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851 results on '"Martinez-Picado, Javier"'

1. Vaccine breakthrough hypoxemic COVID-19 pneumonia in patients with auto-Abs neutralizing type I IFNs

Author

Bastard, Paul, Vazquez, Sara, Liu, Jamin, Laurie, Matthew T, Wang, Chung Yu, Gervais, Adrian, Le Voyer, Tom, Bizien, Lucy, Zamecnik, Colin, Philippot, Quentin, Rosain, Jérémie, Catherinot, Emilie, Willmore, Andrew, Mitchell, Anthea M, Bair, Rebecca, Garçon, Pierre, Kenney, Heather, Fekkar, Arnaud, Salagianni, Maria, Poulakou, Garyphallia, Siouti, Eleni, Sahanic, Sabina, Tancevski, Ivan, Weiss, Günter, Nagl, Laurenz, Manry, Jérémy, Duvlis, Sotirija, Arroyo-Sánchez, Daniel, Artal, Estela Paz, Rubio, Luis, Perani, Cristiano, Bezzi, Michela, Sottini, Alessandra, Quaresima, Virginia, Roussel, Lucie, Vinh, Donald C, Reyes, Luis Felipe, Garzaro, Margaux, Hatipoglu, Nevin, Boutboul, David, Tandjaoui-Lambiotte, Yacine, Borghesi, Alessandro, Aliberti, Anna, Cassaniti, Irene, Venet, Fabienne, Monneret, Guillaume, Halwani, Rabih, Sharif-Askari, Narjes Saheb, Danielson, Jeffrey, Burrel, Sonia, Morbieu, Caroline, Stepanovskyy, Yurii, Bondarenko, Anastasia, Volokha, Alla, Boyarchuk, Oksana, Gagro, Alenka, Neuville, Mathilde, Neven, Bénédicte, Keles, Sevgi, Hernu, Romain, Bal, Antonin, Novelli, Antonio, Novelli, Giuseppe, Saker, Kahina, Ailioaie, Oana, Antolí, Arnau, Jeziorski, Eric, Rocamora-Blanch, Gemma, Teixeira, Carla, Delaunay, Clarisse, Lhuillier, Marine, Le Turnier, Paul, Zhang, Yu, Mahevas, Matthieu, Pan-Hammarström, Qiang, Abolhassani, Hassan, Bompoil, Thierry, Dorgham, Karim, Gorochov, Guy, Laouenan, Cédric, Rodríguez-Gallego, Carlos, Ng, Lisa FP, Renia, Laurent, Pujol, Aurora, Belot, Alexandre, Raffi, François, Allende, Luis M, Martinez-Picado, Javier, Ozcelik, Tayfun, Imberti, Luisa, Notarangelo, Luigi D, Troya, Jesus, Solanich, Xavier, Zhang, Shen-Ying, Puel, Anne, Wilson, Michael R, Trouillet-Assant, Sophie, Abel, Laurent, and Jouanguy, Emmanuelle

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Prevention, Emerging Infectious Diseases, Coronaviruses, Pneumonia & Influenza, Pneumonia, Lung, Infectious Diseases, Immunization, Clinical Research, Biotechnology, Vaccine Related, Infection, Good Health and Well Being, Humans, COVID-19, COVID-19 Vaccines, SARS-CoV-2, Vaccines, Vaccination, Interferon Type I, RNA, Messenger, COVID HGE Consortium, French COVID Study Group, COMET Consortium, Clinical sciences
Abstract

Life-threatening "breakthrough" cases of critical COVID-19 are attributed to poor or waning antibody (Ab) response to SARS-CoV-2 vaccines in individuals already at risk. Preexisting auto-Abs neutralizing type I IFNs underlie at least 15% of critical COVID-19 pneumonia cases in unvaccinated individuals; their contribution to hypoxemic breakthrough cases in vaccinated people is unknown. We studied a cohort of 48 individuals (aged 20 to 86 years) who received two doses of a messenger RNA (mRNA) vaccine and developed a breakthrough infection with hypoxemic COVID-19 pneumonia 2 weeks to 4 months later. Ab levels to the vaccine, neutralization of the virus, and auto-Abs to type I IFNs were measured in the plasma. Forty-two individuals had no known deficiency of B cell immunity and a normal Ab response to the vaccine. Among them, 10 (24%) had auto-Abs neutralizing type I IFNs (aged 43 to 86 years). Eight of these 10 patients had auto-Abs neutralizing both IFN-α2 and IFN-ω, whereas two neutralized IFN-ω only. No patient neutralized IFN-β. Seven neutralized type I IFNs at 10 ng/ml and three at 100 pg/ml only. Seven patients neutralized SARS-CoV-2 D614G and Delta efficiently, whereas one patient neutralized Delta slightly less efficiently. Two of the three patients neutralizing only type I IFNs at 100 pg/ml neutralized both D614G and Delta less efficiently. Despite two mRNA vaccine inoculations and the presence of circulating Abs capable of neutralizing SARS-CoV-2, auto-Abs neutralizing type I IFNs may underlie a notable proportion of hypoxemic COVID-19 pneumonia cases, highlighting the importance of this particularly vulnerable population.

Published
2023

2. Correction: Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

Author

Matuozzo, Daniela, Talouarn, Estelle, Marchal, Astrid, Zhang, Peng, Manry, Jeremy, Seeleuthner, Yoann, Zhang, Yu, Bolze, Alexandre, Chaldebas, Matthieu, Milisavljevic, Baptiste, Gervais, Adrian, Bastard, Paul, Asano, Takaki, Bizien, Lucy, Barzaghi, Federica, Abolhassani, Hassan, Tayoun, Ahmad Abou, Aiuti, Alessandro, Darazam, Ilad Alavi, Allende, Luis M., Alonso-Arias, Rebeca, Arias, Andrés Augusto, Aytekin, Gokhan, Bergman, Peter, Bondesan, Simone, Bryceson, Yenan T., Bustos, Ingrid G., Cabrera-Marante, Oscar, Carcel, Sheila, Carrera, Paola, Casari, Giorgio, Chaïbi, Khalil, Colobran, Roger, Condino-Neto, Antonio, Covill, Laura E., Delmonte, Ottavia M., Zein, Loubna El, Flores, Carlos, Gregersen, Peter K., Gut, Marta, Haerynck, Filomeen, Halwani, Rabih, Hancerli, Selda, Hammarström, Lennart, Hatipoğlu, Nevin, Karbuz, Adem, Keles, Sevgi, Kyheng, Christèle, Leon-Lopez, Rafael, Franco, Jose Luis, Mansouri, Davood, Martinez-Picado, Javier, Akcan, Ozge Metin, Migeotte, Isabelle, Morange, Pierre-Emmanuel, Morelle, Guillaume, Martin-Nalda, Andrea, Novelli, Giuseppe, Novelli, Antonio, Ozcelik, Tayfun, Palabiyik, Figen, Pan-Hammarström, Qiang, de Diego, Rebeca Pérez, Planas-Serra, Laura, Pleguezuelo, Daniel E., Prando, Carolina, Pujol, Aurora, Reyes, Luis Felipe, Rivière, Jacques G., Rodriguez-Gallego, Carlos, Rojas, Julian, Rovere-Querini, Patrizia, Schlüter, Agatha, Shahrooei, Mohammad, Sobh, Ali, Soler-Palacin, Pere, Tandjaoui-Lambiotte, Yacine, Tipu, Imran, Tresoldi, Cristina, Troya, Jesus, van de Beek, Diederik, Zatz, Mayana, Zawadzki, Pawel, Al-Muhsen, Saleh Zaid, Alosaimi, Mohammed Faraj, Alsohime, Fahad M., Baris-Feldman, Hagit, Butte, Manish J., Constantinescu, Stefan N., Cooper, Megan A., Dalgard, Clifton L., Fellay, Jacques, Heath, James R., Lau, Yu-Lung, Lifton, Richard P., Maniatis, Tom, Mogensen, Trine H., von Bernuth, Horst, Lermine, Alban, Vidaud, Michel, Boland, Anne, Deleuze, Jean-François, Nussbaum, Robert, Kahn-Kirby, Amanda, Mentre, France, Tubiana, Sarah, Gorochov, Guy, Tubach, Florence, Hausfater, Pierre, Meyts, Isabelle, Zhang, Shen-Ying, Puel, Anne, Notarangelo, Luigi D., Boisson-Dupuis, Stephanie, Su, Helen C., Boisson, Bertrand, Jouanguy, Emmanuelle, Casanova, Jean-Laurent, Zhang, Qian, Abel, Laurent, and Cobat, Aurélie

Published
2024
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3. Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

Author

Matuozzo, Daniela, Talouarn, Estelle, Marchal, Astrid, Zhang, Peng, Manry, Jeremy, Seeleuthner, Yoann, Zhang, Yu, Bolze, Alexandre, Chaldebas, Matthieu, Milisavljevic, Baptiste, Gervais, Adrian, Bastard, Paul, Asano, Takaki, Bizien, Lucy, Barzaghi, Federica, Abolhassani, Hassan, Abou Tayoun, Ahmad, Aiuti, Alessandro, Alavi Darazam, Ilad, Allende, Luis M, Alonso-Arias, Rebeca, Arias, Andrés Augusto, Aytekin, Gokhan, Bergman, Peter, Bondesan, Simone, Bryceson, Yenan T, Bustos, Ingrid G, Cabrera-Marante, Oscar, Carcel, Sheila, Carrera, Paola, Casari, Giorgio, Chaïbi, Khalil, Colobran, Roger, Condino-Neto, Antonio, Covill, Laura E, Delmonte, Ottavia M, El Zein, Loubna, Flores, Carlos, Gregersen, Peter K, Gut, Marta, Haerynck, Filomeen, Halwani, Rabih, Hancerli, Selda, Hammarström, Lennart, Hatipoğlu, Nevin, Karbuz, Adem, Keles, Sevgi, Kyheng, Christèle, Leon-Lopez, Rafael, Franco, Jose Luis, Mansouri, Davood, Martinez-Picado, Javier, Metin Akcan, Ozge, Migeotte, Isabelle, Morange, Pierre-Emmanuel, Morelle, Guillaume, Martin-Nalda, Andrea, Novelli, Giuseppe, Novelli, Antonio, Ozcelik, Tayfun, Palabiyik, Figen, Pan-Hammarström, Qiang, de Diego, Rebeca Pérez, Planas-Serra, Laura, Pleguezuelo, Daniel E, Prando, Carolina, Pujol, Aurora, Reyes, Luis Felipe, Rivière, Jacques G, Rodriguez-Gallego, Carlos, Rojas, Julian, Rovere-Querini, Patrizia, Schlüter, Agatha, Shahrooei, Mohammad, Sobh, Ali, Soler-Palacin, Pere, Tandjaoui-Lambiotte, Yacine, Tipu, Imran, Tresoldi, Cristina, Troya, Jesus, van de Beek, Diederik, Zatz, Mayana, Zawadzki, Pawel, Al-Muhsen, Saleh Zaid, Alosaimi, Mohammed Faraj, Alsohime, Fahad M, Baris-Feldman, Hagit, Butte, Manish J, Constantinescu, Stefan N, Cooper, Megan A, Dalgard, Clifton L, Fellay, Jacques, Heath, James R, Lau, Yu-Lung, Lifton, Richard P, Maniatis, Tom, Mogensen, Trine H, von Bernuth, Horst, Lermine, Alban, and Vidaud, Michel

Subjects
Clinical Research, Infectious Diseases, Pneumonia & Influenza, Genetics, Human Genome, Prevention, 2.1 Biological and endogenous factors, Aetiology, Humans, Young Adult, Adult, Middle Aged, COVID-19, SARS-CoV-2, Toll-Like Receptor 3, Toll-Like Receptor 7, Interferon Type I, Autoantibodies, COVID Human Genetic Effort, COVIDeF Study Group, French COVID Cohort Study Group, CoV-Contact Cohort, COVID-STORM Clinicians, COVID Clinicians, Orchestra Working Group, Amsterdam UMC Covid-19 Biobank, NIAID-USUHS COVID Study Group, Immunity, Rare variants, Type I interferon, Clinical Sciences
Abstract

BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in ~ 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P = 1.1 × 10-4) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR = 3.70[95%CI 1.3-8.2], P = 2.1 × 10-4). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR = 19.65[95%CI 2.1-2635.4], P = 3.4 × 10-3), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR = 4.40[9%CI 2.3-8.4], P = 7.7 × 10-8). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD] = 43.3 [20.3] years) than the other patients (56.0 [17.3] years; P = 1.68 × 10-5).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old.

Published
2023

4. Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection

Author

Abel, Laurent, Aiuti, Alessandro, Al-Muhsen, Saleh, Al-Mulla, Fahd, Amara, Ali, Anderson, Mark S., Andreakos, Evangelos, Arias, Andrés A., Arkin, Lisa M., Feldman, Hagit Baris, Bastard, Paul, Belot, Alexandre, Biggs, Catherine M., Bogunovic, Dusan, Bolze, Alexandre, Bondarenko, Anastasiia, Borghesi, Alessandro, Bousfiha, Ahmed A., Brodin, Petter, Bryceson, Yenan, Butte, Manish J., Casanova, Jean-Laurent, Casari, Giorgio, Christodoulou, John, Cobat, Aurélie, Colobran, Roger, Condino-Neto, Antonio, Constantinescu, Stefan N., Cooper, Megan A., Dalgard, Clifton L., Desai, Murkesh, Drolet, Beth A., Duval, Xavier, El Baghdadi, Jamila, Eloy, Philippine, Espinosa-Padilla, Sara, Fellay, Jacques, Flores, Carlos, Franco, José Luis, Froidure, Antoine, Gorochov, Guy, Gregersen, Peter K., Grimbacher, Bodo, Haerynck, Filomeen, Hagin, David, Halwani, Rabih, Hammarström, Lennart, Heath, James R., Hsieh, Elena W.Y., Husebye, Eystein, Imai, Kohsuke, Itan, Yuval, Jouanguy, Emmanuelle, Kaja, Elżbieta, Karamitros, Timokratis, Kisand, Kai, Ku, Cheng-Lung, Lau, Yu-Lung, Ling, Yun, Lucas, Carrie L., Maniatis, Tom, Mansouri, Davood, Maródi, László, Mentré, France, Meyts, Isabelle, Milner, Joshua D., Mironska, Kristina, Mogensen, Trine H., Morio, Tomohiro, Ng, Lisa F.P., Notarangelo, Luigi D., Novelli, Antonio, Novelli, Giuseppe, O'Farrelly, Cliona, Okada, Satoshi, Okamoto, Keisuke, Ozcelik, Tayfun, Pan-Hammarström, Qiang, Pape, Jean W., Perez de Diego, Rebeca, Perez-Tur, Jordi, Perlin, David S., Pesole, Graziano, Planas, Anna M., Prando, Carolina, Pujol, Aurora, Puel, Anne, Quintana-Murci, Lluis, Ramaswamy, Sathishkumar, Renia, Laurent, Resnick, Igor, Rodríguez-Gallego, Carlos, Sancho-Shimizu, Vanessa, Sediva, Anna, Seppänen, Mikko R.J., Shahrooei, Mohammad, Shcherbina, Anna, Slaby, Ondrej, Snow, Andrew L., Soler-Palacín, Pere, Soumelis, Vassili, Spaan, András N., Tancevski, Ivan, Tangye, Stuart G., Tayoun, Ahmad Abou, Temel, Şehime Gülsün, Thorball, Christian, Tiberghien, Pierre, Trouillet-Assant, Sophie, Turvey, Stuart E., Uddin, K. M. Furkan, Uddin, Mohammed J., van de Beek, Diederik, Vinh, Donald C., von Bernuth, Horst, Wauters, Joost, Zatz, Mayana, Zawadzki, Pawel, Zhang, Qian, Zhang, Shen-Ying, Bureau, Serge, Vacher, Yannick, Gysembergh-Houal, Anne, Demerville, Lauren, Benleulmi-Chaachoua, Abla, Abad, Sebastien, Abassi, Radhiya, Abdellaoui, Abdelrafie, Abdelmalek, Abdelkrim, Abdoul, Hendy, Abergel, Helene, Abeud, Fariza, Abgrall, Sophie, Abisror, Noemie, Adechian, Marylise, Aderdour, Nordine, Admane, Hakeem Farid, Adnet, Frederic, Afritt, Sara, Agostini, Helene, Aguilar, Claire, Agut, Sophie, Aiello, Tommaso Francesco, Kaci, Marc Ait, Oufella, Hafid Ait, Ajeenthiravasan, Gokula, Alauzy, Virginie, Alby-Laurent, Fanny, Allard, Lucie, Alyanakian, Marie-Alexandra, Borrero, Blanca Amador, Amam, Sabrina, Amrouche, Lucile, Andronikof, Marc, Anglicheau, Dany, Anguel, Nadia, Annane, Djillali, Aounzou, Mohammed, Aparicio, Caroline, Aratus, Gladys, Arlet, Jean-Benoit, Arzoine, Jeremy, Aslangul, Elisabeth, Assefi, Mona, Aubry, Adeline, Audiffred, Laetitia, Audureau, Etienne, Auger, Christelle Nathalie, Auregan, Jean-Charles, Awotar, Celine, Milla, Sonia Ayllon, Azan, Delphine, Azemar, Laurene, Azzouguen, Billal, Elrufaai, Marwa Bachir, Badsi, Aïda, Bakouboula, Prissile, Balcerowiak, Coline, Balde, Fanta, Baldivia, Elodie, Bangamingo, Eliane-Flore, Baptiste, Amandine, Baran-Marszak, Fanny, Barau, Caroline, Barget, Nathalie, Baronnet, Flore, Barthelemy, Romain, Baudel, Jean-Luc, Baudry, Camille, Baudry, Elodie, Beaugerie, Laurent, Belamri, Adel, Belaube, Nicolas, Belilita, Rhida, Bellassen, Pierre, Belmokhtar, Rawan, Beltran, Isabel, Benainous, Ruben, Benallaoua, Mourad, Benamouzig, Robert, Benbara, Amélie, Benhida, Jaouad, Benkhelouf, Anis, Benlagha, Jihene, Benmostafa, Chahinez, Benothmane, Skander, Bentifraouine, Miassa, Berard, Laurence, Bernier, Quentin, Berti, Enora, Bertier, Astrid, Berton, Laure, Bessis, Simon, Beurton, Alexandra, Bianco, Celine, Bianquis, Clara, Bidar, Frank, Blanche, Philippe, Blayau, Clarisse, Bleibtreu, Alexandre, Blin, Emmanuelle, Bloch-Queyrat, Coralie, Boissier, Marie-Christophe, Bollens, Diane, Bolzoni, Marion, Bompard, Rudy pierre, Bonnet, Nicolas, Bonnouvrier, Justine, Botha, Shirmonecrystal, Boucenna, Wissam, Bouchama, Fatiha, Bouchaud, Olivier, Bouchghoul, Hanane, Boudjebla, Taoueslylia, Boudjema, Noel, Bouffard, Catherine, Bougle, Adrien, Bouguerra, Meriem, Bouras, Leila, Bourcier, Agnes, Durand, Anne Bourgarit, Bourrier, Anne, Bouscarat, Fabrice, Bouvry, Diane, Bouziri, Nesrine, Bouzrara, Ons, Bribier, Sarah, Brugier, Delphine, Brunel, Melanie, Bui, Eida, Buisson, Anne, Bukreyeva, Iryna, Bureau, Côme, Cadranel, Jacques, Cailhol, Johann, Calin, Ruxandra, Vega, Clara Campos, Canavaggio, Pauline, Cancella, Marta, Cantin, Delphine, Cao, Albert, Carbillon, Lionel, Carlier, Nicolas, Cassard, Clementine, Castor, Guylaine, Cauchy, Marion, Cha, Olivier, Chaigne, Benjamin, Challal, Salima, Champion, Karine, Chariot, Patrick, Chas, Julie, Chauveau, Simon, Chauvin, Anthony, Chauvin, Clement, Chavarot, Nathalie, Chebbout, Kamélia, Cherai, Mustapha, Cherubini, Ilaria, Chevalier, Amelie, Chiarabini, Thibault, Chinet, Thierry, Chocron, Richard, Choinier, Pascaline, Chommeloux, Juliette, Choquet, Christophe, Choupeaux, Laure, Chousterman, Benjamin, Ciocan, Dragosmarius, Clarke, Ada, Clavere, Gaëlle, Clavier, Florian, Clement, Karine, Clerc, Sebastien, Cohen, Yves, Cohen, Fleur, Cohen, Adrien, Coilly, Audrey, Colboc, Hester, Colin, Pauline, Collet, Magalie, Comarmond, Chloé, Combacon, Emeline, Combes, Alain, Comparon, Celine, Constantin, Jean-Michel, Cordel, Hugues, Cordier, Anne-Gael, Costantini, Adrien, Chalumeau, Nathalie Costedoat, Couffignal, Camille, Coupeau, Doriane, Creange, Alain, Lamarre, Yannie Cuvillier, Da Silveira, Charlène, Guibal El Kayani, Sandrine Dautheville, De Castro, Nathalie, De Rycke, Yann, Del Pozo, Lucie, Delannoy, Quentin, Delay, Mathieu, Deleris, Robin, Delforge, Juliette, Delphine, Laëtitia, Demare, Noemie, Demeret, Sophie, Demoule, Alexandre, Deniau, Aurore, Depret, François, Derolez, Sophie, Derradji, Ouda, Derridj, Nawal, Descamps, Vincent, Deschamps, Lydia, Desconclois, Celine, Desnos, Cyrielle, Desongins, Karine, Dhote, Robin, Diallo, Benjamin, Didier, Morgane, Diemer, Myriam, Diez, Stephane, Djadi-Prat, Juliette, Djamouri Monnory, Fatima-Zohra, Djebara, Siham, Djebra, Naoual, Djietcheu, Minette, Djillali, Hadjer, Djouadi, Nouara, Donneger, Severine, Santos, Catarina Dos, Dournon, Nathalie, Dres, Martin, Droctove, Laura, Drogrey, Marie, Dropy, Margot, Drouet, Elodie, Dubosq, Valérie, Dubreucq, Evelyne, Dubus, Estelle, Duchemann, Boris, Duchenoy, Thibault, Dudoignon, Emmanuel, Dufau, Romain, Dumas, Florence, Duran, Clara, Duron, Emmanuelle, Durrbach, Antoine, Duvivier, Claudine, Ebstein, Nathan, El Khalifa, Jihane, Elabbadi, Alexandre, Elie, Caroline, Ernotte, Gabriel, Esling, Anne, Etienne, Martin, Eyer, Xavier, Fartoukh, Muriel Sarah, Fayali, Takoua, Fermaut, Marion, Fiorentino, Arianna, Fliss, Souha, Fournier, Marie-Céline, Fournier, Benjamin, Francois, Hélène, Freynet, Olivia, Frigout, Yvann, Fromont, Isaure, Fuentes, Axelle, Furet, Thomas, Galand, Joris, Garnier, Marc, Gaubert, Agnes, Gaudry, Stéphane, Gaugain, Samuel, Gauthier, Damien, Gautier, Maxime, Georgin-Lavialle, Sophie, Geromin, Daniela, Ghalayini, Mohamed, Ghaleh, Bijan, Ghezal, Myriam, Gibelin, Aude, Gimeno, Linda, Girard, Benoit, Leprieur, Bénédicte Giroux, Gomes, Doryan, Gomes-Pires, Elisabete, Gouge, Anne, Gouja, Amel, Goulet, Helene, Goupil, Sylvain, De Bouille, Jeanne Goupil, Gras, Julien, Greffe, Segolene, Grimaldi, Lamiae, Guedeney, Paul, Guidet, Bertrand, Guillo, Matthias, Gulczynski, Mariechristelle, Hadjam, Tassadit, Haguenauer, Didier, Hammal, Soumeya, Hammoudi, Nadjib, Hanon, Olivier, Harrois, Anarole, Hausfater, Pierre, Hautem, Coraline, Hekimian, Guillaume, Heming, Nicholas, Hermine, Olivier, Ho, Sylvie, Houllier, Marie, Huot, Benjamin, Huscenot, Tessa, Saied, Wafa Ibn, Ikherbane, Ghilas, Imarazene, Meriem, Ingiliz, Patrick, Iratni, Lina, Jaureguiberry, Stephane, Jean-Marc, Jean-Francois, Jeyarajasingham, Deleena, Jouany, Pauline, Jouis, Veronique, Jourdaine, Clement, Kafif, Ouifiya, Kallala, Rim, Katsahian, Sandrine, Kelesyan, Lilit, Keo, Vixra, Ketz, Flora, Khamis, Warda, Khelili, Enfel, Khellaf, Mehdi, Kotokpo Youkou, Christy Gaëlla, Kounis, Ilias, Kpalma, Gaelle, Krause, Jessica, Labbe, Vincent, Lacombe, Karine, Lacorte, Jean-Marc, Lafont, Anne Gaelle, Lafont, Emmanuel, Lagha, Lynda, Lamhaut, Lionel, Lancelot, Aymeric, Landman, Cecilia, Lanternier, Fanny, Larcheveque, Cecile, Combe, Caroline Lascoux, Lassel, Ludovic, Laverdant, Benjamin, Lavergne, Christophe, Lavillegrand, Jean-Rémi, Lazureanu, Pompilia, Le Guennec, Loïc, Leberre, Lamia, Leblanc, Claire, Leboyer, Marion, Lecomte, Francois, Lecorre, Marine, Leenhardt, Romain, Lefebvre, Marylou, Lefebvre, Bénédicte, Legendre, Paul, Leger, Anne, Legros, Laurence, Legrosse, Justyna, Lehuunghia, Sébastien, Lemarec, Julien, Leporrier-Ext, Jeremie, Lesein, Manon, Lesur, Hubert, Levy, Vincent, Levy, Albert, Lopes, Edwige, Lopes, Amanda, Lopez, Vanessa, Lopinto, Julien, Lortholary, Olivier, Louadah, Badr, Loze, Bénédicte, Lucas, Marie-Laure, Lucasamichi, Axelle, Luong, Liem Binh, Magazimama-Ext, Arouna, Maingret, David, Mameri, Lakhdar, Manivet, Philippe, Mansouri, Cylia, Marcault, Estelle, Marey, Jonathan, Marin, Nathalie, Marois, Clémence, Martin, Olivier, Martineau, Lou, Martinez-Lopez, Cannelle, Martyniuck, Pierre, De Farcy, Pauline Mary, Marzouk, Nessrine, Masmoudi, Rafik, Mebazaa, Alexandre, Mechai, Frédéric, Mecozzi, Fabio, Mediouni, Chamseddine, Megarbane, Bruno, Meghadecha, Mohamed, Mejean, Élodie, Mekinian, Arsene, Abdelhadi, Nour Mekki, Mekni, Rania, Meliti, Thinhinan Sabrina, Lima, Breno Melo, Meng, Paris, Merbah, Soraya, Messani, Fadhila, Messaoudi, Yasmine, Mewasing, Baboo-Irwinsingh, Meziane, Lydia, Michelot-Burger, Carole, Mignot, Françoise, Minka, Fadi Hillary, Miyara, Makoto, Moine, Pierre, Molina, Jean-Michel, Montegnies-Boulet, Anaïs, Monti, Alexandra, Montlahuc, Claire, Montout, Anne-Lise, Moores, Alexandre, Morbieu, Caroline, Mortelette, Helene, Mouly, Stéphane, Muzaffar, Rosita, Nacerddine, Cherifa Iness, Nadal, Marine, Nadif, Hajer, Nassarmadji, Kladoum, Natella, Pierre, Ndingamondze, Sandrine, Neraal, Stefan, Nguyen, Caroline, N'Guyen, Bao, Larmurier, Isabelle Nion, Nlomenyengue, Luc, Noel, Nicolas, Nunes, Hilario, Omar, Edris, Ouazene, Zineb, Ouedraogo, Elise, Ouelaa, Wassila, Oukhedouma, Anissa, Amara, Yasmina Ould, Oya, Herve, Oziel, Johanna, Padilla, Thomas, Paillaud, Elena, Paiva, Solenne, Parfait, Beatrice, Parize, Perrine, Parizot, Christophe, Parrot, Antoine, Pavot, Arthur, Peaudecerf, Laetitia, Pene, Frédéric, Pepin, Marion, Pernet, Julie, Pernin, Claire, Petit, Mylène, Peyrony, Olivier, Pietri, Marie-Pierre, Pietri, Olivia, De Chambrun, Marc Pineton, Pinson, Michelle, Pintado, Claire, Piquard, Valentine, Pires, Christine, Planquette, Benjamin, Poirier, Sandrine, Pomel, Anne-Laure, Pons, Stéphanie, Ponscarme, Diane, Pourcelot, Annegaelle, Pourcher, Valérie, Pouvaret, Anne, Prever, Florian, Previlon, Miresta, Prevost, Margot, Provoost, Marie-Julie, Quemeneur, Cyril, Rafat, Cédric, Rami, Agathe, Ranque, Brigitte, Raphael, Maurice, Raphalen, Jean Herle, Rastoin, Anna, Raux, Mathieu, Rebai, Amani, Reby, Michael, Regent, Alexis, Regrag, Asma, Resche-Rigon, Matthieu, Ressaire, Quentin, Richard, Christian, Richard, Mariecaroline, Robert, Maxence, Rohaut, Benjamin, Rolland-Debord, Camille, Ropers, Jacques, Roque-Afonso, Anne-Marie, Rosso, Charlotte, Rousseaux, Mélanie, Rousseaux, Nabila, Roux, Swasti, Roux, Lorène, Rouzaud, Claire, Rozes, Antoine, Rubenstein, Emma, Sabate, Jean-Marc, Sabet, Sheila, Sacleux, Sophie-Caroline, Kermanach, Nathalie Saidenberg, Saliba, Faouzi, Salmon, Dominique, Savale, Laurent, Savary, Guillaume, Sberro, Rebecca, Scemla, Anne, Schlemmer, Frederic, Schwartz, Mathieu, Sedfi, Saïd, Sefir-Kribel, Samia, Seksik, Philippe, Sellier, Pierre, Selves, Agathe, Sembach, Nicole, Semerano, Luca, Senat, Marie-Victoire, Sene, Damien, Serris, Alexandra, Sese, Lucile, Sghiouar, Naima, Sigaux, Johanna, Siguier, Martin, Silvain, Johanne, Simon, Noémie, Simon, Tabassome, Skandri, Lina Innes, Slimani, Miassa, Snauwaert, Aurélie, Sokol, Harry, Soliman, Heithem, Soltani, Nisrine, Soyer, Benjamin, Steg, Gabriel, Suarez, Lydia, Szwebel, Tali-Anne, Taffame, Kossi, Tandjaoui-Lambiotte, Yacine, Tantet, Claire, Tateo, Mariagrazia, Theodose, Igor, Thiebaud, Pierre clement, Thomas, Caroline, Tiercelet, Kelly, Tisserand, Julie, Tomczak, Carole, Torelino, Krystel, Touam-Ext, Fatima, Toumi, Lilia, Toury, Gustave, Toy-Miou, Mireille, Dinh Thanh Lien, Olivia Tran, Trandinh, Alexy, Treluyer, Jean-Marc, Trinque, Baptiste, Truchot, Jennifer, Tubach, Florence, Tubiana, Sarah, Tunesi, Simone, Turpin, Matthieu, Turpin, Agathe, Urbina, Tomas, Narvaez, Rafael Usubillaga, Uzunhan, Yurdagul, Vaittinadaayar, Prabakar, Valent, Arnaud, Valentian, Maelle, Valin, Nadia, Vallet, Hélène, Vaz, Marina, Vazquezibarra, Miguel-Alejandro, Vedie, Benoit, Velly, Laetitia, Verstuyft, Celine, Viallette, Cedric, Vicaut, Eric, Vignes, Dorothee, Vimpere, Damien, Virlouvet, Myriam, Voiriot, Guillaume, Voisot, Lena, Weiss, Emmanuel, Weiss, Nicolas, Winchenne, Anaïs, Yordanov, Youri, Zafrani, Lara, Zaidan, Mohamad, Zaidi, Wissem, Zak, Cathia, Zarhrate-Ghoul, Aida, Zatout, Ouassila, Zeino, Suzanne, Zeitouni, Michel, Zemirli, Naïma, Zerah, Lorene, Zia, Ounsa, Ziol, Marianne, Zolario, Oceane, Zuber, Julien, Andrejak, Claire, Angoulvant, François, Bachelet, Delphine, Bartoli, Marie, Basmaci, Romain, Behillil, Sylvie, Beluze, Marine, Benkerrou, Dehbia, Bhavsar, Krishna, Bouadma, Lila, Bouchez, Sabelline, Bouscambert, Maude, Cervantes-Gonzalez, Minerva, Chair, Anissa, Chirouze, Catherine, Coelho, Alexandra, Couffin-Cadiergues, Sandrine, d’Ortenzio, Eric, Debray, Marie-Pierre, Deconinck, Laurene, Deplanque, Dominique, Descamps, Diane, Desvallée, Mathilde, Diallo, Alpha, Diouf, Alphonsine, Dorival, Céline, Dubos, François, Elharrar, Brigitte, Enouf, Vincent, Esperou, Hélène, Esposito-Farese, Marina, Etienne, Manuel, Devouge, Eglantine Ferrand, Gault, Nathalie, Gaymard, Alexandre, Ghosn, Jade, Gigante, Tristan, Gilg, Morgane, Guedj, Jérémie, Hoctin, Alexandre, Hoffmann, Isabelle, Houas, Ikram, Hulot, Jean-Sébastien, Jaafoura, Salma, Kaguelidou, Florentia, Kali, Sabrina, Khalil, Antoine, Khan, Coralie, Laouénan, Cédric, Laribi, Samira, Le, Minh, Le Hingrat, Quentin, Le Mestre, Soizic, Le Nagard, Hervé, Lescure, François-Xavier, Letrou, Sophie, Levy, Yves, Lina, Bruno, Lingas, Guillaume, Lucet, Jean-Christophe, Malvy, Denis, Mambert, Marina, Meziane, Amina, Mouquet, Hugo, Mullaert, Jimmy, Neant, Nadège, Nguyen, Duc, Noret, Marion, Nseir, Saad, Papadopoulos, Aurélie, Paul, Christelle, Peiffer-Smadja, Nathan, Perpoint, Thomas, Petrov-Sanchez, Ventzislava, Peytavin, Gilles, Pham, Huong, Picone, Olivier, Puéchal, Oriane, Rabaud, Christian, Rosa-Calatrava, Manuel, Rossignol, Bénédicte, Rossignol, Patrick, Roy, Carine, Schneider, Marion, Su, Richa, Tardivon, Coralie, Tellier, Marie-Capucine, Téoulé, François, Terrier, Olivier, Timsit, Jean-François, Tual, Christelle, Van Der Werf, Sylvie, Vanel, Noémie, Veislinger, Aurélie, Visseaux, Benoit, Wiedemann, Aurélie, Yazdanpanah, Yazdan, Alavoine, Loubna, Burdet, Charles, Charpentier, Charlotte, Dechanet, Aline, Ecobichon, Jean-Luc, Frezouls, Wahiba, Houhou, Nadhira, Lehacaut, Jonathan, Manchon, Pauline, Nouroudine, Mariama, Quintin, Caroline, Thy, Michael, van der Werf, Sylvie, Vignali, Valérie, Chahine, Abir, Waucquier, Nawal, Migaud, Maria-Claire, Djossou, Félix, Mergeay-Fabre, Mayka, Lucarelli, Aude, Demar, Magalie, Bruneau, Léa, Gérardin, Patrick, Maillot, Adrien, Payet, Christine, Laviolle, Bruno, Laine, Fabrice, Paris, Christophe, Desille-Dugast, Mireille, Fouchard, Julie, Pistone, Thierry, Perreau, Pauline, Gissot, Valérie, Goas, Carole L.E., Montagne, Samatha, Richard, Lucie, Bouiller, Kévin, Desmarets, Maxime, Meunier, Alexandre, Bourgeon, Marilou, Lefévre, Benjamin, Jeulin, Hélène, Legrand, Karine, Lomazzi, Sandra, Tardy, Bernard, Gagneux-Brunon, Amandine, Bertholon, Frédérique, Botelho-Nevers, Elisabeth, Kouakam, Christelle, Nicolas, Leturque, Roufai, Layidé, Amat, Karine, Espérou, Hélène, Hendou, Samia, Foti, Giuseppe, Citerio, Giuseppe, Contro, Ernesto, Pesci, Alberto, Valsecchi, Maria Grazia, Cazzaniga, Marina, Bellani, Giacomo, Abad, Jorge, Accordino, Giulia, Angelini, Micol, Aguilera-Albesa, Sergio, Aguiló-Cucurull, Aina, Özkan, Esra Akyüz, Darazam, Ilad Alavi, Roblero Albisures, Jonathan Antonio, Aldave, Juan C., Ramos, Miquel Alfonso, Khan, Taj Ali, Aliberti, Anna, Nadji, Seyed Alireza, Alkan, Gulsum, AlKhater, Suzan A., Allardet-Servent, Jerome, Allende, Luis M., Alonso-Arias, Rebeca, Alshahrani, Mohammed S., Alsina, Laia, Amoura, Zahir, Antolí, Arnau, Arrestier, Romain, Aubart, Mélodie, Auguet, Teresa, Avramenko, Iryna, Aytekin, Gökhan, Azot, Axelle, Bahram, Seiamak, Bajolle, Fanny, Baldanti, Fausto, Baldolli, Aurélie, Ballester, Maite, Barrou, Benoit, Barzaghi, Federica, Basso, Sabrina, Bayhan, Gulsum Iclal, Bezrodnik, Liliana, Bilbao, Agurtzane, Blanchard-Rohner, Geraldine, Blanco, Ignacio, Blandinières, Adeline, Blázquez-Gamero, Daniel, Bloomfield, Marketa, Bolivar-Prados, Mireia, Borie, Raphael, Botdhlo-Nevers, Elisabeth, Bousquet, Aurore, Boutolleau, David, Bouvattier, Claire, Boyarchuk, Oksana, Bravais, Juliette, Briones, M. Luisa, Brunner, Marie-Eve, Bruno, Raffaele, Bueno, Maria Rita P., Bukhari, Huda, Bustamante, Jacinta, Cáceres Agra, Juan José, Capra, Ruggero, Carapito, Raphael, Carrabba, Maria, Casasnovas, Carlos, Caseris, Marion, Cassaniti, Irene, Castelle, Martin, Castelli, Francesco, Castillo de Vera, Martín, Castro, Mateus V., Catherinot, Emilie, Celik, Jale Bengi, Ceschi, Alessandro, Chalumeau, Martin, Charbit, Bruno, Boulanger, Cécile, Clavé, Père, Clotet, Bonaventura, Codina, Anna, Comarmond, Cloé, Comoli, Patrizia, Corsico, Angelo G., Coşkuner, Taner, Cvetkovski, Aleksandar, Cyrus, Cyril, Dalmau, David, Danion, François, Darley, David Ross, Das, Vincent, Dauby, Nicolas, Dauger, Stéphane, De Munte, Paul, de Pontual, Loic, Dehban, Amin, Delplancq, Geoffroy, Desguerre, Isabelle, Di Sabatino, Antonio, Diehl, Jean-Luc, Dobbelaere, Stephanie, Domínguez-Garrido, Elena, Dubost, Clément, Ekwall, Olov, Bozdemir, Şefika Elmas, Elnagdy, Marwa H., Emiroglu, Melike, Endo, Akifumi, Erdeniz, Emine Hafize, Aytekin, Selma Erol, Etxart Lasa, Maria Pilar, Euvrard, Romain, Fabio, Giovanna, Faivre, Laurence, Falck, Antonin, Fartoukh, Muriel, Faure, Morgane, Arquero, Miguel Fernandez, Ferrer, Ricard, Ferreres, Jose, Francois, Bruno, Fumadó, Victoria, Fung, Kitty S.C., Fusco, Francesca, Gagro, Alenka, Solis, Blanca Garcia, Garçon, Pierre, Gaussem, Pascale, Gayretli, Zeynep, Gil-Herrera, Juana, Gilardin, Laurent, Gatineau, Audrey Giraud, Girona-Alarcón, Mònica, Cifuentes Godínez, Karen Alejandra, Goffard, Jean-Christophe, Gonzales, Nacho, Gonzalez-Granado, Luis I., González-Montelongo, Rafaela, Guerder, Antoine, Gülhan, Belgin, Gumucio, Victor Daniel, Hanitsch, Leif Gunnar, Gunst, Jan, Gut, Marta, Hadjadj, Jérôme, Hancerli, Selda, Hariyan, Tetyana, Hatipoglu, Nevin, Heppekcan, Deniz, Hernandez-Brito, Elisa, Ho, Po-ki, Holanda-Peña, María Soledad, Horcajada, Juan P., Hraiech, Sami, Humbert, Linda, Hung, Ivan F.N., Iglesias, Alejandro D., Íñigo-Campos, Antonio, Jamme, Matthieu, Arranz, María Jesús, Jimeno, Marie-Thérèse, Jordan, Iolanda, Kanık-Yüksek, Saliha, Kara, Yalcin, Karahan, Aydın, Karbuz, Adem, Yasar, Kadriye Kart, Kasapcopur, Ozgur, Kashimada, Kenichi, Keles, Sevgi, Demirkol, Yasemin Kendir, Kido, Yasutoshi, Kizil, Can, Kılıç, Ahmet Osman, Klocperk, Adam, Koutsoukou, Antonia, Król, Zbigniew J., Ksouri, Hatem, Kuentz, Paul, Kwan, Arthur M.C., Kwan, Yat Wah M., Kwok, Janette S.Y., Lagier, Jean-Christophe, Lam, David S.Y., Lampropoulou, Vicky, Le Bourgeois, Fleur, Leo, Yee-Sin, Lopez, Rafael Leon, Leung, Daniel, Levin, Michael, Levy, Michael, Lévy, Romain, Li, Zhi, Lilleri, Daniele, Adrian Bolanos Lima, Edson Jose, Linglart, Agnes, López-Collazo, Eduardo, Lorenzo-Salazar, José M., Louapre, Céline, Lubetzki, Catherine, Lung, Kwok-Cheung, Luyt, Charles-Edouard, Lye, David C., Magnone, Cinthia, Marchioni, Enrico, Marioli, Carola, Marjani, Majid, Marques, Laura, Pereira, Jesus Marquez, Martín-Nalda, Andrea, Pueyo, David Martínez, Martinez-Picado, Javier, Marzana, Iciar, Mata-Martínez, Carmen, Mathian, Alexis, Matos, Larissa R.B., Matthews, Gail V., Mayaux, Julien, McLaughlin-Garcia, Raquel, Meersseman, Philippe, Mège, Jean-Louis, Mekontso-Dessap, Armand, Melki, Isabelle, Meloni, Federica, Meritet, Jean-François, Merlani, Paolo, Akcan, Özge Metin, Mezidi, Mehdi, Migeotte, Isabelle, Millereux, Maude, Million, Matthieu, Mirault, Tristan, Mircher, Clotilde, Mirsaeidi, Mehdi, Mizoguchi, Yoko, Modi, Bhavi P., Mojoli, Francesco, Moncomble, Elsa, Melián, Abián Montesdeoca, Martinez, Antonio Morales, Morandeira, Francisco, Morange, Pierre-Emmanuel, Mordacq, Clémence, Morelle, Guillaume, Mouly, Stéphane J., Muñoz-Barrera, Adrián, Nafati, Cyril, Nagashima, Shintaro, Nakagama, Yu, Neven, Bénédicte, Neves, João Farela, Ng, Yuk-Yung, Hubert Nielly, Medina, Yeray Novoa, Cuadros, Esmeralda Nuñez, Karabela, Semsi Nur, Ocejo-Vinyals, J. Gonzalo, Oualha, Mehdi, Ouedrani, Amani, Özçelik, Tayfun, Ozkaya-Parlakay, Aslinur, Pagani, Michele, Papadaki, Maria, Parola, Philippe, Pascreau, Tiffany, Paul, Stéphane, Paz-Artal, Estela, Pedraza, Sigifredo, González Pellecer, Nancy Carolina, Pellegrini, Silvia, Pérez de Diego, Rebeca, Pérez-Fernández, Xosé Luis, Philippe, Aurélien, Philippot, Quentin, Picod, Adrien, Pineton de Chambrun, Marc, Piralla, Antonio, Planas-Serra, Laura, Ploin, Dominique, Poissy, Julien, Poncelet, Géraldine, Poulakou, Garyphallia, Pouletty, Marie S., Pourshahnazari, Persia, Qiu-Chen, Jia Li, Quentric, Paul, Rambaud, Thomas, Raoult, Didier, Raoult, Violette, Rebillat, Anne-Sophie, Redin, Claire, Resmini, Léa, Ricart, Pilar, Richard, Jean-Christophe, Rigo-Bonnin, Raúl, Rivet, Nadia, Rivière, Jacques G., Rocamora-Blanch, Gemma, Rodero, Mathieu P., Rodrigo, Carlos, Rodriguez, Luis Antonio, Rodriguez-Gallego, Carlos, Rodriguez-Palmero, Agustí, Romero, Carolina Soledad, Rothenbuhler, Anya, Roux, Damien, Rovina, Nikoletta, Rozenberg, Flore, Ruch, Yvon, Ruiz, Montse, Ruiz del Prado, Maria Yolanda, Ruiz-Rodriguez, Juan Carlos, Sabater-Riera, Joan, Saks, Kai, Salagianni, Maria, Sanchez, Oliver, Sánchez-Montalvá, Adrián, Sánchez-Ramón, Silvia, Schidlowski, Laire, Schluter, Agatha, Schmidt, Julien, Schmidt, Matthieu, Schuetz, Catharina, Schweitzer, Cyril E., Scolari, Francesco, Seijo, Luis, Seminario, Analia Gisela, Seng, Piseth, Senoglu, Sevtap, Seppänen, Mikko, Llovich, Alex Serra, Siguret, Virginie, Siouti, Eleni, Smadja, David M., Smith, Nikaia, Sobh, Ali, Solanich, Xavier, Solé-Violán, Jordi, Soler, Catherine, Sözeri, Betül, Stella, Giulia Maria, Stepanovskiy, Yuriy, Stoclin, Annabelle, Taccone, Fabio, Taupin, Jean-Luc, Tavernier, Simon J., Tello, Loreto Vidaur, Terrier, Benjamin, Thiery, Guillaume, Thorn, Karolina, Thumerelle, Caroline, Tipu, Imran, Tolstrup, Martin, Tomasoni, Gabriele, Toubiana, Julie, Alvarez, Josep Trenado, Triantafyllia, Vasiliki, Troya, Jesús, Tsang, Owen T.Y., Tserel, Liina, Tso, Eugene Y.K., Tucci, Alessandra, Tüter Öz, Şadiye Kübra, Ursini, Matilde Valeria, Utsumi, Takanori, Vabres, Pierre, Valencia-Ramos, Juan, Van Den Rym, Ana Maria, Vandernoot, Isabelle, Velez-Santamaria, Valentina, Zuniga Veliz, Silvia Patricia, Vidigal, Mateus C., Viel, Sébastien, Villain, Cédric, Vilaire-Meunier, Marie E., Villar-García, Judit, Vincent, Audrey, Van der Linden, Dimitri, Volokha, Alla, Vuotto, Fanny, Wauters, Els, Wu, Alan K.L., Wu, Tak-Chiu, Yahşi, Aysun, Yesilbas, Osman, Yildiz, Mehmet, Young, Barnaby E., Yükselmiş, Ufuk, Zecca, Marco, Zuccaro, Valentina, Van Praet, Jens, Lambrecht, Bart N., Van Braeckel, Eva, Bosteels, Cédric, Hoste, Levi, Hoste, Eric, Bauters, Fré, De Clercq, Jozefien, Heijmans, Catherine, Slabbynck, Hans, Naesens, Leslie, Florkin, Benoit, Young, Mary-Anne, Willis, Amanda, Lapuente-Suanzes, Paloma, de Andrés-Martín, Ana, Berkell, Matilda, Carelli, Valerio, Fiorentino, Alessia, Malhotra, Surbhi, Mattiaccio, Alessandro, Pippucci, Tommaso, Seri, Marco, Tacconelli, Evelina, van Agtmael, Michiel, Algera, Anne Geke, Appelman, Brent, van Baarle, Frank, Bax, Diane, Beudel, Martijn, Bogaard, Harm Jan, Bomers, Marije, Bonta, Peter, Bos, Lieuwe, Botta, Michela, de Brabander, Justin, de Bree, Godelieve, de Bruin, Sanne, Buis, David T.P., Bugiani, Marianna, Bulle, Esther, Chouchane, Osoul, Cloherty, Alex, Dijkstra, Mirjam, Dongelmans, Dave A., Dujardin, Romein W.G., Elbers, Paul, Fleuren, Lucas, Geerlings, Suzanne, Geijtenbeek, Theo, Girbes, Armand, Goorhuis, Bram, Grobusch, Martin P., Hafkamp, Florianne, Hagens, Laura, Hamann, Jorg, Harris, Vanessa, Hemke, Robert, Hermans, Sabine M., Heunks, Leo, Hollmann, Markus, Horn, Janneke, Hovius, Joppe W., de Jong, Menno D., Koning, Rutger, Lim, Endry H.T., van Mourik, Niels, Nellen, Jeaninne, Nossent, Esther J., Paulus, Frederique, Peters, Edgar, Pina-Fuentes, Dan A.I., van der Poll, Tom, Preckel, Bennedikt, Prins, Jan M., Raasveld, Jorinde, Reijnders, Tom, de Rotte, Maurits C.F. J., Schinkel, Michiel, Schultz, Marcus J., Schrauwen, Femke A.P., Schuurmans, Alex, Schuurmans, Jaap, Sigaloff, Kim, Slim, Marleen A., Smeele, Patrick, Smit, Marry, Stijnis, Cornelis S., Stilma, Willemke, Teunissen, Charlotte, Thoral, Patrick, Tsonas, Anissa M., Tuinman, Pieter R., van der Valk, Marc, Veelo, Denise P., Volleman, Carolien, de Vries, Heder, Vught, Lonneke A., van Vugt, Michèle, Wouters, Dorien, Zwinderman, A.H., Brouwer, Matthijs C., Wiersinga, W. Joost, Vlaar, Alexander P.J., Tompkins, Miranda F., Alba, Camille, Hupalo, Daniel N., Rosenberger, John, Sukumar, Gauthaman, Wilkerson, Matthew D., Zhang, Xijun, Lack, Justin, Oler, Andrew J., Dobbs, Kerry, Delmonte, Ottavia M., Danielson, Jeffrey J., Biondi, Andrea, Bettini, Laura Rachele, D’Angiò, Mariella, Beretta, Ilaria, Imberti, Luisa, Sottini, Alessandra, Quaresima, Virginia, Quiros-Roldan, Eugenia, Rossi, Camillo, Castagnoli, Riccardo, Montagna, Daniela, Licari, Amelia, Marseglia, Gian Luigi, Marchal, Astrid, Cirulli, Elizabeth T., Neveux, Iva, Bellos, Evangelos, Thwaites, Ryan S., Schiabor Barrett, Kelly M., Zhang, Yu, Nemes-Bokun, Ivana, Kalinova, Mariya, Catchpole, Andrew, Lack, Justin B., Chiu, Christopher, and Grzymski, Joseph J.

Published
2024
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5. Africa-specific human genetic variation near CHD1L associates with HIV-1 load

Author

McLaren, Paul J., Porreca, Immacolata, Iaconis, Gennaro, Mok, Hoi Ping, Mukhopadhyay, Subhankar, Karakoc, Emre, Cristinelli, Sara, Pomilla, Cristina, Bartha, István, Thorball, Christian W., Tough, Riley H., Angelino, Paolo, Kiar, Cher S., Carstensen, Tommy, Fatumo, Segun, Porter, Tarryn, Jarvis, Isobel, Skarnes, William C., Bassett, Andrew, DeGorter, Marianne K., Sathya Moorthy, Mohana Prasad, Tuff, Jeffrey F., Kim, Eun-Young, Walter, Miriam, Simons, Lacy M., Bashirova, Arman, Buchbinder, Susan, Carrington, Mary, Cossarizza, Andrea, De Luca, Andrea, Goedert, James J., Goldstein, David B., Haas, David W., Herbeck, Joshua T., Johnson, Eric O., Kaleebu, Pontiano, Kilembe, William, Kirk, Gregory D., Kootstra, Neeltje A., Kral, Alex H., Lambotte, Olivier, Luo, Ma, Mallal, Simon, Martinez-Picado, Javier, Meyer, Laurence, Miro, José M., Moodley, Pravi, Motala, Ayesha A., Mullins, James I., Nam, Kireem, Obel, Niels, Pirie, Fraser, Plummer, Francis A., Poli, Guido, Price, Matthew A., Rauch, Andri, Theodorou, Ioannis, Trkola, Alexandra, Walker, Bruce D., Winkler, Cheryl A., Zagury, Jean-François, Montgomery, Stephen B., Ciuffi, Angela, Hultquist, Judd F., Wolinsky, Steven M., Dougan, Gordon, Lever, Andrew M. L., Gurdasani, Deepti, Groom, Harriet, Sandhu, Manjinder S., and Fellay, Jacques

Published
2023
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6. ABX464 Decreases the Total Human Immunodeficiency Virus (HIV) Reservoir and HIV Transcription Initiation in CD4+ T Cells From Antiretroviral Therapy–Suppressed Individuals Living With HIV

Author

Moron-Lopez, Sara, Bernal, Silvia, Wong, Joseph K, Martinez-Picado, Javier, and Yukl, Steven A

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Clinical Research, Genetics, Infectious Diseases, Clinical Trials and Supportive Activities, Minority Health, Health Disparities, HIV/AIDS, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Infection, CD4-Positive T-Lymphocytes, DNA, Viral, HIV Infections, HIV-1, Humans, Proviruses, Quinolines, RNA, Viral Load, ABX464, antiviral drugs, HIV-1 DNA, HIV-1 RNA, HIV-1 transcription, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

BackgroundAntiretroviral therapy (ART) intensification and disruption of latency have been suggested as strategies to eradicate HIV. ABX464 is a novel antiviral that inhibits HIV RNA biogenesis. We investigated its effect on HIV transcription and total and intact HIV DNA in CD4+ T cells from ART-suppressed participants enrolled in the ABIVAX-005 clinical trial (NCT02990325).MethodsPeripheral CD4+ T cells were available for analysis from 9 ART-suppressed participants who were treated daily with 150 mg of ABX464 for 4 weeks. Total and intact HIV DNA and initiated, 5'elongated, unspliced, polyadenylated, and multiply-spliced HIV transcripts were quantified at weeks 0, 4, and 8 using ddPCR.ResultsWe observed a significant decrease in total HIV DNA (P = .008, median fold change (mfc) = 0.8) and a lower median level of intact HIV DNA (P = not significant [n.s.], mfc = 0.8) after ABX464 treatment. Moreover, we observed a decrease in initiated HIV RNA per million CD4+ T cells and per provirus (P = .05, mfc = 0.7; P = .004, mfc = 0.5, respectively), a trend toward a decrease in the 5'elongated HIV RNA per provirus (P = .07, mfc = 0.5), and a lower median level of unspliced HIV RNA (P = n.s., mfc = 0.6), but no decrease in polyadenylated or multiply-spliced HIV RNA.ConclusionsIn this substudy, ABX464 had a dual effect of decreasing total HIV DNA (and possibly intact proviruses) and HIV transcription per provirus. To further characterize its specific mechanism of action, long-term administration of ABX464 should be studied in a larger cohort.Clinical trials registrationNCT02990325.

Published
2022

8. In-depth virological and immunological characterization of HIV-1 cure after CCR5Δ32/Δ32 allogeneic hematopoietic stem cell transplantation

Author

Jensen, Björn-Erik Ole, Knops, Elena, Cords, Leon, Lübke, Nadine, Salgado, Maria, Busman-Sahay, Kathleen, Estes, Jacob D., Huyveneers, Laura E. P., Perdomo-Celis, Federico, Wittner, Melanie, Gálvez, Cristina, Mummert, Christiane, Passaes, Caroline, Eberhard, Johanna M., Münk, Carsten, Hauber, Ilona, Hauber, Joachim, Heger, Eva, De Clercq, Jozefien, Vandekerckhove, Linos, Bergmann, Silke, Dunay, Gábor A., Klein, Florian, Häussinger, Dieter, Fischer, Johannes C., Nachtkamp, Kathrin, Timm, Joerg, Kaiser, Rolf, Harrer, Thomas, Luedde, Tom, Nijhuis, Monique, Sáez-Cirión, Asier, Schulze zur Wiesch, Julian, Wensing, Annemarie M. J., Martinez-Picado, Javier, and Kobbe, Guido

Published
2023
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11. TL1A–DR3 Plasma Levels Are Predictive of HIV-1 Disease Control, and DR3 Costimulation Boosts HIV-1–Specific T Cell Responses

Author

Oriol-Tordera, Bruna, Olvera, Alex, Duran-Castells, Clara, Llano, Anuska, Mothe, Beatriz, Massanella, Marta, Dalmau, Judith, Ganoza, Carmela, Sanchez, Jorge, Calle, Maria Luz, Clotet, Bonaventura, Martinez-Picado, Javier, Negredo, Eugènia, Blanco, Julià, Hartigan-O'Connor, Dennis, Brander, Christian, and Ruiz-Riol, Marta

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Genetics, Prevention, HIV/AIDS, Infectious Diseases, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Animals, Antibodies, Monoclonal, Murine-Derived, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes, Female, HIV Infections, HIV-1, Humans, Male, Mice, Receptors, Tumor Necrosis Factor, Member 25, Tumor Necrosis Factor Ligand Superfamily Member 15, Biochemistry and cell biology
Abstract

Relative control of HIV-1 infection has been linked to genetic and immune host factors. In this study, we analyzed 96 plasma proteome arrays from chronic untreated HIV-1-infected individuals using the classificatory random forest approach to discriminate between uncontrolled disease (plasma viral load [pVL] >50,000 RNA copies/ml; CD4 counts 283 cells/mm3, n = 47) and relatively controlled disease (pVL

Published
2020

12. Early intervention with 3BNC117 and romidepsin at antiretroviral treatment initiation in people with HIV-1: a phase 1b/2a, randomized trial

Author

Gunst, Jesper D., Pahus, Marie H., Rosás-Umbert, Miriam, Lu, I-Na, Benfield, Thomas, Nielsen, Henrik, Johansen, Isik S., Mohey, Rajesh, Østergaard, Lars, Klastrup, Vibeke, Khan, Maryam, Schleimann, Mariane H., Olesen, Rikke, Støvring, Henrik, Denton, Paul W., Kinloch, Natalie N., Copertino, Dennis C., Ward, Adam R., Alberto, Winiffer D. Conce, Nielsen, Silke D., Puertas, Maria C., Ramos, Victor, Reeves, Jacqueline D., Petropoulos, Christos J., Martinez-Picado, Javier, Brumme, Zabrina L., Jones, R. Brad, Fox, Julie, Tolstrup, Martin, Nussenzweig, Michel C., Caskey, Marina, Fidler, Sarah, and Søgaard, Ole S.

Published
2022
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13. Recommendations for measuring HIV reservoir size in cure-directed clinical trials.

Author

Abdel-Mohsen, Mohamed, Richman, Douglas, Siliciano, Robert F, Nussenzweig, Michel C, Howell, Bonnie J, Martinez-Picado, Javier, Chomont, Nicolas, Bar, Katharine J, Yu, Xu G, Lichterfeld, Mathias, Alcami, Jose, Hazuda, Daria, Bushman, Frederic, Siliciano, Janet D, Betts, Michael R, Spivak, Adam M, Planelles, Vicente, Hahn, Beatrice H, Smith, Davey M, Ho, Ya-Chi, Buzon, Maria J, Gaebler, Christian, Paiardini, Mirko, Li, Qingsheng, Estes, Jacob D, Hope, Thomas J, Kostman, Jay, Mounzer, Karam, Caskey, Marina, Fox, Lawrence, Frank, Ian, Riley, James L, Tebas, Pablo, Montaner, Luis J, and BEAT-HIV Delaney Collaboratory to Cure HIV-1 infection

Subjects
BEAT-HIV Delaney Collaboratory to Cure HIV-1 infection, Medical and Health Sciences, Immunology
Abstract

Therapeutic strategies are being clinically tested either to eradicate latent HIV reservoirs or to achieve virologic control in the absence of antiretroviral therapy. Attaining this goal will require a consensus on how best to measure the numbers of persistently infected cells with the potential to cause viral rebound after antiretroviral-therapy cessation in assessing the results of cure-directed strategies in vivo. Current measurements assess various aspects of the HIV provirus and its functionality and produce divergent results. Here, we provide recommendations from the BEAT-HIV Martin Delaney Collaboratory on which viral measurements should be prioritized in HIV-cure-directed clinical trials.

Published
2020

14. Tuberculosis-associated IFN-I induces Siglec-1 on tunneling nanotubes and favors HIV-1 spread in macrophages

Author

Dupont, Maeva, Souriant, Shanti, Balboa, Luciana, Manh, Thien-Phong Vu, Pingris, Karine, Rousset, Stella, Cougoule, Céline, Rombouts, Yoann, Poincloux, Renaud, Neji, Myriam Ben, Allers, Carolina, Kaushal, Deepak, Kuroda, Marcelo J, Benet, Susana, Martinez-Picado, Javier, Izquierdo-Useros, Nuria, del Carmen Sasiain, Maria, Maridonneau-Parini, Isabelle, Neyrolles, Olivier, Vérollet, Christel, and Lugo-Villarino, Geanncarlo

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Rare Diseases, HIV/AIDS, Lung, Tuberculosis, 2.1 Biological and endogenous factors, Aetiology, Infection, Good Health and Well Being, Animals, Cells, Cultured, Coinfection, Female, Gene Expression Profiling, HIV Infections, HIV-1, Humans, Interferon Type I, Macaca mulatta, Macrophages, Alveolar, Male, Nanotubes, Sialic Acid Binding Ig-like Lectin 1, Tuberculosis, Pulmonary, HIV, cell biology, co-infection, human, infectious disease, interferons, macrophages, microbiology, mycobacterium tuberculosis, rhesus macaque, tunneling natotubes, Biochemistry and Cell Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

While tuberculosis (TB) is a risk factor in HIV-1-infected individuals, the mechanisms by which Mycobacterium tuberculosis (Mtb) worsens HIV-1 pathogenesis remain scarce. We showed that HIV-1 infection is exacerbated in macrophages exposed to TB-associated microenvironments due to tunneling nanotube (TNT) formation. To identify molecular factors associated with TNT function, we performed a transcriptomic analysis in these macrophages, and revealed the up-regulation of Siglec-1 receptor. Siglec-1 expression depends on Mtb-induced production of type I interferon (IFN-I). In co-infected non-human primates, Siglec-1 is highly expressed by alveolar macrophages, whose abundance correlates with pathology and activation of IFN-I/STAT1 pathway. Siglec-1 localizes mainly on microtubule-containing TNT that are long and carry HIV-1 cargo. Siglec-1 depletion decreases TNT length, diminishes HIV-1 capture and cell-to-cell transfer, and abrogates the exacerbation of HIV-1 infection induced by Mtb. Altogether, we uncover a deleterious role for Siglec-1 in TB-HIV-1 co-infection and open new avenues to understand TNT biology.

Published
2020

15. Sustained aviraemia despite anti-retroviral therapy non-adherence in male children following in utero hiv transmission

Author

Bengu, Nomonde, primary, Cromhout, Gabriela, additional, Adland, Emily, additional, Govender, Katya, additional, Herbert, Nicholas, additional, Lim, Nicholas, additional, Fillis, Rowena, additional, Sprenger, Kenneth, additional, Vieira, Vinicius, additional, Kannie, Samantha, additional, van Lobenstein, Jeroen, additional, Chinniah, Kogielambal, additional, Kapongo, Constant, additional, Bhoola, Roopesh, additional, Krishna, Malini, additional, Mchunu, Noxolo, additional, Pascucci, Giuseppe Rubens, additional, Cotugno, Nicola, additional, Palma, Paolo, additional, Tagarro, Alfredo, additional, Rojo, Pablo, additional, Roider, Julia, additional, Garcia-Guerrero, Maria C., additional, Ochsenbauer, Christina, additional, Groll, Andreas, additional, Reddy, Kavidha, additional, Giaquinto, Carlo, additional, Rossi, Paolo, additional, Hong, Seohyun, additional, Dong, Krista, additional, Ansari, M. Azim, additional, Puertas, Maria C., additional, Ndung’u, Thumbi, additional, Capparelli, Edmund, additional, Lichterfeld, Mathias, additional, Martinez-Picado, Javier, additional, Kappes, John C., additional, Archary, Moherndran, additional, and Goulder, Philip, additional

Published
2024
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16. Dynamics of virological and immunological markers of HIV persistence after allogeneic haematopoietic stem-cell transplantation in the IciStem cohort: a prospective observational cohort study

Author

Salgado, Maria, primary, Gálvez, Cristina, additional, Nijhuis, Monique, additional, Kwon, Mi, additional, Cardozo-Ojeda, E Fabian, additional, Badiola, Jon, additional, Gorman, Matthew J, additional, Huyveneers, Laura E P, additional, Urrea, Victor, additional, Bandera, Alessandra, additional, Jensen, Björn-Erik Ole, additional, Vandekerckhove, Linos, additional, Jurado, Manuel, additional, Raj, Kavita, additional, Schulze zur Wiesch, Julian, additional, Bailén, Rebeca, additional, Eberhard, Johanna M, additional, Nabergoj, Mitja, additional, Hütter, Gero, additional, Saldaña-Moreno, Raquel, additional, Oldford, Sharon, additional, Barrett, Lisa, additional, Ramirez, Maria Luisa Montes, additional, Garba, Salisu, additional, Gupta, Ravi Kumar, additional, Revollo, Boris, additional, Ferra-Coll, Christelle, additional, Kuball, Jurgen, additional, Alter, Galit, additional, Sáez-Cirión, Asier, additional, Diez-Martin, Jose Luis, additional, Duke, Elizabeth R, additional, Schiffer, Joshua T, additional, Wensing, Annemarie, additional, Martinez-Picado, Javier, additional, Muscatello, Antonio, additional, Calmy, Alexandra, additional, Chapel, Anais, additional, Mamez, Anne-Claire, additional, Passaes, Caroline, additional, Brisseau, Clarissa, additional, Olivarria, Eduardo, additional, Knops, Elena, additional, Heger, Eva, additional, Bikhezar, Fatima, additional, Perdomo-Celis, Federico, additional, Kobbe, Guido, additional, Gabriel, Ian H, additional, Lunzen, Jan V, additional, Dalmau, Judith, additional, Martín-Carbonero, Luz, additional, Puertas, Mari Carmen, additional, Garcia-Guerrero, Mari Carmen, additional, de Scheerder, Marie-Angélique, additional, Angin, Mathieu, additional, Lübke, Nadine, additional, Balsalobre, Pascual, additional, de Paz, Raquel, additional, Kaiser, Rolf, additional, Kerre, Tessa, additional, Harrer, Thomas, additional, Luedde, Tom, additional, and Rocha, Vanderson, additional

Published
2024
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17. Author Correction: Africa-specific human genetic variation near CHD1L associates with HIV-1 load

Author

McLaren, Paul J., Porreca, Immacolata, Iaconis, Gennaro, Mok, Hoi Ping, Mukhopadhyay, Subhankar, Karakoc, Emre, Cristinelli, Sara, Pomilla, Cristina, Bartha, István, Thorball, Christian W., Tough, Riley H., Angelino, Paolo, Kiar, Cher S., Carstensen, Tommy, Fatumo, Segun, Porter, Tarryn, Jarvis, Isobel, Skarnes, William C., Bassett, Andrew, DeGorter, Marianne K., Sathya Moorthy, Mohana Prasad, Tuff, Jeffrey F., Kim, Eun-Young, Walter, Miriam, Simons, Lacy M., Bashirova, Arman, Buchbinder, Susan, Carrington, Mary, Cossarizza, Andrea, De Luca, Andrea, Goedert, James J., Goldstein, David B., Haas, David W., Herbeck, Joshua T., Johnson, Eric O., Kaleebu, Pontiano, Kilembe, William, Kirk, Gregory D., Kootstra, Neeltje A., Kral, Alex H., Lambotte, Olivier, Luo, Ma, Mallal, Simon, Martinez-Picado, Javier, Meyer, Laurence, Miro, José M., Moodley, Pravi, Motala, Ayesha A., Mullins, James I., Nam, Kireem, Obel, Niels, Pirie, Fraser, Plummer, Francis A., Poli, Guido, Price, Matthew A., Rauch, Andri, Theodorou, Ioannis, Trkola, Alexandra, Walker, Bruce D., Winkler, Cheryl A., Zagury, Jean-François, Montgomery, Stephen B., Ciuffi, Angela, Hultquist, Judd F., Wolinsky, Steven M., Dougan, Gordon, Lever, Andrew M. L., Gurdasani, Deepti, Groom, Harriet, Sandhu, Manjinder S., and Fellay, Jacques

Published
2023
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18. Recommendations for analytical antiretroviral treatment interruptions in HIV research trials—report of a consensus meeting

Author

Julg, Boris, Dee, Lynda, Ananworanich, Jintanat, Barouch, Dan H, Bar, Katharine, Caskey, Marina, Colby, Donn J, Dawson, Liza, Dong, Krista L, Dubé, Karine, Eron, Joseph, Frater, John, Gandhi, Rajesh T, Geleziunas, Romas, Goulder, Philip, Hanna, George J, Jefferys, Richard, Johnston, Rowena, Kuritzkes, Daniel, Li, Jonathan Z, Likhitwonnawut, Udom, van Lunzen, Jan, Martinez-Picado, Javier, Miller, Veronica, Montaner, Luis J, Nixon, Douglas F, Palm, David, Pantaleo, Giuseppe, Peay, Holly, Persaud, Deborah, Salzwedel, Jessica, Salzwedel, Karl, Schacker, Timothy, Sheikh, Virginia, Søgaard, Ole S, Spudich, Serena, Stephenson, Kathryn, Sugarman, Jeremy, Taylor, Jeff, Tebas, Pablo, Tiemessen, Caroline T, Tressler, Randall, Weiss, Carol D, Zheng, Lu, Robb, Merlin L, Michael, Nelson L, Mellors, John W, Deeks, Steven G, and Walker, Bruce D

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Sexually Transmitted Infections, Infectious Diseases, Clinical Research, Clinical Trials and Supportive Activities, Infection, Anti-Retroviral Agents, HIV Infections, Humans, Sustained Virologic Response, Viral Load, Withholding Treatment, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

Analytical antiretroviral treatment interruption (ATI) is an important feature of HIV research, seeking to achieve sustained viral suppression in the absence of antiretroviral therapy (ART) when the goal is to measure effects of novel therapeutic interventions on time to viral load rebound or altered viral setpoint. Trials with ATIs also intend to determine host, virological, and immunological markers that are predictive of sustained viral control off ART. Although ATI is increasingly incorporated into proof-of-concept trials, no consensus has been reached on strategies to maximise its utility and minimise its risks. In addition, differences in ATI trial designs hinder the ability to compare efficacy and safety of interventions across trials. Therefore, we held a meeting of stakeholders from many interest groups, including scientists, clinicians, ethicists, social scientists, regulators, people living with HIV, and advocacy groups, to discuss the main challenges concerning ATI studies and to formulate recommendations with an emphasis on strategies for risk mitigation and monitoring, ART resumption criteria, and ethical considerations. In this Review, we present the major points of discussion and consensus views achieved with the goal of informing the conduct of ATIs to maximise the knowledge gained and minimise the risk to participants in clinical HIV research.

Published
2019

19. Gut microbiome signatures linked to HIV-1 reservoir size and viremia control

Author

Borgognone, Alessandra, Noguera-Julian, Marc, Oriol, Bruna, Noël-Romas, Laura, Ruiz-Riol, Marta, Guillén, Yolanda, Parera, Mariona, Casadellà, Maria, Duran, Clara, Puertas, Maria C., Català-Moll, Francesc, De Leon, Marlon, Knodel, Samantha, Birse, Kenzie, Manzardo, Christian, Miró, José M., Clotet, Bonaventura, Martinez-Picado, Javier, Moltó, José, Mothe, Beatriz, Burgener, Adam, Brander, Christian, and Paredes, Roger

Published
2022
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20. Lectins enhance SARS-CoV-2 infection and influence neutralizing antibodies

Author

Lempp, Florian A., Soriaga, Leah B., Montiel-Ruiz, Martin, Benigni, Fabio, Noack, Julia, Park, Young-Jun, Bianchi, Siro, Walls, Alexandra C., Bowen, John E., Zhou, Jiayi, Kaiser, Hannah, Joshi, Anshu, Agostini, Maria, Meury, Marcel, Dellota, Jr, Exequiel, Jaconi, Stefano, Cameroni, Elisabetta, Martinez-Picado, Javier, Vergara-Alert, Júlia, Izquierdo-Useros, Nuria, Virgin, Herbert W., Lanzavecchia, Antonio, Veesler, David, Purcell, Lisa A., Telenti, Amalio, and Corti, Davide

Published
2021
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21. CD32 is expressed on cells with transcriptionally active HIV but does not enrich for HIV DNA in resting T cells

Author

Abdel-Mohsen, Mohamed, Kuri-Cervantes, Leticia, Grau-Exposito, Judith, Spivak, Adam M, Nell, Racheal A, Tomescu, Costin, Vadrevu, Surya Kumari, Giron, Leila B, Serra-Peinado, Carla, Genescà, Meritxell, Castellví, Josep, Wu, Guoxin, Del Rio Estrada, Perla M, González-Navarro, Mauricio, Lynn, Kenneth, King, Colin T, Vemula, Sai, Cox, Kara, Wan, Yanmin, Li, Qingsheng, Mounzer, Karam, Kostman, Jay, Frank, Ian, Paiardini, Mirko, Hazuda, Daria, Reyes-Terán, Gustavo, Richman, Douglas, Howell, Bonnie, Tebas, Pablo, Martinez-Picado, Javier, Planelles, Vicente, Buzon, Maria J, Betts, Michael R, and Montaner, Luis J

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, Infection, Good Health and Well Being, Anti-Retroviral Agents, CD4-Positive T-Lymphocytes, HIV Infections, Humans, In Vitro Techniques, Lymphocytes, Receptors, CCR4, Receptors, CCR6, Receptors, CXCR3, Receptors, IgG, Biological Sciences, Medical and Health Sciences, Medical biotechnology, Biomedical engineering
Abstract

The persistence of HIV reservoirs, including latently infected, resting CD4+ T cells, is the major obstacle to cure HIV infection. CD32a expression was recently reported to mark CD4+ T cells harboring a replication-competent HIV reservoir during antiretroviral therapy (ART) suppression. We aimed to determine whether CD32 expression marks HIV latently or transcriptionally active infected CD4+ T cells. Using peripheral blood and lymphoid tissue of ART-treated HIV+ or SIV+ subjects, we found that most of the circulating memory CD32+ CD4+ T cells expressed markers of activation, including CD69, HLA-DR, CD25, CD38, and Ki67, and bore a TH2 phenotype as defined by CXCR3, CCR4, and CCR6. CD32 expression did not selectively enrich for HIV- or SIV-infected CD4+ T cells in peripheral blood or lymphoid tissue; isolated CD32+ resting CD4+ T cells accounted for less than 3% of the total HIV DNA in CD4+ T cells. Cell-associated HIV DNA and RNA loads in CD4+ T cells positively correlated with the frequency of CD32+ CD69+ CD4+ T cells but not with CD32 expression on resting CD4+ T cells. Using RNA fluorescence in situ hybridization, CD32 coexpression with HIV RNA or p24 was detected after in vitro HIV infection (peripheral blood mononuclear cell and tissue) and in vivo within lymph node tissue from HIV-infected individuals. Together, these results indicate that CD32 is not a marker of resting CD4+ T cells or of enriched HIV DNA-positive cells after ART; rather, CD32 is predominately expressed on a subset of activated CD4+ T cells enriched for transcriptionally active HIV after long-term ART.

Published
2018

22. Differential Immunodominance Hierarchy of CD8+ T-Cell Responses in HLA-B*27:05- and -B*27:02-Mediated Control of HIV-1 Infection

Author

Adland, Emily, Hill, Matilda, Lavandier, Nora, Csala, Anna, Edwards, Anne, Chen, Fabian, Radkowski, Marek, Kowalska, Justyna D, Paraskevis, Dimitrios, Hatzakis, Angelos, Valenzuela-Ponce, Humberto, Pfafferott, Katja, Williams, Ian, Pellegrino, Pierre, Borrow, Persephone, Mori, Masahiko, Rockstroh, Jürgen, Prado, Julia G, Mothe, Beatriz, Dalmau, Judith, Martinez-Picado, Javier, Tudor-Williams, Gareth, Frater, John, Stryhn, Anette, Buus, Soren, Teran, Gustavo Reyes, Mallal, Simon, John, Mina, Buchbinder, Susan, Kirk, Gregory, Martin, Jeffrey, Michael, Nelson, Fellay, Jacques, Deeks, Steve, Walker, Bruce, Avila-Rios, Santiago, Cole, David, Brander, Christian, Carrington, Mary, and Goulder, Philip

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Infectious Diseases, HIV/AIDS, Clinical Research, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, CD8-Positive T-Lymphocytes, Genes, MHC Class I, HIV Infections, HIV-1, HLA-B27 Antigen, Humans, Immunodominant Epitopes, Viral Load, gag Gene Products, Human Immunodeficiency Virus, nef Gene Products, Human Immunodeficiency Virus, CD8(+) T cell, HIV Gag, HIV Nef, HLA, HLA-B*27, human immunodeficiency virus, CD8+ T cell, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract

The well-characterized association between HLA-B*27:05 and protection against HIV disease progression has been linked to immunodominant HLA-B*27:05-restricted CD8+ T-cell responses toward the conserved Gag KK10 (residues 263 to 272) and polymerase (Pol) KY9 (residues 901 to 909) epitopes. We studied the impact of the 3 amino acid differences between HLA-B*27:05 and the closely related HLA-B*27:02 on the HIV-specific CD8+ T-cell response hierarchy and on immune control of HIV. Genetic epidemiological data indicate that both HLA-B*27:02 and HLA-B*27:05 are associated with slower disease progression and lower viral loads. The effect of HLA-B*27:02 appeared to be consistently stronger than that of HLA-B*27:05. In contrast to HLA-B*27:05, the immunodominant HIV-specific HLA-B*27:02-restricted CD8+ T-cell response is to a Nef epitope (residues 142 to 150 [VW9]), with Pol KY9 subdominant and Gag KK10 further subdominant. This selection was driven by structural differences in the F pocket, mediated by a polymorphism between these two HLA alleles at position 81. Analysis of autologous virus sequences showed that in HLA-B*27:02-positive subjects, all three of these CD8+ T-cell responses impose selection pressure on the virus, whereas in HLA-B*27:05-positive subjects, there is no Nef VW9-mediated selection pressure. These studies demonstrate that HLA-B*27:02 mediates protection against HIV disease progression that is at least as strong as or stronger than that mediated by HLA-B*27:05. In combination with the protective Gag KK10 and Pol KY9 CD8+ T-cell responses that dominate HIV-specific CD8+ T-cell activity in HLA-B*27:05-positive subjects, a Nef VW9-specific response is additionally present and immunodominant in HLA-B*27:02-positive subjects, mediated through a polymorphism at residue 81 in the F pocket, that contributes to selection pressure against HIV.IMPORTANCE CD8+ T cells play a central role in successful control of HIV infection and have the potential also to mediate the eradication of viral reservoirs of infection. The principal means by which protective HLA class I molecules, such as HLA-B*27:05 and HLA-B*57:01, slow HIV disease progression is believed to be via the particular HIV-specific CD8+ T cell responses restricted by those alleles. We focus here on HLA-B*27:05, one of the best-characterized protective HLA molecules, and the closely related HLA-B*27:02, which differs by only 3 amino acids and which has not been well studied in relation to control of HIV infection. We show that HLA-B*27:02 is also protective against HIV disease progression, but the CD8+ T-cell immunodominance hierarchy of HLA-B*27:02 differs strikingly from that of HLA-B*27:05. These findings indicate that the immunodominant HLA-B*27:02-restricted Nef response adds to protection mediated by the Gag and Pol specificities that dominate anti-HIV CD8+ T-cell activity in HLA-B*27:05-positive subjects.

Published
2018

25. SARS-CoV-2 interaction with Siglec-1 mediates trans-infection by dendritic cells

Author

Perez-Zsolt, Daniel, Muñoz-Basagoiti, Jordana, Rodon, Jordi, Elosua-Bayes, Marc, Raïch-Regué, Dàlia, Risco, Cristina, Sachse, Martin, Pino, Maria, Gumber, Sanjeev, Paiardini, Mirko, Chojnacki, Jakub, Erkizia, Itziar, Muñiz-Trabudua, Xabier, Ballana, Ester, Riveira-Muñoz, Eva, Noguera-Julian, Marc, Paredes, Roger, Trinité, Benjamin, Tarrés-Freixas, Ferran, Blanco, Ignacio, Guallar, Victor, Carrillo, Jorge, Blanco, Julià, Telenti, Amalio, Heyn, Holger, Segalés, Joaquim, Clotet, Bonaventura, Martinez-Picado, Javier, Vergara-Alert, Júlia, and Izquierdo-Useros, Nuria

Published
2021
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26. Author Correction to: SARS-CoV-2 interaction with Siglec-1 mediates trans-infection by dendritic cells

Author

Perez-Zsolt, Daniel, Muñoz-Basagoiti, Jordana, Rodon, Jordi, Elosua-Bayes, Marc, Raïch-Regué, Dàlia, Risco, Cristina, Sachse, Martin, Pino, Maria, Gumber, Sanjeev, Paiardini, Mirko, Chojnacki, Jakub, Erkizia, Itziar, Muñiz-Trabudua, Xabier, Ballana, Ester, Riveira-Muñoz, Eva, Noguera-Julian, Marc, Paredes, Roger, Trinité, Benjamin, Tarrés-Freixas, Ferran, Blanco, Ignacio, Guallar, Victor, Carrillo, Jorge, Blanco, Julià, Telenti, Amalio, Heyn, Holger, Segalés, Joaquim, Clotet, Bonaventura, Martinez-Picado, Javier, Vergara-Alert, Júlia, and Izquierdo-Useros, Nuria

Published
2022
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27. Targeting Viral Transcription for HIV Cure Strategies.

Author

Izquierdo-Pujol, Jon, Puertas, Maria C., Martinez-Picado, Javier, and Morón-López, Sara

Subjects
HIV infections, HIV, RNA regulation, GENOME editing, HIV-positive persons
Abstract

Combination antiretroviral therapy (ART) suppresses viral replication to undetectable levels, reduces mortality and morbidity, and improves the quality of life of people living with HIV (PWH). However, ART cannot cure HIV infection because it is unable to eliminate latently infected cells. HIV latency may be regulated by different HIV transcription mechanisms, such as blocks to initiation, elongation, and post-transcriptional processes. Several latency-reversing (LRA) and -promoting agents (LPA) have been investigated in clinical trials aiming to eliminate or reduce the HIV reservoir. However, none of these trials has shown a conclusive impact on the HIV reservoir. Here, we review the cellular and viral factors that regulate HIV-1 transcription, the potential pharmacological targets and genetic and epigenetic editing techniques that have been or might be evaluated to disrupt HIV-1 latency, the role of miRNA in post-transcriptional regulation of HIV-1, and the differences between the mechanisms regulating HIV-1 and HIV-2 expression. [ABSTRACT FROM AUTHOR]

Published
2024
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28. HIGH-FREQUENCY failure of combination antiretroviral therapy in paediatric HIV infection is associated with unmet maternal needs causing maternal NON-ADHERENCE

Author

Millar, Jane R., Bengu, Nomonde, Fillis, Rowena, Sprenger, Ken, Ntlantsana, Vuyokazi, Vieira, Vinicius A., Khambati, Nisreen, Archary, Moherndran, Muenchhoff, Maximilian, Groll, Andreas, Grayson, Nicholas, Adamson, John, Govender, Katya, Dong, Krista, Kiepiela, Photini, Walker, Bruce D., Bonsall, David, Connor, Thomas, Bull, Matthew J., Nxele, Nelisiwe, Roider, Julia, Ismail, Nasreen, Adland, Emily, Puertas, Maria C., Martinez-Picado, Javier, Matthews, Philippa C., Ndung'u, Thumbi, and Goulder, Philip

Published
2020
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29. Evidence for HIV-1 cure after CCR5Δ32/Δ32 allogeneic haemopoietic stem-cell transplantation 30 months post analytical treatment interruption: a case report

Author

Gupta, Ravindra Kumar, Peppa, Dimitra, Hill, Alison L, Gálvez, Cristina, Salgado, Maria, Pace, Matthew, McCoy, Laura E, Griffith, Sarah A, Thornhill, John, Alrubayyi, Aljawharah, Huyveneers, Laura E P, Nastouli, Eleni, Grant, Paul, Edwards, Simon G, Innes, Andrew J, Frater, John, Nijhuis, Monique, Wensing, Anne Marie J, Martinez-Picado, Javier, and Olavarria, Eduardo

Published
2020
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30. Persistent HIV-1 replication during antiretroviral therapy

Author

Martinez-Picado, Javier and Deeks, Steven G

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, HIV/AIDS, 2.2 Factors relating to the physical environment, Aetiology, Infection, Anti-Retroviral Agents, HIV Infections, HIV-1, Humans, Lymphoid Tissue, Virus Replication, abnormal levels of immune activation and inflammation, cell-to-cell infection, HIV residual replication during ART, limited drug penetration within tissues, presence of immune sanctuaries, Public Health and Health Services, Virology, Clinical sciences, Medical microbiology, Epidemiology
Abstract

Purpose of reviewThe present review will highlight some of the recent findings regarding the capacity of HIV-1 to replicate during antiretroviral therapy (ART).Recent findingsAlthough ART is highly effective at inhibiting HIV replication, it is not curative. Several mechanisms contribute to HIV persistence during ART, including HIV latency, immune dysfunction, and perhaps persistent low-level spread of the virus to uninfected cells (replication). The success in curing HIV will depend on efficiently targeting these three aspects. The degree to which HIV replicates during ART remains controversial. Most studies have failed to find any evidence of HIV evolution in blood, even with samples collected over many years, although a recent very intensive study of three individuals suggested that the virus population does shift, at least during the first few months of therapy. Stronger but still not definitive evidence for replication comes from a series of studies in which standard regimens were intensified with an integration inhibitor, resulting in changes in episomal DNA (blood) and cell-associated RNA (tissue). Limited drug penetration within tissues and the presence of immune sanctuaries have been argued as potential mechanisms allowing HIV to spread during ART. Mathematical models suggest that HIV replication and evolution is possible even without the selection of fully drug-resistant variants. As persistent HIV replication could have clinical consequences and might limit the efficacy of curative interventions, determining if HIV replicates during ART and why, should remain a key focus of the HIV research community.SummaryResidual viral replication likely persists in lymphoid tissues, at least in a subset of individuals. Abnormal levels of immune activation might contribute to sustain virus replication.

Published
2016

31. Exploring the HIV-1 Rev Recognition Element (RRE)–Rev Inhibitory Capacity and Antiretroviral Action of Benfluron Analogs

Author

Chumillas, Sergi, primary, Loharch, Saurabh, additional, Beltrán, Manuela, additional, Szewczyk, Mateusz P., additional, Bernal, Silvia, additional, Puertas, Maria C., additional, Martinez-Picado, Javier, additional, Alcamí, José, additional, Bedoya, Luis M., additional, Marchán, Vicente, additional, and Gallego, José, additional

Published
2023
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32. Robust HIV-specific CD4+ and CD8+ T-cell responses distinguish the rare phenotype of elite control in adolescents living with HIV from viraemic non-progressors

Author

Vieira, Vinicius A., Millar, Jane, Adland, Emily, Muenchhoff, Maximilian, Roider, Julia, Guash, Claudia Fortuny, Peluso, Denise, Thomé, Beatriz, Garcia-Guerrero, Maria C., Puertas, Mari C., Bamford, Alasdair, Brander, Christian, Carrington, Mary, Martinez-Picado, Javier, Frater, John, Tudor-Williams, Gareth, and Goulder, Philip

Published
2021
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33. Robust HIV-specific CD4+ and CD8+ T-cell responses distinguish elite control in adolescents living with HIV from viremic nonprogressors

Author

Vieira, Vinicius A., Millar, Jane, Adland, Emily, Muenchhoff, Maximilian, Roider, Julia, Guash, Claudia Fortuny, Peluso, Denise, Thomé, Beatriz, Garcia-Guerrero, Maria C., Puertas, Mari C., Bamford, Alasdair, Brander, Christian, Carrington, Mary, Martinez-Picado, Javier, Frater, John, Tudor-Williams, Gareth, and Goulder, Philip

Published
2022
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34. Therapeutic Vaccination Refocuses T-cell Responses Towards Conserved Regions of HIV-1 in Early Treated Individuals (BCN 01 study)

Author

Mothe, Beatriz, Manzardo, Christian, Sanchez-Bernabeu, Alvaro, Coll, Pep, Morón-López, Sara, Puertas, Maria C., Rosas-Umbert, Miriam, Cobarsi, Patricia, Escrig, Roser, Perez-Alvarez, Núria, Ruiz, Irene, Rovira, Cristina, Meulbroek, Michael, Crook, Alison, Borthwick, Nicola, Wee, Edmund G., Yang, Hongbing, Miró, Jose M., Dorrell, Lucy, Clotet, Bonaventura, Martinez-Picado, Javier, Brander, Christian, and Hanke, Tomáš

Published
2019
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35. Different Plasma Markers of Inflammation Are Influenced by Immune Recovery and cART Composition or Intensification in Treated HIV Infected Individuals

Author

Massanella, Marta, Ouchi, Dan, Marfil, Silvia, Llibre, Josep M, Puertas, Maria C, Buzón, María J, Richman, Douglas D, Orna, Elisa, Stevenson, Mario, Gatell, Josep M, Domingo, Pere, Negredo, Eugènia, Martinez-Picado, Javier, Clotet, Bonaventura, and Blanco, Julià

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Clinical Research, Emerging Infectious Diseases, Infectious Diseases, HIV/AIDS, Clinical Trials and Supportive Activities, Inflammatory and immune system, Infection, Adult, Biomarkers, Female, HIV Infections, HIV Integrase Inhibitors, Humans, Inflammation, Male, Middle Aged, Prospective Studies, Raltegravir Potassium, General Science & Technology
Abstract

BackgroundHIV-1 infection increases plasma levels of inflammatory markers. Combination antiretroviral therapy (cART) does not restore inflammatory markers to normal levels. Since intensification of cART with raltegravir reduced CD8 T-cell activation in the Discor-Ral and IntegRal studies, we have evaluated the effect of raltegravir intensification on several soluble inflammation markers in these studies.MethodsLongitudinal plasma samples (0-48 weeks) from the IntegRal (n = 67, 22 control and 45 intensified individuals) and the Discor-Ral studies (44 individuals with CD4 T-cell counts

Published
2014

36. Impact of Obefazimod on Viral Persistence, Inflammation, and Immune Activation in People With Human Immunodeficiency Virus on Suppressive Antiretroviral Therapy

Author

Bernal, Silvia, primary, Puertas, Maria C, additional, Morón-López, Sara, additional, Cranston, Ross D, additional, Urrea, Víctor, additional, Dalmau, Judith, additional, Salgado, María, additional, Gálvez, Cristina, additional, Erkizia, Itziar, additional, McGowan, Ian, additional, Scherrer, Didier, additional, Revollo, Boris, additional, Sirera, Guillem, additional, Santos, José Ramón, additional, Clotet, Bonaventura, additional, Paredes, Roger, additional, and Martinez-Picado, Javier, additional

Published
2023
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39. HIV-1 remission following CCR5[DELTA]32/[DELTA]32 haematopoietic stem-cell transplantation

Author

Gupta, Ravindra K., Abdul-Jawad, Sultan, McCoy, Laura E., Mok, Hoi Ping, Peppa, Dimitra, Salgado, Maria, and Martinez-Picado, Javier

Subjects
HIV infections -- Care and treatment, Regression (Disease) -- Research, Stem cell transplantation -- Patient outcomes, Cancer research, Lymphomas, Lymphocytes, Vincristine, Tumors, Efavirenz, Hematopoietic stem cell transplantation, RNA, Antibodies, DNA, T cells, Raltegravir, Rilpivirine, Antiretroviral agents, HIV, Stem cells, Emtricitabine, Highly active antiretroviral therapy, Surgery, Genetic research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

A cure for HIV-1 remains unattainable as only one case has been reported, a decade ago.sup.1,2. The individual--who is known as the 'Berlin patient'--underwent two allogeneic haematopoietic stem-cell transplantation (HSCT) procedures using a donor with a homozygous mutation in the HIV coreceptor CCR5 (CCR5[DELTA]32/[DELTA]32) to treat his acute myeloid leukaemia. Total body irradiation was given with each HSCT. Notably, it is unclear which treatment or patient parameters contributed to this case of long-term HIV remission. Here we show that HIV-1 remission may be possible with a less aggressive and toxic approach. An adult infected with HIV-1 underwent allogeneic HSCT for Hodgkin's lymphoma using cells from a CCR5[DELTA]32/[DELTA]32 donor. He experienced mild gut graft-versus-host disease. Antiretroviral therapy was interrupted 16 months after transplantation. HIV-1 remission has been maintained over a further 18 months. Plasma HIV-1 RNA has been undetectable at less than one copy per millilitre along with undetectable HIV-1 DNA in peripheral CD4 T lymphocytes. Quantitative viral outgrowth assays from peripheral CD4 T lymphocytes show no reactivatable virus using a total of 24 million resting CD4 T cells. CCR5-tropic, but not CXCR4-tropic, viruses were identified in HIV-1 DNA from CD4 T cells of the patient before the transplant. CD4 T cells isolated from peripheral blood after transplantation did not express CCR5 and were susceptible only to CXCR4-tropic virus ex vivo. HIV-1 Gag-specific CD4 and CD8 T cell responses were lost after transplantation, whereas cytomegalovirus-specific responses were detectable. Similarly, HIV-1-specific antibodies and avidities fell to levels comparable to those in the Berlin patient following transplantation. Although at 18 months after the interruption of treatment it is premature to conclude that this patient has been cured, these data suggest that a single allogeneic HSCT with homozygous CCR5[DELTA]32 donor cells may be sufficient to achieve HIV-1 remission with reduced intensity conditioning and no irradiation, and the findings provide further support for the development of HIV-1 remission strategies based on preventing CCR5 expression. An adult infected with HIV-1 who underwent allogeneic haematopoietic stem-cell transplantation for Hodgkin's lymphoma using cells from a CCR5[DELTA]32/[DELTA]32 donor achieved full remission of HIV-1 for 18 months after transplantation and 16 months after cessation of antiretroviral therapy., Author(s): Ravindra K. Gupta [sup.1] [sup.2] [sup.3] [sup.4] [sup.5] , Sultan Abdul-Jawad [sup.1] , Laura E. McCoy [sup.1] , Hoi Ping Mok [sup.4] , Dimitra Peppa [sup.3] [sup.6] , Maria [...]

Published
2019
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40. Barriers to a cure for HIV: new ways to target and eradicate HIV-1 reservoirs

Author

Katlama, Christine, Deeks, Steven G, Autran, Brigitte, Martinez-Picado, Javier, van Lunzen, Jan, Rouzioux, Christine, Miller, Michael, Vella, Stefano, Schmitz, Joern E, Ahlers, Jeffrey, Richman, Douglas D, and Sekaly, Rafick P

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, HIV/AIDS, Aetiology, 2.2 Factors relating to the physical environment, Infection, Anti-HIV Agents, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Drug Therapy, Combination, HIV Infections, HIV-1, Humans, RNA, Viral, Receptors, CCR5, Virus Latency, Virus Replication, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

Antiretroviral therapy for HIV infection needs lifelong access and strict adherence to regimens that are both expensive and associated with toxic effects. A curative intervention will be needed to fully stop the epidemic. The failure to eradicate HIV infection during long-term antiretroviral therapy shows the intrinsic stability of the viral genome in latently infected CD4T cells and other cells, and possibly a sustained low-level viral replication. Heterogeneity in latently infected cell populations and homoeostatic proliferation of infected cells might affect the dynamics of virus production and persistence. Despite potent antiretroviral therapy, chronic immune activation, inflammation, and immune dysfunction persist, and are likely to have important effects on the size and distribution of the viral reservoir. The inability of the immune system to recognise cells harbouring latent virus and to eliminate cells actively producing virus is the biggest challenge to finding a cure. We look at new approaches to unravelling the complex virus-host interactions that lead to persistent infection and latency, and discuss the rationale for combination of novel treatment strategies with available antiretroviral treatment options to cure HIV.

Published
2013

42. Definition of the viral targets of protective HIV-1-specific T cell responses

Author

Mothe, Beatriz, Llano, Anuska, Ibarrondo, Javier, Daniels, Marcus, Miranda, Cristina, Zamarreño, Jennifer, Bach, Vanessa, Zuniga, Rosario, Pérez-Álvarez, Susana, Berger, Christoph T, Puertas, Maria C, Martinez-Picado, Javier, Rolland, Morgane, Farfan, Marilu, Szinger, James J, Hildebrand, William H, Yang, Otto O, Sanchez-Merino, Victor, Brumme, Chanson J, Brumme, Zabrina L, Heckerman, David, Allen, Todd M, Mullins, James I, Gómez, Guadalupe, Goulder, Philip J, Walker, Bruce D, Gatell, Jose M, Clotet, Bonaventura, Korber, Bette T, Sanchez, Jorge, and Brander, Christian

Abstract

Abstract Background The efficacy of the CTL component of a future HIV-1 vaccine will depend on the induction of responses with the most potent antiviral activity and broad HLA class I restriction. However, current HIV vaccine designs are largely based on viral sequence alignments only, not incorporating experimental data on T cell function and specificity. Methods Here, 950 untreated HIV-1 clade B or -C infected individuals were tested for responses to sets of 410 overlapping peptides (OLP) spanning the entire HIV-1 proteome. For each OLP, a "protective ratio" (PR) was calculated as the ratio of median viral loads (VL) between OLP non-responders and responders. Results For both clades, there was a negative relationship between the PR and the entropy of the OLP sequence. There was also a significant additive effect of multiple responses to beneficial OLP. Responses to beneficial OLP were of significantly higher functional avidity than responses to non-beneficial OLP. They also had superior in-vitro antiviral activities and, importantly, were at least as predictive of individuals' viral loads than their HLA class I genotypes. Conclusions The data thus identify immunogen sequence candidates for HIV and provide an approach for T cell immunogen design applicable to other viral infections.

Published
2011

43. Common genetic variation and the control of HIV-1 in humans.

Author

Fellay, Jacques, Ge, Dongliang, Shianna, Kevin V, Colombo, Sara, Ledergerber, Bruno, Cirulli, Elizabeth T, Urban, Thomas J, Zhang, Kunlin, Gumbs, Curtis E, Smith, Jason P, Castagna, Antonella, Cozzi-Lepri, Alessandro, De Luca, Andrea, Easterbrook, Philippa, Günthard, Huldrych F, Mallal, Simon, Mussini, Cristina, Dalmau, Judith, Martinez-Picado, Javier, Miro, José M, Obel, Niels, Wolinsky, Steven M, Martinson, Jeremy J, Detels, Roger, Margolick, Joseph B, Jacobson, Lisa P, Descombes, Patrick, Antonarakis, Stylianos E, Beckmann, Jacques S, O'Brien, Stephen J, Letvin, Norman L, McMichael, Andrew J, Haynes, Barton F, Carrington, Mary, Feng, Sheng, Telenti, Amalio, Goldstein, David B, and NIAID Center for HIV/AIDS Vaccine Immunology (CHAVI)

Subjects
NIAID Center for HIV/AIDS Vaccine Immunology, Humans, HIV-1, HIV Infections, Disease Progression, Viral Load, Major Histocompatibility Complex, Genotype, Phenotype, Polymorphism, Single Nucleotide, Alleles, Adult, Female, Male, Genetic Variation, Kaplan-Meier Estimate, Polymorphism, Single Nucleotide, Genetics, Developmental Biology
Abstract

To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians.

Published
2009

44. Role of Siglecs in viral infections: A double-edged sword interaction

Author

Raïch-Regué, Dàlia, primary, Resa-Infante, Patricia, additional, Gallemí, Marçal, additional, Laguia, Fernando, additional, Muñiz-Trabudua, Xabier, additional, Muñoz-Basagoiti, Jordana, additional, Perez-Zsolt, Daniel, additional, Chojnacki, Jakub, additional, Benet, Susana, additional, Clotet, Bonaventura, additional, Martinez-Picado, Javier, additional, and Izquierdo-Useros, Nuria, additional

Published
2023
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46. Sustained aviremia despite anti-retroviral therapy non-adherence in male children after in utero HIV transmission

Author

Bengu, Nomonde, Cromhout, Gabriela, Adland, Emily, Govender, Katya, Herbert, Nicholas, Lim, Nicholas, Fillis, Rowena, Sprenger, Kenneth, Vieira, Vinicius, Kannie, Samantha, van Lobenstein, Jeroen, Chinniah, Kogielambal, Kapongo, Constant, Bhoola, Roopesh, Krishna, Malini, Mchunu, Noxolo, Pascucci, Giuseppe Rubens, Cotugno, Nicola, Palma, Paolo, Tagarro, Alfredo, Rojo, Pablo, Roider, Julia, Garcia-Guerrero, Maria C., Ochsenbauer, Christina, Groll, Andreas, Reddy, Kavidha, Giaquinto, Carlo, Rossi, Paolo, Hong, Seohyun, Dong, Krista, Ansari, M. Azim, Puertas, Maria C., Ndung’u, Thumbi, Capparelli, Edmund, Lichterfeld, Mathias, Martinez-Picado, Javier, Kappes, John C., Archary, Moherndran, and Goulder, Philip

Abstract

After sporadic reports of post-treatment control of HIV in children who initiated combination anti-retroviral therapy (cART) early, we prospectively studied 284 very-early-cART-treated children from KwaZulu-Natal, South Africa, after vertical HIV transmission to assess control of viremia. Eighty-four percent of the children achieved aviremia on cART, but aviremia persisting to 36 or more months was observed in only 32%. We observed that male infants have lower baseline plasma viral loads (P= 0.01). Unexpectedly, a subset (n= 5) of males maintained aviremia despite unscheduled complete discontinuation of cART lasting 3–10 months (n= 4) or intermittent cART adherence during 17-month loss to follow-up (n= 1). We further observed, in vertically transmitted viruses, a negative correlation between type I interferon (IFN-I) resistance and viral replication capacity (VRC) (P< 0.0001) that was markedly stronger for males than for females (r= −0.51 versus r= −0.07 for IFN-α). Although viruses transmitted to male fetuses were more IFN-I sensitive and of higher VRC than those transmitted to females in the full cohort (P< 0.0001 and P= 0.0003, respectively), the viruses transmitted to the five males maintaining cART-free aviremia had significantly lower replication capacity (P< 0.0001). These data suggest that viremic control can occur in some infants with in utero–acquired HIV infection after early cART initiation and may be associated with innate immune sex differences.

Published
2024
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47. Plasma-derived extracellular vesicles from Plasmodium vivax patients signal spleen fibroblasts via NF-kB facilitating parasite cytoadherence

Author

Toda, Haruka, Diaz-Varela, Miriam, Segui-Barber, Joan, Roobsoong, Wanlapa, Baro, Barbara, Garcia-Silva, Susana, Galiano, Alicia, Gualdrón-López, Melisa, Almeida, Anne C. G., Brito, Marcelo A. M., de Melo, Gisely Cardoso, Aparici-Herraiz, Iris, Castro-Cavadía, Carlos, Monteiro, Wuelton Marcelo, Borràs, Eva, Sabidó, Eduard, Almeida, Igor C., Chojnacki, Jakub, Martinez-Picado, Javier, Calvo, Maria, Armengol, Pilar, Carmona-Fonseca, Jaime, Yasnot, Maria Fernanda, Lauzurica, Ricardo, Marcilla, Antonio, Peinado, Hector, Galinski, Mary R., Lacerda, Marcus V. G., Sattabongkot, Jetsumon, Fernandez-Becerra, Carmen, and del Portillo, Hernando A.

Published
2020
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48. Author Correction: Sex-specific innate immune selection of HIV-1 in utero is associated with increased female susceptibility to infection

Author

Adland, Emily, Millar, Jane, Bengu, Nomonde, Muenchhoff, Maximilian, Fillis, Rowena, Sprenger, Kenneth, Ntlantsana, Vuyokasi, Roider, Julia, Vieira, Vinicius, Govender, Katya, Adamson, John, Nxele, Nelisiwe, Ochsenbauer, Christina, Kappes, John, Mori, Luisa, van Lobenstein, Jeroen, Graza, Yeney, Chinniah, Kogielambal, Kapongo, Constant, Bhoola, Roopesh, Krishna, Malini, Matthews, Philippa C., Poderos, Ruth Penya, Lluch, Marta Colomer, Puertas, Maria C., Prado, Julia G., McKerrow, Neil, Archary, Moherndran, Ndung’u, Thumbi, Groll, Andreas, Jooste, Pieter, Martinez-Picado, Javier, Altfeld, Marcus, and Goulder, Philip

Published
2020
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49. Sex-specific innate immune selection of HIV-1 in utero is associated with increased female susceptibility to infection

Author

Adland, Emily, Millar, Jane, Bengu, Nomonde, Muenchhoff, Maximilian, Fillis, Rowena, Sprenger, Kenneth, Ntlantsana, Vuyokasi, Roider, Julia, Vieira, Vinicius, Govender, Katya, Adamson, John, Nxele, Nelisiwe, Ochsenbauer, Christina, Kappes, John, Mori, Luisa, van Lobenstein, Jeroen, Graza, Yeney, Chinniah, Kogielambal, Kapongo, Constant, Bhoola, Roopesh, Krishna, Malini, Matthews, Philippa C., Poderos, Ruth Penya, Lluch, Marta Colomer, Puertas, Maria C., Prado, Julia G., McKerrow, Neil, Archary, Moherndran, Ndung’u, Thumbi, Groll, Andreas, Jooste, Pieter, Martinez-Picado, Javier, Altfeld, Marcus, and Goulder, Philip

Published
2020
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