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1,052 results on '"Fellay, Jacques"'

1. Proteome-wide prediction of mode of inheritance and molecular mechanism underlying genetic diseases using structural interactomics

Author

Saadat, Ali and Fellay, Jacques

Subjects
Quantitative Biology - Quantitative Methods, Quantitative Biology - Genomics
Abstract

Genetic diseases can be classified according to their modes of inheritance and their underlying molecular mechanisms. Autosomal dominant disorders often result from DNA variants that cause loss-of-function, gain-of-function, or dominant-negative effects, while autosomal recessive diseases are primarily linked to loss-of-function variants. In this study, we introduce a graph-of-graphs approach that leverages protein-protein interaction networks and high-resolution protein structures to predict the mode of inheritance of diseases caused by variants in autosomal genes, and to classify dominant-associated proteins based on their functional effect. Our approach integrates graph neural networks, structural interactomics and topological network features to provide proteome-wide predictions, thus offering a scalable method for understanding genetic disease mechanisms.

Published
2024

2. DNA Language Model and Interpretable Graph Neural Network Identify Genes and Pathways Involved in Rare Diseases

Author

Saadat, Ali and Fellay, Jacques

Subjects
Quantitative Biology - Quantitative Methods, Quantitative Biology - Genomics
Abstract

Identification of causal genes and pathways is a critical step for understanding the genetic underpinnings of rare diseases. We propose novel approaches to gene prioritization and pathway identification using DNA language model, graph neural networks, and genetic algorithm. Using HyenaDNA, a long-range genomic foundation model, we generated dynamic gene embeddings that reflect changes caused by deleterious variants. These gene embeddings were then utilized to identify candidate genes and pathways. We validated our method on a cohort of rare disease patients with partially known genetic diagnosis, demonstrating the re-identification of known causal genes and pathways and the detection of novel candidates. These findings have implications for the prevention and treatment of rare diseases by enabling targeted identification of new drug targets and therapeutic pathways.

Published
2024
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3. Fine-tuning the ESM2 protein language model to understand the functional impact of missense variants

Author

Saadat, Ali and Fellay, Jacques

Subjects
Quantitative Biology - Quantitative Methods, Quantitative Biology - Genomics
Abstract

Elucidating the functional effect of missense variants is of crucial importance, yet challenging. To understand the impact of such variants, we fine-tuned the ESM2 protein language model to classify 20 protein features at amino acid resolution. We used the resulting models to: 1) identify protein features that are enriched in either pathogenic or benign missense variants, 2) compare the characteristics of proteins with reference or alternate alleles to understand how missense variants affect protein functionality. We show that our model can be used to reclassify some variants of unknown significance. We also demonstrate the usage of our models for understanding the potential effect of variants on protein features.

Published
2024

5. 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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6. Back-to-Africa introductions of Mycobacterium tuberculosis as the main cause of tuberculosis in Dar es Salaam, Tanzania.

Author

Zwyer, Michaela, Rutaihwa, Liliana, Windels, Etthel, Hella, Jerry, Menardo, Fabrizio, Sasamalo, Mohamed, Sommer, Gregor, Schmülling, Lena, Borrell, Sonia, Reinhard, Miriam, Dötsch, Anna, Hiza, Hellen, Stritt, Christoph, Sikalengo, George, Fenner, Lukas, De Jong, Bouke, Kato-Maeda, Midori, Jugheli, Levan, Ernst, Joel, Niemann, Stefan, Jeljeli, Leila, Ballif, Marie, Egger, Matthias, Rakotosamimanana, Niaina, Yeboah-Manu, Dorothy, Asare, Prince, Malla, Bijaya, Dou, Horng, Zetola, Nicolas, Wilkinson, Robert, Cox, Helen, Carter, E, Gnokoro, Joachim, Yotebieng, Marcel, Gotuzzo, Eduardo, Abimiku, Alashle, Avihingsanon, Anchalee, Xu, Zhi, Fellay, Jacques, Portevin, Damien, Reither, Klaus, Stadler, Tanja, Gagneux, Sebastien, and Brites, Daniela

Subjects
Humans, Mycobacterium tuberculosis, Tanzania, Tuberculosis, Genotype, Virulence
Abstract

In settings with high tuberculosis (TB) endemicity, distinct genotypes of the Mycobacterium tuberculosis complex (MTBC) often differ in prevalence. However, the factors leading to these differences remain poorly understood. Here we studied the MTBC population in Dar es Salaam, Tanzania over a six-year period, using 1,082 unique patient-derived MTBC whole-genome sequences (WGS) and associated clinical data. We show that the TB epidemic in Dar es Salaam is dominated by multiple MTBC genotypes introduced to Tanzania from different parts of the world during the last 300 years. The most common MTBC genotypes deriving from these introductions exhibited differences in transmission rates and in the duration of the infectious period, but little differences in overall fitness, as measured by the effective reproductive number. Moreover, measures of disease severity and bacterial load indicated no differences in virulence between these genotypes during active TB. Instead, the combination of an early introduction and a high transmission rate accounted for the high prevalence of L3.1.1, the most dominant MTBC genotype in this setting. Yet, a longer co-existence with the host population did not always result in a higher transmission rate, suggesting that distinct life-history traits have evolved in the different MTBC genotypes. Taken together, our results point to bacterial factors as important determinants of the TB epidemic in Dar es Salaam.

Published
2023

7. 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

9. 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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10. 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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11. Joint host-pathogen genomic analysis identifies hepatitis B virus mutations associated with human NTCP and HLA class I variation

Author

Xu, Zhi Ming, Gnouamozi, Gnimah Eva, Rüeger, Sina, Shea, Patrick R., Buti, Maria, Chan, Henry LY., Marcellin, Patrick, Lawless, Dylan, Naret, Olivier, Zeller, Matthias, Schneuing, Arne, Scheck, Andreas, Junier, Thomas, Moradpour, Darius, Podlaha, Ondrej, Suri, Vithika, Gaggar, Anuj, Subramanian, Mani, Correia, Bruno, Gfeller, David, Urban, Stephan, and Fellay, Jacques

Published
2024
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12. A high-resolution HLA reference panel capturing global population diversity enables multi-ancestry fine-mapping in HIV host response

Author

Luo, Yang, Kanai, Masahiro, Choi, Wanson, Li, Xinyi, Sakaue, Saori, Yamamoto, Kenichi, Ogawa, Kotaro, Gutierrez-Arcelus, Maria, Gregersen, Peter K, Stuart, Philip E, Elder, James T, Forer, Lukas, Schönherr, Sebastian, Fuchsberger, Christian, Smith, Albert V, Fellay, Jacques, Carrington, Mary, Haas, David W, Guo, Xiuqing, Palmer, Nicholette D, Chen, Yii-Der Ida, Rotter, Jerome I, Taylor, Kent D, Rich, Stephen S, Correa, Adolfo, Wilson, James G, Kathiresan, Sekar, Cho, Michael H, Metspalu, Andres, Esko, Tonu, Okada, Yukinori, Han, Buhm, McLaren, Paul J, and Raychaudhuri, Soumya

Subjects
Biological Sciences, Genetics, Biotechnology, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Alleles, Amino Acids, Gene Frequency, Genetic Variation, Genetics, Population, HIV Infections, HIV-1, HLA Antigens, Haplotypes, Host-Pathogen Interactions, Humans, Linkage Disequilibrium, Physical Chromosome Mapping, Reference Standards, Selection, Genetic, Viral Load, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Fine-mapping to plausible causal variation may be more effective in multi-ancestry cohorts, particularly in the MHC, which has population-specific structure. To enable such studies, we constructed a large (n = 21,546) HLA reference panel spanning five global populations based on whole-genome sequences. Despite population-specific long-range haplotypes, we demonstrated accurate imputation at G-group resolution (94.2%, 93.7%, 97.8% and 93.7% in admixed African (AA), East Asian (EAS), European (EUR) and Latino (LAT) populations). Applying HLA imputation to genome-wide association study data for HIV-1 viral load in three populations (EUR, AA and LAT), we obviated effects of previously reported associations from population-specific HIV studies and discovered a novel association at position 156 in HLA-B. We pinpointed the MHC association to three amino acid positions (97, 67 and 156) marking three consecutive pockets (C, B and D) within the HLA-B peptide-binding groove, explaining 12.9% of trait variance.

Published
2021

14. Revolutionizing Medical Data Sharing Using Advanced Privacy Enhancing Technologies: Technical, Legal and Ethical Synthesis

Author

Scheibner, James, Raisaro, Jean Louis, Troncoso-Pastoriza, Juan Ramón, Ienca, Marcello, Fellay, Jacques, Vayena, Effy, and Hubaux, Jean-Pierre

Subjects
Computer Science - Cryptography and Security, Computer Science - Computers and Society
Abstract

Multisite medical data sharing is critical in modern clinical practice and medical research. The challenge is to conduct data sharing that preserves individual privacy and data usability. The shortcomings of traditional privacy-enhancing technologies mean that institutions rely on bespoke data sharing contracts. These contracts increase the inefficiency of data sharing and may disincentivize important clinical treatment and medical research. This paper provides a synthesis between two novel advanced privacy enhancing technologies (PETs): Homomorphic Encryption and Secure Multiparty Computation (defined together as Multiparty Homomorphic Encryption or MHE). These PETs provide a mathematical guarantee of privacy, with MHE providing a performance advantage over separately using HE or SMC. We argue MHE fulfills legal requirements for medical data sharing under the General Data Protection Regulation (GDPR) which has set a global benchmark for data protection. Specifically, the data processed and shared using MHE can be considered anonymized data. We explain how MHE can reduce the reliance on customized contractual measures between institutions. The proposed approach can accelerate the pace of medical research whilst offering additional incentives for healthcare and research institutes to employ common data interoperability standards., Comment: 19 pages, 2 figures, 1 table

Published
2020

15. Secondary structure of the human mitochondrial genome affects formation of deletions

Author

Shamanskiy, Victor, Mikhailova, Alina A., Tretiakov, Evgenii O., Ushakova, Kristina, Mikhailova, Alina G., Oreshkov, Sergei, Knorre, Dmitry A., Ree, Natalia, Overdevest, Jonathan B., Lukowski, Samuel W., Gostimskaya, Irina, Yurov, Valerian, Liou, Chia-Wei, Lin, Tsu-Kung, Kunz, Wolfram S., Reymond, Alexandre, Mazunin, Ilya, Bazykin, Georgii A., Fellay, Jacques, Tanaka, Masashi, Khrapko, Konstantin, Gunbin, Konstantin, and Popadin, Konstantin

Published
2023
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16. Integrated analysis of whole blood oxylipin and cytokine responses after bacterial, viral, and T cell stimulation reveals new immune networks

Author

Abel, Laurent, Alcover, Andres, Aschard, Hugues, Bousso, Philippe, Bourke, Nollaig, Brodin, Petter, Bruhns, Pierre, Cerf-Bensussan, Nadine, Cumano, Ana, D’Enfert, Christophe, Deriano, Ludovic, Dillies, Marie-Agnès, Di Santo, James, Eberl, Gérard, Enninga, Jost, Fellay, Jacques, Gomperts-Boneca, Ivo, Hasan, Milena, Hedestam, Gunilla Karlsson, Hercberg, Serge, Ingersoll, Molly A., Lantz, Olivier, Kenny, Rose Anne, Ménager, Mickaël, Mouquet, Hugo, O'Farrelly, Cliona, Patin, Etienne, Pellegrini, Sandra, Rausell, Antonio, Rieux-Laucat, Frédéric, Rogge, Lars, Fontes, Magnus, Sakuntabhai, Anavaj, Schwartz, Olivier, Schwikowski, Benno, Shorte, Spencer, Tangy, Frédéric, Toubert, Antoine, Touvier, Mathilde, Ungeheuer, Marie-Noëlle, Zimmer, Christophe, Albert, Matthew L., Duffy, Darragh, Quintana-Murci, Lluis, Villain, Etienne, Chanson, Aurélie, Mainka, Malwina, Kampschulte, Nadja, Le Faouder, Pauline, Bertrand-Michel, Justine, Brandolini-Bunlon, Marion, Charbit, Bruno, Musvosvi, Munyaradzi, Bilek, Nicole, Scriba, Thomas J., Schebb, Nils Helge, and Gladine, Cécile

Published
2023
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17. A metagenome-wide association study of HIV disease progression in HIV controllers

Author

Real, Luis Miguel, Sáez, María E., Corma-Gómez, Anais, Gonzalez-Pérez, Antonio, Thorball, Christian, Ruiz, Rocío, Jimenez-Leon, María Reyes, Gonzalez-Serna, Alejandro, Gasca-Capote, Carmen, Bravo, María José, Royo, José Luis, Perez-Gomez, Alberto, Camacho-Sojo, María Inés, Gallego, Isabel, Vitalle, Joana, Bachiller, Sara, Gutierrez-Valencia, Alicia, Vidal, Francisco, Fellay, Jacques, Lichterfeld, Mathias, and Ruiz-Mateos, Ezequiel

Published
2023
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20. Weight, Anthropometric and Metabolic Changes After Discontinuing Antiretroviral Therapy Containing Tenofovir Alafenamide in People With HIV.

Author

Damas, José, Munting, Aline, Fellay, Jacques, Haerry, David, Marzolini, Catia, Tarr, Philip E, Steffen, Ana, Braun, Dominique L, Stoeckle, Marcel, Bernasconi, Enos, Tshikung, Olivier Nawej, Fux, Christoph A, Darling, Katharine E A, Béguelin, Charles, Wandeler, Gilles, Cavassini, Matthias, Surial, Bernard, and (SHCS), the Swiss HIV Cohort Study

Subjects
LAMIVUDINE, RILPIVIRINE, ANTIRETROVIRAL agents, AFRICAN Americans, RESEARCH funding, BODY weight, DRUG therapy, TENOFOVIR, HIV-positive persons, LIPIDS, HIV infections, DESCRIPTIVE statistics, LONGITUDINAL method, CHOLESTEROL, WAIST-hip ratio, ANTHROPOMETRY, CONFIDENCE intervals, TRIGLYCERIDES, TIME
Abstract

Background Antiretroviral therapy (ART)-related weight gain is of particular concern in people with HIV (PWH). Although weight gain was observed among PWH receiving tenofovir alafenamide (TAF), little is known about the potential reversibility after TAF discontinuation. We evaluated weight and metabolic changes 12 months after TAF discontinuation in the Swiss HIV Cohort Study. Methods We included participants who received at least 6 months of TAF-containing ART between January 2016 and March 2023. Using multivariable mixed-effect models, changes in weight and lipid levels were compared between individuals who continued TAF and those who switched to one of the following TAF-free regimens: (1) tenofovir disoproxil fumarate (TDF)-based ART, (2) dolutegravir/lamivudine (DTG/3TC), or (3) long-acting cabotegravir/rilpivirine (CAB/RPV). Results Of 6555 participants (median age 54 years, 24.3% female, 13% Black), 5485 (83.7%) continued, and 1070 (16.3%) stopped TAF. Overall, discontinuing TAF was associated with an adjusted mean weight change of −0.54 kg (95% confidence interval [CI] −.98 to −.11) after 12 months. In stratified analyses, switching from TAF to TDF led to an adjusted mean weight decrease of −1.84 kg (95% CI −2.72 to −.97), and to a decrease in mean total cholesterol (−0.44 mmol/L) and triglycerides (−0.38 mmol/L) after 12 months. Switching from TAF-based ART to DTG/3TC (−0.17 kg, 95% CI −.82 to.48) or long-acting CAB/RPV (−0.64 kg, 95% CI −2.16 to.89) did not lead to reductions in weight. Conclusions Replacing TAF with TDF in PWH led to a decrease in body weight and an improved lipid profile within 1 year. Weight changes were not observed among individuals who switched to DTG/3TC or long-acting CAB/RPV. [ABSTRACT FROM AUTHOR]

Published
2024
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21. 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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22. Killer cell immunoglobulin-like receptor 3DL1 variation modifies HLA-B*57 protection against HIV-1

Author

Martin, Maureen P, Naranbhai, Vivek, Shea, Patrick R, Qi, Ying, Ramsuran, Veron, Vince, Nicolas, Gao, Xiaojiang, Thomas, Rasmi, Brumme, Zabrina L, Carlson, Jonathan M, Wolinsky, Steven M, Goedert, James J, Walker, Bruce D, Segal, Florencia P, Deeks, Steven G, Haas, David W, Migueles, Stephen A, Connors, Mark, Michael, Nelson, Fellay, Jacques, Gostick, Emma, Llewellyn-Lacey, Sian, Price, David A, Lafont, Bernard A, Pymm, Phillip, Saunders, Philippa M, Widjaja, Jacqueline, Wong, Shu Cheng, Vivian, Julian P, Rossjohn, Jamie, Brooks, Andrew G, and Carrington, Mary

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Genetics, HIV/AIDS, Human Genome, Clinical Research, Sexually Transmitted Infections, 2.1 Biological and endogenous factors, Aetiology, Infection, Good Health and Well Being, Adult, Cohort Studies, Female, Genetic Variation, HIV Infections, HIV-1, HLA-B Antigens, Humans, Male, Middle Aged, Receptors, KIR3DL1, AIDS/HIV, Innate immunity, MHC class 1, NK cells, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

HLA-B*57 control of HIV involves enhanced CD8+ T cell responses against infected cells, but extensive heterogeneity exists in the level of HIV control among B*57+ individuals. Using whole-genome sequencing of untreated B*57+ HIV-1-infected controllers and noncontrollers, we identified a single variant (rs643347A/G) encoding an isoleucine-to-valine substitution at position 47 (I47V) of the inhibitory killer cell immunoglobulin-like receptor KIR3DL1 as the only significant modifier of B*57 protection. The association was replicated in an independent cohort and across multiple outcomes. The modifying effect of I47V was confined to B*57:01 and was not observed for the closely related B*57:03. Positions 2, 47, and 54 tracked one another nearly perfectly, and 2 KIR3DL1 allotypes differing only at these 3 positions showed significant differences in binding B*57:01 tetramers, whereas the protective allotype showed lower binding. Thus, variation in an immune NK cell receptor that binds B*57:01 modifies its protection. These data highlight the exquisite specificity of KIR-HLA interactions in human health and disease.

Published
2018

23. 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

24. Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells

Author

Ramsuran, Veron, Naranbhai, Vivek, Horowitz, Amir, Qi, Ying, Martin, Maureen P, Yuki, Yuko, Gao, Xiaojiang, Walker-Sperling, Victoria, Del Prete, Gregory Q, Schneider, Douglas K, Lifson, Jeffrey D, Fellay, Jacques, Deeks, Steven G, Martin, Jeffrey N, Goedert, James J, Wolinsky, Steven M, Michael, Nelson L, Kirk, Gregory D, Buchbinder, Susan, Haas, David, Ndung’u, Thumbi, Goulder, Philip, Parham, Peter, Walker, Bruce D, Carlson, Jonathan M, and Carrington, Mary

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Women's Health, Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Infection, Alleles, CD4 Lymphocyte Count, Cohort Studies, HIV, HIV Infections, HLA Antigens, Humans, Killer Cells, Natural, Ligands, NK Cell Lectin-Like Receptor Subfamily C, Protein Sorting Signals, Viremia, General Science & Technology
Abstract

The highly polymorphic human leukocyte antigen (HLA) locus encodes cell surface proteins that are critical for immunity. HLA-A expression levels vary in an allele-dependent manner, diversifying allele-specific effects beyond peptide-binding preference. Analysis of 9763 HIV-infected individuals from 21 cohorts shows that higher HLA-A levels confer poorer control of HIV. Elevated HLA-A expression provides enhanced levels of an HLA-A-derived signal peptide that specifically binds and determines expression levels of HLA-E, the ligand for the inhibitory NKG2A natural killer (NK) cell receptor. HLA-B haplotypes that favor NKG2A-mediated NK cell licensing (i.e., education) exacerbate the deleterious effect of high HLA-A on HIV control, consistent with NKG2A-mediated inhibition impairing NK cell clearance of HIV-infected targets. Therapeutic blockade of HLA-E:NKG2A interaction may yield benefit in HIV disease.

Published
2018

26. Author Correction: Increased prevalence of clonal hematopoiesis of indeterminate potential amongst people living with HIV

Author

Bick, Alexander G., Popadin, Konstantin, Thorball, Christian W., Uddin, Md Mesbah, Zanni, Markella V., Yu, Bing, Cavassini, Matthias, Rauch, Andri, Tarr, Philip, Schmid, Patrick, Bernasconi, Enos, Günthard, Huldrych F., Libby, Peter, Boerwinkle, Eric, McLaren, Paul J., Ballantyne, Christie M., Grinspoon, Steven, Natarajan, Pradeep, and Fellay, Jacques

Published
2022
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27. Increased prevalence of clonal hematopoiesis of indeterminate potential amongst people living with HIV

Author

Bick, Alexander G., Popadin, Konstantin, Thorball, Christian W., Uddin, Md Mesbah, Zanni, Markella V., Yu, Bing, Cavassini, Matthias, Rauch, Andri, Tarr, Philip, Schmid, Patrick, Bernasconi, Enos, Günthard, Huldrych F., Libby, Peter, Boerwinkle, Eric, McLaren, Paul J., Ballantyne, Christie M., Grinspoon, Steven, Natarajan, Pradeep, and Fellay, Jacques

Published
2022
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30. Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection

Author

Marchal, Astrid, primary, Cirulli, Elizabeth T., additional, Neveux, Iva, additional, Bellos, Evangelos, additional, Thwaites, Ryan S., additional, Schiabor Barrett, Kelly M., additional, Zhang, Yu, additional, Nemes-Bokun, Ivana, additional, Kalinova, Mariya, additional, Catchpole, Andrew, additional, Tangye, Stuart G., additional, Spaan, András N., additional, Lack, Justin B., additional, Ghosn, Jade, additional, Burdet, Charles, additional, Gorochov, Guy, additional, Tubach, Florence, additional, Hausfater, Pierre, additional, Dalgard, Clifton L., additional, Zhang, Shen-Ying, additional, Zhang, Qian, additional, Chiu, Christopher, additional, Fellay, Jacques, additional, Grzymski, Joseph J., additional, Sancho-Shimizu, Vanessa, additional, Abel, Laurent, additional, Casanova, Jean-Laurent, additional, Cobat, Aurélie, additional, and Bolze., Alexandre, additional

Published
2024
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31. From Your Nose to Your Toes: A Review of Severe Acute Respiratory Syndrome Coronavirus 2 Pandemic‒Associated Pernio

Author

Aiuti, Alessandro, Belot, Alexandre, Bolze, Alexandre, Bondarenko, Anastasiia, Sediva, Anna, Shcherbina, Anna, Planas, Anna M., Condino-Neto, Antonio, Pujol, Aurora, Drolet, Beth A., Catherine, Biggs, Flores, Carlos, Rodríguez-Gallego, Carlos, Prando, Carolina, Dalgard, Clifton L., O'Farrelly, Cliona, Roger, Colobran, Mansouri, Davoud, van de Beek, Diederik, Vinh, Donald C., Hsieh, Elena, Andreakos, Evangelos, Haerynck, Filomeen, Uddin, Furkan, Casari, Giorgio, Novelli, Giuseppe, Pesole, Graziano, Meyts, Isabelle, Tancevski, Ivan, Fellay, Jacques, Casanova, Jean-Laurent, Tur, Jordi, Kisand, Kai, Okamoto, Keisuke, Mironska, Kristina, Abel, Laurent, Renia, Laurent, Ng, Lisa F.P., Shahrooei, Mohammed, Soler-Palacín, Pere, Brodin, Petter, Pan-Hammarström, Qiang, Halwani, Rabih, Perez de Diego, Rebeca, Al-Muhsen, Saleh, Espinosa-Padilla, Sara, Okada, Satoshi, Ozcelik, Tayfun, Tayoun, Ahmad Abou, Karamitros, Timokratis, Mogensen, Trine H., Lau, Yu-Lung, Arkin, Lisa M., Moon, John J., Tran, Jennifer M., Asgari, Samira, O’Farrelly, Cliona, Cowen, Edward W., Mays, Jacqueline W., and Singh, Anne Marie

Published
2021
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32. HLA tapasin independence : broader peptide repertoire and HIV control

Author

Bashirova, Arman A., Viard, Mathias, Naranbhai, Vivek, Grifoni, Alba, Garcia-Beltran, Wilfredo, Akdag, Marjan, Yuki, Yuko, Gao, Xiaojiang, O’hUigin, Colm, Raghavan, Malini, Wolinsky, Steven, Bream, Jay H., Duggal, Priya, Martinson, Jeremy, Michael, Nelson L., Kirk, Gregory D., Buchbinder, Susan P., Haas, David, Goedert, James J., Deeks, Steven G., Fellay, Jacques, Walker, Bruce, Goulder, Philip, Cresswell, Peter, Elliott, Tim, Sette, Alessandro, Carlson, Jonathan, and Carrington, Mary

Published
2020

34. HLA-B*14:02-Restricted Env-Specific CD8+ T-Cell Activity Has Highly Potent Antiviral Efficacy Associated with Immune Control of HIV Infection

Author

Leitman, Ellen M, Willberg, Christian B, Tsai, Ming-Han, Chen, Huabiao, Buus, Søren, Chen, Fabian, Riddell, Lynn, Haas, David, Fellay, Jacques, Goedert, James J, Piechocka-Trocha, Alicja, Walker, Bruce D, Martin, Jeffrey, Deeks, Steven, Wolinsky, Steven M, Martinson, Jeremy, Martin, Maureen, Qi, Ying, Sáez-Cirión, Asier, Yang, Otto O, Matthews, Philippa C, Carrington, Mary, and Goulder, Philip JR

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Immunization, Vaccine Related, HIV/AIDS, Sexually Transmitted Infections, Clinical Research, Prevention, Vaccine Related (AIDS), 2.1 Biological and endogenous factors, Inflammatory and immune system, Infection, Good Health and Well Being, Adult, CD8-Positive T-Lymphocytes, HIV Envelope Protein gp160, HIV Infections, HIV-1, HLA-B14 Antigen, Humans, Immunity, Cellular, Peptides, gag Gene Products, Human Immunodeficiency Virus, CD8(+) T cells, HIV, HLA-B*14, immune control, CD8+ T cells, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract

Immune control of human immunodeficiency virus type 1 (HIV) infection is typically associated with effective Gag-specific CD8+ T-cell responses. We here focus on HLA-B*14, which protects against HIV disease progression, but the immunodominant HLA-B*14-restricted anti-HIV response is Env specific (ERYLKDQQL, HLA-B*14-EL9). A subdominant HLA-B*14-restricted response targets Gag (DRYFKTLRA, HLA-B*14-DA9). Using HLA-B*14/peptide-saporin-conjugated tetramers, we show that HLA-B*14-EL9 is substantially more potent at inhibiting viral replication than HLA-B*14-DA9. HLA-B*14-EL9 also has significantly higher functional avidity (P < 0.0001) and drives stronger selection pressure on the virus than HLA-B*14-DA9. However, these differences were HLA-B*14 subtype specific, applying only to HLA-B*14:02 and not to HLA-B*14:01. Furthermore, the HLA-B*14-associated protection against HIV disease progression is significantly greater for HLA-B*14:02 than for HLA-B*14:01, consistent with the superior antiviral efficacy of the HLA-B*14-EL9 response. Thus, although Gag-specific CD8+ T-cell responses may usually have greater anti-HIV efficacy, factors independent of protein specificity, including functional avidity of individual responses, are also critically important to immune control of HIV.IMPORTANCE In HIV infection, although cytotoxic T lymphocytes (CTL) play a potentially critical role in eradication of viral reservoirs, the features that constitute an effective response remain poorly defined. We focus on HLA-B*14, unique among HLAs associated with control of HIV in that the dominant CTL response is Env specific, not Gag specific. We demonstrate that Env-specific HLA-B*14-restricted activity is substantially more efficacious than the subdominant HLA-B*14-restricted Gag response. Env immunodominance over Gag and strong Env-mediated selection pressure on HIV are observed only in subjects expressing HLA-B*14:02, and not HLA-B*14:01. This reflects the increased functional avidity of the Env response over Gag, substantially more marked for HLA-B*14:02. Finally, we show that HLA-B*14:02 is significantly more strongly associated with viremic control than HLA-B*14:01. These findings indicate that, although Gag-specific CTL may usually have greater anti-HIV efficacy than Env responses, factors independent of protein specificity, including functional avidity, may carry greater weight in mediating effective control of HIV.

Published
2017

35. Inborn errors of type I interferon immunity in patients with symptomatic acute hepatitis E

Author

Saadat, Ali, Gouttenoire, Jérôme; https://orcid.org/0000-0002-7715-1494, Ripellino, Paolo; https://orcid.org/0000-0002-8662-9656, Semela, David, Amar, Soraya, Frey, Beat M; https://orcid.org/0000-0002-2514-8621, Fontana, Stefano, Mdawar-Bailly, Elise, Moradpour, Darius; https://orcid.org/0000-0003-1977-6792, Fellay, Jacques; https://orcid.org/0000-0002-8240-939X, Fraga, Montserrat, HEV Human Genetics Collaborators, Saadat, Ali, Gouttenoire, Jérôme; https://orcid.org/0000-0002-7715-1494, Ripellino, Paolo; https://orcid.org/0000-0002-8662-9656, Semela, David, Amar, Soraya, Frey, Beat M; https://orcid.org/0000-0002-2514-8621, Fontana, Stefano, Mdawar-Bailly, Elise, Moradpour, Darius; https://orcid.org/0000-0003-1977-6792, Fellay, Jacques; https://orcid.org/0000-0002-8240-939X, Fraga, Montserrat, and HEV Human Genetics Collaborators

Abstract

BACKGROUND AND AIMS: The clinical spectrum of human infection by HEV ranges from asymptomatic to severe acute hepatitis. Furthermore, HEV can cause diverse neurological manifestations, especially Parsonage-Turner syndrome. Here, we used a large-scale human genomic approach to search for genetic determinants of severe clinical presentations of HEV infection. APPROACH AND RESULTS: We performed whole genome sequencing in 3 groups of study participants with PCR-proven acute HEV infection: (1) 24 patients with symptomatic acute hepatitis E; (2) 12 patients with HEV-associated Parsonage-Turner syndrome; and (3) 16 asymptomatic blood donors (controls). For variant calling and annotation, we used GATK4 best practices followed by Variant Effect Predictor (VEP) and Annovar. For variant classification, we implemented the ACMG/AMP Bayesian classification framework in R. Variants with a probability of pathogenicity >0.9 were considered damaging. We used all genes with at least 1 damaging variant as input for pathway enrichment analyses. We observed a significant enrichment of type I interferon response pathways in the symptomatic hepatitis group: 10 out of 24 patients carried a damaging variant in one of 9 genes encoding either intracellular viral sensors (IFIH1, DDX58, TLR3, POLR3B, POLR3C) or other molecules involved in type I interferon response [interferon regulatory factor 7 (IRF7), MYD88, OAS3, GAPDH]. We did not find any enriched pathway in the Parsonage-Turner syndrome group or in the controls. CONCLUSIONS: Our results highlight the essential role of type I interferon in preventing symptomatic acute hepatitis E.

Published
2024

36. Prevalence of actionable pharmacogenetic variants and high‐risk drug prescriptions: A Swiss hospital‐based cohort study.

Author

Hodel, Flavia, De Min, Maria B., Thorball, Christian Wandall, Redin, Claire, Vollenweider, Peter, Girardin, François, and Fellay, Jacques

Subjects
DRUG side effects, MEDICAL care, ELECTRONIC health records, DRUG prescribing, DRUG metabolism, PHARMACOGENOMICS
Abstract

Drug type and dosing recommendation have been designed and optimized based on average response in the general population. Yet, there is significant inter‐individual variability in drug response, which results in treatment inefficacy or adverse drug reactions in a subset of patients. This is partly due to genetic factors that typically affect drug metabolism or clearance. To verify the relevance and applicability of international pharmacogenetic guidelines in the Swiss population, we genotyped 1533 patients from a hospital‐based biobank who received at least 30 different drugs, as documented in their electronic health record. We then assessed the prevalence of clinically actionable variants in 13 high‐risk pharmacogenes. We compared the allele frequencies obtained in the hospital‐based cohort with those of a Swiss population‐based cohort of 4791 individuals. The prevalence of clinically actionable variants was comparable between the two cohorts, with most study participants (97.3%) carrying at least one actionable pharmacogenetic variant. We then assessed the frequency of high‐risk prescriptions due to actionable gene–drug interactions and observed that 31% of patients in the hospital‐based cohort were prescribed at least one drug for which they carried a high‐risk variant, and for which international guidelines recommend a change of drug or dosage. Our analysis confirms the high prevalence of actionable pharmacogenetic variants in the Swiss population. It also shows that a substantial minority of patients are exposed to drugs for which they carry potentially problematic variants. Implementing a genetically informed approach to drug prescribing could have a positive impact on the quality of healthcare delivery. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Using viral diversity to identify HIV-1 variants under HLA-dependent selection in a systematic viral genome-wide screen.

Author

Neuner-Jehle, Nadia, Zeeb, Marius, Thorball, Christian W., Fellay, Jacques, Metzner, Karin J., Frischknecht, Paul, Neumann, Kathrin, Leeman, Christine, Rauch, Andri, Stöckle, Marcel, Huber, Michael, Perreau, Matthieu, Bernasconi, Enos, Notter, Julia, Hoffmann, Matthias, Leuzinger, Karoline, Günthard, Huldrych F., Pasin, Chloé, and Kouyos, Roger D.

Subjects
HLA histocompatibility antigens, WHOLE genome sequencing, VIRAL load, IMMUNE recognition, VIRAL mutation
Abstract

The pathogenesis of HIV-1 infection is governed by a highly dynamic, time-dependent interaction between the host and the viral genome. In this study, we developed a novel systematic approach to assess the host-virus interaction, using average pairwise viral diversity as a proxy for time since infection, and applied this method to nearly whole viral genome sequences (n = 4,464), human leukocyte antigen (HLA) genotyping data (n = 1,044), and viral RNA load (VL) measurements during the untreated chronic phase (n = 829) of Swiss HIV Cohort Study participants. Our systematic genome-wide screen revealed for 98 HLA/viral-variant pairs a signature of immune-driven selection in the form of an HLA-dependent effect of infection time on the presence of HIV amino acid variants. Of these pairs, 12 were found to have an effect on VL. Furthermore, 28/58 pairs were validated by time-to-event analyses and 48/92 by computational HLA-epitope predictions. Our diversity-based approach allows a powerful and systematic investigation of the interaction between the virus and cellular immunity, revealing a notable subset of such interaction effects. From an evolutionary perspective, these observations underscore the complexity of HLA-mediated selection pressures on the virus that shape viral evolution and pathogenesis. Author summary: The intricate interplay between viruses and the human immune system is reflected in dynamic associations between the viral and the human genomes. These often take the form of escape dynamics, in which the virus acquires mutations that allow it to evade immune recognition. We developed a novel viral diversity-based method to screen for such interactions across the viral genome systematically and applied it to a unique dataset of HIV-1 sequences and human leukocyte antigen (HLA) variants. We could identify time-dependent interactions between 98 pairs of HLA and viral variants. Among these pairs, 12 were associated with the concentration of viral RNA, longitudinal time-to-event analyses confirmed 28, and 48 were consistent with computational predictions of viral peptide binding to HLA molecules. Our results highlight how the highly dynamic interaction between the viral genome and the immune system shapes viral evolution, and our approach offers new opportunities to systematically study such interactions from real-world cross-sectional data. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Epistatic interaction between ERAP2 and HLA modulates HIV-1 adaptation and disease outcome in an Australian population.

Author

Al-kaabi, Marwah, Deshpande, Pooja, Firth, Martin, Pavlos, Rebecca, Chopra, Abha, Basiri, Hamed, Currenti, Jennifer, Alves, Eric, Kalams, Spyros, Fellay, Jacques, Phillips, Elizabeth, Mallal, Simon, John, Mina, and Gaudieri, Silvana

Subjects
T cells, HIV, HIV infections, HLA histocompatibility antigens, VIRAL load, SINGLE nucleotide polymorphisms, AUSTRALIANS
Abstract

A strong genetic predictor of outcome following untreated HIV-1 infection is the carriage of specific alleles of human leukocyte antigens (HLAs) that present viral epitopes to T cells. Residual variation in outcome measures may be attributed, in part, to viral adaptation to HLA-restricted T cell responses. Variants of the endoplasmic reticulum aminopeptidases (ERAPs) influence the repertoire of T cell epitopes presented by HLA alleles as they trim pathogen-derived peptide precursors to optimal lengths for antigen presentation, along with other functions unrelated to antigen presentation. We investigated whether ERAP variants influence HLA-associated HIV-1 adaptation with demonstrable effects on overall HIV-1 disease outcome. Utilizing host and viral data of 249 West Australian individuals with HIV-1 subtype B infection, we identified a novel association between two linked ERAP2 single nucleotide polymorphisms (SNPs; rs2248374 and rs2549782) with plasma HIV RNA concentration (viral load) (P adjusted = 0.0024 for both SNPs). Greater HLA-associated HIV-1 adaptation in the HIV-1 Gag gene correlated significantly with higher viral load, lower CD4+ T cell count and proportion; P = 0.0103, P = 0.0061, P = 0.0061, respectively). When considered together, there was a significant interaction between the two ERAP2 SNPs and HLA-associated HIV-1 adaptation on viral load (P = 0.0111). In a comprehensive multivariate model, addition of ERAP2 haplotypes and HLA associated adaptation as an interaction term to known HLA and CCR5 determinants and demographic factors, increased the explanatory variance of population viral load from 17.67% to 45.1% in this dataset. These effects were not replicated in publicly available datasets with comparably sized cohorts, suggesting that any true global epistasis may be dependent on specific HLA-ERAP allelic combinations. Our data raises the possibility that ERAP2 variants may shape peptide repertoires presented to HLA class I-restricted T cells to modulate the degree of viral adaptation within individuals, in turn contributing to disease variability at the population level. Analyses of other populations and experimental studies, ideally with locally derived ERAP genotyping and HLA-specific viral adaptations are needed to elucidate this further. Author summary: HIV infection outcome is variable between individuals and understanding the factors that impact this variation is important for efforts towards a HIV cure or vaccine. Here, we found that the level of HIV in the blood is affected by whether an individual carries a specific form of ERAP2, a molecule that influences processing and presentation of the virus to the immune system, as well as the degree to which HIV has mutated to adapt to immune responses. We also show that the interaction of ERAP2 and other known genetic factors explains greater variation in infection outcome than these factors alone. These findings expand our knowledge of the potential importance of viral processing and presentation in the immune response to HIV. [ABSTRACT FROM AUTHOR]

Published
2024
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39. Self-reported neurocognitive complaints in the Swiss HIV Cohort Study: a viral genome-wide association study.

Author

Zeeb, Marius, Pasin, Chloé, Cavassini, Matthias, Bieler-Aeschlimann, Mélanie, Frischknecht, Paul, Kusejko, Katharina, Fellay, Jacques, Blanquart, François, Metzner, Karin J, Neumann, Kathrin, Jörimann, Lisa, Tschumi, Jasmin, Bernasconi, Enos, Huber, Michael, Kovari, Helen, Leuzinger, Karoline, Notter, Julia, Perreau, Matthieu, Rauch, Andri, and Ramette, Alban

Published
2024
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43. Privacy in the Genomic Era

Author

Naveed, Muhammad, Ayday, Erman, Clayton, Ellen W., Fellay, Jacques, Gunter, Carl A., Hubaux, Jean-Pierre, Malin, Bradley A., and Wang, XiaoFeng

Subjects
Computer Science - Cryptography and Security, K.6.5
Abstract

Genome sequencing technology has advanced at a rapid pace and it is now possible to generate highly-detailed genotypes inexpensively. The collection and analysis of such data has the potential to support various applications, including personalized medical services. While the benefits of the genomics revolution are trumpeted by the biomedical community, the increased availability of such data has major implications for personal privacy; notably because the genome has certain essential features, which include (but are not limited to) (i) an association with traits and certain diseases, (ii) identification capability (e.g., forensics), and (iii) revelation of family relationships. Moreover, direct-to-consumer DNA testing increases the likelihood that genome data will be made available in less regulated environments, such as the Internet and for-profit companies. The problem of genome data privacy thus resides at the crossroads of computer science, medicine, and public policy. While the computer scientists have addressed data privacy for various data types, there has been less attention dedicated to genomic data. Thus, the goal of this paper is to provide a systematization of knowledge for the computer science community. In doing so, we address some of the (sometimes erroneous) beliefs of this field and we report on a survey we conducted about genome data privacy with biomedical specialists. Then, after characterizing the genome privacy problem, we review the state-of-the-art regarding privacy attacks on genomic data and strategies for mitigating such attacks, as well as contextualizing these attacks from the perspective of medicine and public policy. This paper concludes with an enumeration of the challenges for genome data privacy and presents a framework to systematize the analysis of threats and the design of countermeasures as the field moves forward.

Published
2014

44. Blacklisting variants common in private cohorts but not in public databases optimizes human exome analysis

Author

Maffucci, Patrick, Bigio, Benedetta, Rapaport, Franck, Cobat, Aurélie, Borghesi, Alessandro, Lopez, Marie, Patin, Etienne, Bolze, Alexandre, Shang, Lei, Bendavid, Matthieu, Scott, Eric M., Stenson, Peter D., Cunningham-Rundles, Charlotte, Cooper, David N., Gleeson, Joseph G., Fellay, Jacques, Quintana-Murci, Lluis, Casanova, Jean-Laurent, Abel, Laurent, Boisson, Bertrand, and Itan, Yuval

Published
2019

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