaye D, Schroeder, Bryan, Segondy, Michel, Selhorst, Philippe, Sempala, Sylvester, Servais, Jean, Shaik, Ansari, Shao, Yiming, Slim, Amine, Soares, Marcelo A, Songok, Elijah, Stewart, Debbie, Stokes, Julie, Subbarao, Shambavi, Sutthent, Ruengpung, Takehisa, Jun, Tanuri, Amilcar, Tee, Kok Keng, Thapa, Kiran, Thomson, Michael, Tran, Tyna, Urassa, Willy, Ushijima, Hiroshi, van de Perre, Philippe, van der Groen, Guido, van Laethem, Kristel, van Oosterhout, Joep, van Sighem, Ard, van Wijngaerden, Eric, Vandamme, Anne-Mieke, Vercauteren, Jurgen, Vidal, Nicole, Wallace, Lesley, Williamson, Carolyn, Wolday, Dawit, Xu, Jianqing, Yang, Chunfu, Zhang, Linqi, Zhang, Rong, John Radcliffe Hospital [Oxford University Hospital], Centre for Statistics in Medicine, University of Oxford [Oxford], Stellenbosch University, UNAIDS [Genève, Suisse] (ONUSIDA), Institut Pasteur [Paris], Noguchi Memorial Institute for Medical Research [Accra, Ghana] (NMIMR), University of Ghana, Institute of Tropical Medicine [Antwerp] (ITM), State Key Laboratory of Silkworm Genome Biology, Southwest University, Commissariat à l'énergie atomique et aux énergies alternatives - Laboratoire d'Electronique et de Technologie de l'Information (CEA-LETI), Direction de Recherche Technologique (CEA) (DRT (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Georg-Speyer-Haus, The University of Sydney, National AIDS Centre, Istituto Superiore di Sanita [Rome], Harvard School of Public Health, Digital Enterprise Research Institute (DERI-NUIG), National University of Ireland [Galway] (NUI Galway), Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Pathogénèse et contrôle des infections chroniques (PCCI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre Hospitalier Universitaire de Montpellier (CHU Montpellier ), Departments of Medicine and Microbiology, University of Alabama at Birmingham [ Birmingham] (UAB), Robert Koch Institute [Berlin] (RKI), Beihang University (BUAA), Statens Serum Institut [Copenhagen], Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), SANTE/SIDA [Bobo-Dioulasso, Burkina Faso], Institut de Recherche en Sciences de la Santé (IRSS) / Centre Muraz, Department of Microbiology, University of Washington School of Medicine, Department of Microbiology, Medical School, University of Thessaly [Volos] (UTH), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Université Montpellier 1 (UM1), Africa Centre for Health and Population Studies, University of KwaZulu-Natal (UKZN)-Medical Research Council of South Africa, Lab-STICC_UBO_CID_IHSEV, Laboratoire des sciences et techniques de l'information, de la communication et de la connaissance (Lab-STICC), École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS), State Key Laboratory of Infectious Disease Prevention and Control, Chinese Center for Disease Control and Prevention, Laboratory of Virology, CHU Rouen, Normandie Université (NU)-Normandie Université (NU), Universidade Federal do Rio de Janeiro (UFRJ), Departements of Medicine and Microbiology, University of Alabama [Tuscaloosa] (UA), Stichting HIV Monitoring [Amsterdam], Universiteit van Amsterdam (UvA), Département Génétique Internal Médecine, Hôpital Universitaire Leuven, Department of Chemical and Biomolecular Engineering [Baltimore], Johns Hopkins University (JHU), Centers for Disease Control and Prevention [Atlanta] (CDC), Centers for Disease Control and Prevention, China Academy of Chinese Medical Sciences, Chatzidimitriou, Dimitrios [0000-0001-9656-5898], University of Oxford, Institut Pasteur [Paris] (IP), Istituto Superiore di Sanità (ISS), Microbiologie Fondamentale et Pathogénicité (MFP), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques et émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), University of KwaZulu-Natal [Durban, Afrique du Sud] (UKZN)-Medical Research Council of South Africa, Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS), UNAIDS, Noguchi Memorial Institute for Medical Research, University of Ghana, Laboratoire d'Electronique et des Technologies de l'Information (CEA-LETI), Université Grenoble Alpes (UGA)-Direction de Recherche Technologique (CEA) (DRT (CEA)), Beihang University, Recherches Translationnelles sur le VIH et les maladies infectieuses (TransVIHMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Recherche pour le Développement (IRD)-Université Montpellier 1 (UM1)-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Universtié Yaoundé 1 [Cameroun]-Université de Montpellier (UM), Universidade Federal do Rio de Janeiro [Rio de Janeiro] (UFRJ), Nuffield Department of Women's and Reproductive Health (NDWRH), University of Oxford- John Radcliffe Hospital [Oxford University Hospital], South African Centre for Epidemiological Modelling and Analysis, JH is supported by the Oxford University Clinical Academic Graduate School (Oxford, UK) and Linacre College, Oxford University (Oxford, UK)., WHO–UNAIDS Network for HIV Isolation Characterisation : Alash'le G Abimiku, Simon Agwale, Chris Archibald, Boaz Avidor, María Gabriela Barbás, Francoise Barre-Sinoussi, Banson Barugahare, El Hadj Belabbes, Silvia Bertagnolio, Deborah Birx, Aleksei F Bobkov, James Brandful, Helba Bredell, Catherine A Brennan, James Brooks, Marie Bruckova, Luigi Buonaguro, Franco Buonaguro, Stefano Buttò, Anne Buve, Mary Campbell, Jean Carr, Alex Carrera, Manuel Gómez Carrillo, Connie Celum, Beth Chaplin, Macarthur Charles, Dimitrios Chatzidimitriou, Zhiwei Chen, Katsumi Chijiwa, David Cooper, Philip Cunningham, Anoumou Dagnra, Cillian F de Gascun, Julia Del Amo, Elena Delgado, Ursula Dietrich, Dominic Dwyer, Dennis Ellenberger, Barbara Ensoli, Max Essex, Feng Gao, Herve Fleury, Peter N Fonjungo, Vincent Foulongne, Deepak A Gadkari, Federico García, Roger Garsia, Guy Michel Gershy-Damet, Judith R Glynn, Ruth Goodall, Zehava Grossman, Monick Lindenmeyer-Guimarães, Beatrice Hahn, Raph L Hamers, Osamah Hamouda, Ray Handema, Xiang He, Joshua Herbeck, David D Ho, Africa Holguin, Mina Hosseinipour, Gillian Hunt, Masahiko Ito, Mohamed Ali Bel Hadj Kacem, Erin Kahle, Pontiano Kaleebu Kaleebu, Marcia Kalish, Adeeba Kamarulzaman, Chun Kang, Phyllis Kanki, Edward Karamov, Jean-Claude Karasi, Kayitesi Kayitenkore, Tony Kelleher, Dwip Kitayaporn, Leondios G Kostrikis, Claudia Kucherer, Claudia Lara, Thomas Leitner, Kirsi Liitsola, Jai Lingappa, Marek Linka, Ivette Lorenzana de Rivera, Vladimir Lukashov, Shlomo Maayan, Luzia Mayr, Francine McCutchan, Nicolas Meda, Elisabeth Menu, Fred Mhalu, Doreen Mloka, John L Mokili, Brigitte Montes, Orna Mor, Mariza Morgado, Fausta Mosha, Awatef Moussi, James Mullins, Rafael Najera, Mejda Nasr, Nicaise Ndembi, Joel R Neilson, Vivek R Nerurkar, Florian Neuhann, Claudine Nolte, Vlad Novitsky, Philippe Nyambi, Marianna Ofner, Fem J Paladin, Anna Papa, Jean Pape, Neil Parkin, Chris Parry, Martine Peeters, Alexandra Pelletier, Lucía Pérez-Álvarez, Deenan Pillay, Angie Pinto, Trinh Duy Quang, Cecilia Rademeyer, Filimone Raikanikoda, Mark A Rayfield, Jean-Marc Reynes, Tobias Rinke de Wit, Kenneth E Robbins, Morgane Rolland, Christine Rousseau, Jesus Salazar-Gonzales, Hanan Salem, Mika Salminen, Horacio Salomon, Paul Sandstrom, Mario L Santiago, Abdoulaye D Sarr, Bryan Schroeder, Michel Segondy, Philippe Selhorst, Sylvester Sempala, Jean Servais, Ansari Shaik, Yiming Shao, Amine Slim, Marcelo A Soares, Elijah Songok, Debbie Stewart, Julie Stokes, Shambavi Subbarao, Ruengpung Sutthent, Jun Takehisa, Amilcar Tanuri, Kok Keng Tee, Kiran Thapa, Michael Thomson, Tyna Tran, Willy Urassa, Hiroshi Ushijima, Philippevan de Perre, Guidovan der Groen, Kristel van Laethem, Joep van Oosterhout, Ard van Sighem, Eric van Wijngaerden, Anne-Mieke Vandamme, Jurgen Vercauteren, Nicole Vidal, Lesley Wallace, Carolyn Williamson, Dawit Wolday, Jianqing Xu, Chunfu Yang, Linqi Zhang, and Rong Zhang
Subjects: 0301 basic medicine, Serotype, Genotype, Genotyping Techniques, 030106 microbiology, DIVERSITY, MULTICENTER, VACCINE, HIV Infections, Genome, Viral, Biology, Global Health, Serogroup, SUBTYPES, 03 medical and health sciences, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Surveys and Questionnaires, INFECTION, Genetic variation, Global health, Humans, HIV vaccine, Serotyping, AIDS Vaccines, Science & Technology, Molecular epidemiology, Genetic Variation, Subtyping, 3. Good health, Trend analysis, 030104 developmental biology, Infectious Diseases, 13. Climate action, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, HIV-1, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Life Sciences & Biomedicine, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Demography
Abstract: BACKGROUND: Global genetic diversity of HIV-1 is a major challenge to the development of HIV vaccines. We aimed to estimate the regional and global distribution of HIV-1 subtypes and recombinants during 1990-2015. METHODS: We searched PubMed, EMBASE (Ovid), CINAHL (Ebscohost), and Global Health (Ovid) for HIV-1 subtyping studies published between Jan 1, 1990, and Dec 31, 2015. We collected additional unpublished HIV-1 subtyping data through a global survey. We included prevalence studies with HIV-1 subtyping data collected during 1990-2015. We grouped countries into 14 regions and analysed data for four time periods (1990-99, 2000-04, 2005-09, and 2010-15). The distribution of HIV-1 subtypes, circulating recombinant forms (CRFs), and unique recombinant forms (URFs) in individual countries was weighted according to the UNAIDS estimates of the number of people living with HIV (PLHIV) in each country to generate regional and global estimates of HIV-1 diversity in each time period. The primary outcome was the number of samples designated as HIV-1 subtypes A, B, C, D, F, G, H, J, K, CRFs, and URFs. The systematic review is registered with PROSPERO, number CRD42017067164. FINDINGS: This systematic review and global survey yielded 2203 datasets with 383 519 samples from 116 countries in 1990-2015. Globally, subtype C accounted for 46·6% (16 280 897/34 921 639 of PLHIV) of all HIV-1 infections in 2010-15. Subtype B was responsible for 12·1% (4 235 299/34 921 639) of infections, followed by subtype A (10·3%; 3 587 003/34 921 639), CRF02_AG (7·7%; 2 705 110/34 921 639), CRF01_AE (5·3%; 1 840 982/34 921 639), subtype G (4·6%; 1 591 276/34 921 639), and subtype D (2·7%; 926 255/34 921 639). Subtypes F, H, J, and K combined accounted for 0·9% (311 332/34 921 639) of infections. Other CRFs accounted for 3·7% (1 309 082/34 921 639), bringing the proportion of all CRFs to 16·7% (5 844 113/34 921 639). URFs constituted 6·1% (2 134 405/34 921 639), resulting in recombinants accounting for 22·8% (7 978 517/34 921 639) of all global HIV-1 infections. The distribution of HIV-1 subtypes and recombinants changed over time in countries, regions, and globally. At a global level during 2005-15, subtype B increased, subtypes A and D were stable, and subtypes C and G and CRF02_AG decreased. CRF01_AE, other CRFs, and URFs increased, leading to a consistent increase in the global proportion of recombinants over time. INTERPRETATION: Global and regional HIV diversity is complex and evolving, and is a major challenge to HIV vaccine development. Surveillance of the global molecular epidemiology of HIV-1 remains crucial for the design, testing, and implementation of HIV vaccines. FUNDING: None. ispartof: LANCET INFECTIOUS DISEASES vol:19 issue:2 pages:143-155 ispartof: location:United States status: published
Published: 2018
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