143 results on '"Ong, Swee Hoe"'
Search Results
2. Organismal metabolism regulates the expansion of oncogenic PIK3CA mutant clones in normal esophagus
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Herms, Albert, Colom, Bartomeu, Piedrafita, Gabriel, Kalogeropoulou, Argyro, Banerjee, Ujjwal, King, Charlotte, Abby, Emilie, Murai, Kasumi, Caseda, Irene, Fernandez-Antoran, David, Ong, Swee Hoe, Hall, Michael W. J., Bryant, Christopher, Sood, Roshan K., Fowler, Joanna C., Pol, Albert, Frezza, Christian, Vanhaesebroeck, Bart, and Jones, Philip H.
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- 2024
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3. Self-sustaining long-term 3D epithelioid cultures reveal drivers of clonal expansion in esophageal epithelium
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Herms, Albert, Fernandez-Antoran, David, Alcolea, Maria P., Kalogeropoulou, Argyro, Banerjee, Ujjwal, Piedrafita, Gabriel, Abby, Emilie, Valverde-Lopez, Jose Antonio, Ferreira, Inês S., Caseda, Irene, Bejar, Maria T., Dentro, Stefan C., Vidal-Notari, Sara, Ong, Swee Hoe, Colom, Bartomeu, Murai, Kasumi, King, Charlotte, Mahbubani, Krishnaa, Saeb-Parsy, Kourosh, Lowe, Alan R., Gerstung, Moritz, and Jones, Philip H.
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- 2024
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4. Notch1 mutations drive clonal expansion in normal esophageal epithelium but impair tumor growth
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Abby, Emilie, Dentro, Stefan C., Hall, Michael W. J., Fowler, Joanna C., Ong, Swee Hoe, Sood, Roshan, Herms, Albert, Piedrafita, Gabriel, Abnizova, Irina, Siebel, Christian W., Gerstung, Moritz, Hall, Benjamin A., and Jones, Philip H.
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- 2023
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5. AKT-mTORC1 reactivation is the dominant resistance driver for PI3Kβ/AKT inhibitors in PTEN-null breast cancer and can be overcome by combining with Mcl-1 inhibitors
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Dunn, Shanade, Eberlein, Cath, Yu, Jason, Gris-Oliver, Albert, Ong, Swee Hoe, Yelland, Urs, Cureton, Natalie, Staniszewska, Anna, McEwen, Robert, Fox, Millie, Pilling, James, Hopcroft, Philip, Coker, Elizabeth A., Jaaks, Patricia, Garnett, Mathew J., Isherwood, Beverley, Serra, Violeta, Davies, Barry R., Barry, Simon T., Lynch, James T., and Yusa, Kosuke
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- 2022
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6. p53 mutation in normal esophagus promotes multiple stages of carcinogenesis but is constrained by clonal competition
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Murai, Kasumi, Dentro, Stefan, Ong, Swee Hoe, Sood, Roshan, Fernandez-Antoran, David, Herms, Albert, Kostiou, Vasiliki, Abnizova, Irina, Hall, Benjamin A., Gerstung, Moritz, and Jones, Philip H.
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- 2022
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7. KAT7 is a genetic vulnerability of acute myeloid leukemias driven by MLL rearrangements
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Au, Yan Zi, Gu, Muxin, De Braekeleer, Etienne, Gozdecka, Malgorzata, Aspris, Demetrios, Tarumoto, Yusuke, Cooper, Jonathan, Yu, Jason, Ong, Swee Hoe, Chen, Xi, Tzelepis, Konstantinos, Huntly, Brian J. P., Vassiliou, George, and Yusa, Kosuke
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- 2021
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8. Outcompeting p53-Mutant Cells in the Normal Esophagus by Redox Manipulation
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Fernandez-Antoran, David, Piedrafita, Gabriel, Murai, Kasumi, Ong, Swee Hoe, Herms, Albert, Frezza, Christian, and Jones, Philip H.
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- 2019
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9. Species Identification and Profiling of Complex Microbial Communities Using Shotgun Illumina Sequencing of 16S rRNA Amplicon Sequences
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Ong, Swee Hoe, Kukkillaya, Vinutha Uppoor, Wilm, Andreas, Lay, Christophe, Ho, Eliza Xin Pei, Low, Louie, Hibberd, Martin Lloyd, and Nagarajan, Niranjan
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Quantitative Biology - Genomics - Abstract
The high throughput and cost-effectiveness afforded by short-read sequencing technologies, in principle, enable researchers to perform 16S rRNA profiling of complex microbial communities at unprecedented depth and resolution. Existing Illumina sequencing protocols are, however, limited by the fraction of the 16S rRNA gene that is interrogated and therefore limit the resolution and quality of the profiling. To address this, we present the design of a novel protocol for shotgun Illumina sequencing of the bacterial 16S rRNA gene, optimized to capture more than 90% of sequences in the Greengenes database and with nearly twice the resolution of existing protocols. Using several in silico and experimental datasets, we demonstrate that despite the presence of multiple variable and conserved regions, the resulting shotgun sequences can be used to accurately quantify the diversity of complex microbial communities. The reconstruction of a significant fraction of the 16S rRNA gene also enabled high precision (>90%) in species-level identification thereby opening up potential application of this approach for clinical microbial characterization., Comment: 17 pages, 2 tables, 2 figures, supplementary material
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- 2012
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10. Organismal metabolism regulates the expansion of oncogenic PIK3CAmutant clones in normal esophagus
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Herms, Albert, Colom, Bartomeu, Piedrafita, Gabriel, Kalogeropoulou, Argyro, Banerjee, Ujjwal, King, Charlotte, Abby, Emilie, Murai, Kasumi, Caseda, Irene, Fernandez-Antoran, David, Ong, Swee Hoe, Hall, Michael W. J., Bryant, Christopher, Sood, Roshan K., Fowler, Joanna C., Pol, Albert, Frezza, Christian, Vanhaesebroeck, Bart, and Jones, Philip H.
- Abstract
Oncogenic PIK3CAmutations generate large clones in aging human esophagus. Here we investigate the behavior of Pik3camutant clones in the normal esophageal epithelium of transgenic mice. Expression of a heterozygous Pik3caH1047Rmutation drives clonal expansion by tilting cell fate toward proliferation. CRISPR screening and inhibitor treatment of primary esophageal keratinocytes confirmed the PI3K–mTOR pathway increased mutant cell competitive fitness. The antidiabetic drug metformin reduced mutant cell advantage in vivo and in vitro. Conversely, metabolic conditions such as type 1 diabetes or diet-induced obesity enhanced the competitive fitness of Pik3caH1047Rcells. Consistently, we found a higher density of PIK3CAgain-of-function mutations in the esophagus of individuals with high body mass index compared with those with normal weight. We conclude that the metabolic environment selectively influences the evolution of the normal epithelial mutational landscape. Clinically feasible interventions to even out signaling imbalances between wild-type and mutant cells may limit the expansion of oncogenic mutants in normal tissues.
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- 2024
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11. Epidermal Tissue Adapts to Restrain Progenitors Carrying Clonal p53 Mutations
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Murai, Kasumi, Skrupskelyte, Greta, Piedrafita, Gabriel, Hall, Michael, Kostiou, Vasiliki, Ong, Swee Hoe, Nagy, Tibor, Cagan, Alex, Goulding, David, Klein, Allon M., Hall, Benjamin A., and Jones, Philip H.
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- 2018
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12. Genome-wide CRISPR-KO Screen Uncovers mTORC1-Mediated Gsk3 Regulation in Naive Pluripotency Maintenance and Dissolution
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Li, Meng, Yu, Jason S.L., Tilgner, Katarzyna, Ong, Swee Hoe, Koike-Yusa, Hiroko, and Yusa, Kosuke
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- 2018
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13. From clinical sample to complete genome: Comparing methods for the extraction of HIV-1 RNA for high-throughput deep sequencing
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Cornelissen, Marion, Gall, Astrid, Vink, Monique, Zorgdrager, Fokla, Binter, Špela, Edwards, Stephanie, Jurriaans, Suzanne, Bakker, Margreet, Ong, Swee Hoe, Gras, Luuk, van Sighem, Ard, Bezemer, Daniela, de Wolf, Frank, Reiss, Peter, Kellam, Paul, Berkhout, Ben, Fraser, Christophe, and van der Kuyl, Antoinette C.
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- 2017
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14. Comparative analysis of the chicken IFITM locus by targeted genome sequencing reveals evolution of the locus and positive selection in IFITM1 and IFITM3
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Bassano, Irene, Ong, Swee Hoe, Sanz-Hernandez, Maximo, Vinkler, Michal, Kebede, Adebabay, Hanotte, Olivier, Onuigbo, Ebele, Fife, Mark, and Kellam, Paul
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- 2019
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15. Data from Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site
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Fowler, Joanna C., primary, King, Charlotte, primary, Bryant, Christopher, primary, Hall, Michael W.J., primary, Sood, Roshan, primary, Ong, Swee Hoe, primary, Earp, Eleanor, primary, Fernandez-Antoran, David, primary, Koeppel, Jonas, primary, Dentro, Stefan C., primary, Shorthouse, David, primary, Durrani, Amer, primary, Fife, Kate, primary, Rytina, Edward, primary, Milne, Doreen, primary, Roshan, Amit, primary, Mahububani, Krishnaa, primary, Saeb-Parsy, Kourosh, primary, Hall, Benjamin A., primary, Gerstung, Moritz, primary, and Jones, Philip H., primary
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- 2023
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16. Supplementary Data from Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site
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Fowler, Joanna C., primary, King, Charlotte, primary, Bryant, Christopher, primary, Hall, Michael W.J., primary, Sood, Roshan, primary, Ong, Swee Hoe, primary, Earp, Eleanor, primary, Fernandez-Antoran, David, primary, Koeppel, Jonas, primary, Dentro, Stefan C., primary, Shorthouse, David, primary, Durrani, Amer, primary, Fife, Kate, primary, Rytina, Edward, primary, Milne, Doreen, primary, Roshan, Amit, primary, Mahububani, Krishnaa, primary, Saeb-Parsy, Kourosh, primary, Hall, Benjamin A., primary, Gerstung, Moritz, primary, and Jones, Philip H., primary
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- 2023
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17. Epithelioids: Self-sustaining 3D epithelial cultures to study long-term processes
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Herms, Albert, primary, Fernandez-Antoran, David, additional, Alcolea, Maria P., additional, Kalogeropoulou, Argyro, additional, Banerjee, Ujjwal, additional, Piedrafita, Gabriel, additional, Abby, Emilie, additional, Valverde-Lopez, Jose Antonio, additional, Ferreira, Inês S., additional, Dentro, Stefan C., additional, Ong, Swee Hoe, additional, Colom, Bartomeu, additional, Murai, Kasumi, additional, King, Charlotte, additional, Mahbubani, Krishnaa, additional, Saeb-Parsy, Kourosh, additional, Lowe, Alan R, additional, Gerstung, Moritz, additional, and Jones, Philip H, additional
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- 2023
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18. HIV-phyloTSI: Subtype-independent estimation of time since HIV-1 infection for cross-sectional measures of population incidence using deep sequence data
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Golubchik, Tanya, Abeler-Dörner, Lucie, Hall, Matthew, Wymant, Chris, Bonsall, David, Macintyre-Cockett, George, Thomson, Laura, Baeten, Jared, Celum, Connie, Galiwango, Ronald, Kosloff, Barry, Limbada, Mohammed, Mujugira, Andrew, Mugo, Nelly, Gall, Astrid, Blanquart, François, Bakker, Margreet, Bezemer, Daniela, Ong, Swee Hoe, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych, Kivelä, Pia, Kouyos, Roger, Meyer, Laurence, Porter, Kholoud, van Sighem, Ard, van der Valk, Mark, Berkhout, Ben, Kellam, Paul, Cornelissen, Marion, Reiss, Peter, Ayles, Helen, Burns, David, Fidler, Sarah, Grabowski, Mary Kate, Hayes, Richard, Herbeck, Joshua, Kagaayi, Joseph, Kaleebu, Pontiano, Lingappa, Jairam, Ssemwanga, Deogratius, Eshleman, Susan, Cohen, Myron, Ratmann, Oliver, Laeyendecker, Oliver, Fraser, Christophe, Blanquart, François, Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, and On behalf of the HPTN 071 (PopART) Phylogenetics protocol team, the BEEHIVE collaboration and the PANGEA consortium
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[SDV] Life Sciences [q-bio] ,[SDV]Life Sciences [q-bio] - Abstract
Estimating the time since HIV infection (TSI) at population level is essential for tracking changes in the global HIV epidemic. Most methods for determining duration of infection classify samples into recent and non-recent and are unable to give more granular TSI estimates. These binary classifications have a limited recency time window of several months, therefore requiring large sample sizes, and cannot assess the cumulative impact of an intervention. We developed a Random Forest Regression model, HIV-phyloTSI, that combines measures of within-host diversity and divergence to generate TSI estimates from viral deep-sequencing data, with no need for additional variables. HIV-phyloTSI provides a continuous measure of TSI up to 9 years, with a mean absolute error of less than 12 months overall and less than 5 months for infections with a TSI of up to a year. It performed equally well for all major HIV subtypes based on data from African and European cohorts. We demonstrate how HIV-phyloTSI can be used for incidence estimates on a population level.
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- 2022
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19. Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load
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Zhao, Lele; https://orcid.org/0000-0002-2807-1914, Wymant, Chris; https://orcid.org/0000-0002-9847-8226, Blanquart, François; https://orcid.org/0000-0003-0591-2466, Golubchik, Tanya; https://orcid.org/0000-0003-2765-9828, Gall, Astrid, Bakker, Margreet, Bezemer, Daniela; https://orcid.org/0000-0001-9304-0877, Hall, Matthew, Ong, Swee Hoe; https://orcid.org/0000-0002-3629-5387, Albert, Jan, Bannert, Norbert, Fellay, Jacques; https://orcid.org/0000-0002-8240-939X, Grabowski, M Kate, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych F; https://orcid.org/0000-0002-1142-6723, Kivelä, Pia, Kouyos, Roger D; https://orcid.org/0000-0002-9220-8348, Laeyendecker, Oliver, Meyer, Laurence, Porter, Kholoud, van Sighem, Ard; https://orcid.org/0000-0002-6656-0516, van der Valk, Marc, Berkhout, Ben; https://orcid.org/0000-0002-1905-8486, Kellam, Paul, Cornelissen, Marion, Reiss, Peter, Fraser, Christophe, Ferretti, Luca; https://orcid.org/0000-0001-7578-7301, Zhao, Lele; https://orcid.org/0000-0002-2807-1914, Wymant, Chris; https://orcid.org/0000-0002-9847-8226, Blanquart, François; https://orcid.org/0000-0003-0591-2466, Golubchik, Tanya; https://orcid.org/0000-0003-2765-9828, Gall, Astrid, Bakker, Margreet, Bezemer, Daniela; https://orcid.org/0000-0001-9304-0877, Hall, Matthew, Ong, Swee Hoe; https://orcid.org/0000-0002-3629-5387, Albert, Jan, Bannert, Norbert, Fellay, Jacques; https://orcid.org/0000-0002-8240-939X, Grabowski, M Kate, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych F; https://orcid.org/0000-0002-1142-6723, Kivelä, Pia, Kouyos, Roger D; https://orcid.org/0000-0002-9220-8348, Laeyendecker, Oliver, Meyer, Laurence, Porter, Kholoud, van Sighem, Ard; https://orcid.org/0000-0002-6656-0516, van der Valk, Marc, Berkhout, Ben; https://orcid.org/0000-0002-1905-8486, Kellam, Paul, Cornelissen, Marion, Reiss, Peter, Fraser, Christophe, and Ferretti, Luca; https://orcid.org/0000-0001-7578-7301
- Abstract
Set-point viral load (SPVL), a common measure of human immunodeficiency virus (HIV)-1 virulence, is partially determined by viral genotype. Epidemiological evidence suggests that this viral property has been under stabilising selection, with a typical optimum for the virus between 10$^{4}$ and 10$^{5}$ copies of viral RNA per ml. Here we aimed to detect transmission fitness differences between viruses from individuals with different SPVLs directly from phylogenetic trees inferred from whole-genome sequences. We used the local branching index (LBI) as a proxy for transmission fitness. We found that LBI is more sensitive to differences in infectiousness than to differences in the duration of the infectious state. By analysing subtype-B samples from the Bridging the Evolution and Epidemiology of HIV in Europe project, we inferred a significant positive relationship between SPVL and LBI up to approximately 10$^{5}$ copies/ml, with some evidence for a peak around this value of SPVL. This is evidence of selection against low values of SPVL in HIV-1 subtype-B strains, likely related to lower infectiousness, and perhaps a peak in the transmission fitness in the expected range of SPVL. The less prominent signatures of selection against higher SPVL could be explained by an inherent limit of the method or the deployment of antiretroviral therapy.
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- 2022
20. A highly virulent variant of HIV-1 circulating in the Netherlands
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Wymant, Chris, Bezemer, Daniela, Blanquart, François, Ferretti, Luca, Gall, Astrid, Hall, Matthew, Golubchik, Tanya, Bakker, Margreet, Ong, Swee Hoe, Zhao, Lele, Bonsall, David, de Cesare, Mariateresa, MacIntyre-Cockett, George, Abeler-Dörner, Lucie, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Grabowski, M Kate, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych F, Kivelä, Pia, Kouyos, Roger D, Laeyendecker, Oliver, Meyer, Laurence, Porter, Kholoud, Ristola, Matti, van Sighem, Ard, Berkhout, Ben, Kellam, Paul, Cornelissen, Marion, Reiss, Peter, Fraser, Christophe, Aubert, V, Battegay, M, Bernasconi, E, Böni, J, Braun, D L, Bucher, H C, Burton-Jeangros, C, Calmy, A, Cavassini, M, Dollenmaier, G, Egger, M, Elzi, L, Fehr, J, Fellay, J, Furrer, H, Fux, C A, Gorgievski, M, Günthard, H, Haerry, D, Hasse, B, Hirsch, H H, Hoffmann, M, Hösli, I, Kahlert, C, Kaiser, L, Keiser, O, Klimkait, T, Kouyos, R, Kovari, H, Ledergerber, B, Martinetti, G, de Tejada, B Martinez, Marzolini, C, Metzner, K, Müller, N, Nadal, D, Nicca, D, Pantaleo, G, Rauch, A, Regenass, S, Rudin, C, Schöni-Affolter, F, Schmid, P, Speck, R, Stöckle, M, Tarr, P, Trkola, A, Vernazza, P, Weber, R, Yerly, S, van der Valk, M, Geerlings, S E, Goorhuis, A, Hovius, J W, Lempkes, B, Nellen, F J B, van der Poll, T, Prins, J M, Reiss, P, van Vugt, M, Wiersinga, W J, Wit, F W M N, van Duinen, M, van Eden, J, Hazenberg, A, van Hes, A M H, Pijnappel, F J J, Smalhout, S Y, Weijsenfeld, A M, Jurriaans, S, Back, N K T, Zaaijer, H L, Berkhout, B, Cornelissen, M T E, Schinkel, C J, Wolthers, K C, Peters, E J G, van Agtmael, M A, Autar, R S, Bomers, M, Sigaloff, K C E, Heitmuller, M, Laan, L M, Ang, C W, van Houdt, R, Jonges, M, Kuijpers, T W, Pajkrt, D, Scherpbier, H J, de Boer, C, van der Plas, A, van den Berge, M, Stegeman, A, Baas, S, Hage de Looff, L, Buiting, A, Reuwer, A, Veenemans, J, Wintermans, B, Pronk, M J H, Ammerlaan, H S M, van den Bersselaar, D N J, de Munnik, E S, Deiman, B, Jansz, A R, Scharnhorst, V, Tjhie, J, Wegdam, M C A, van Eeden, A, Nellen, J, Brokking, W, Elsenburg, L J M, Nobel, H, van Kasteren, M E E, Berrevoets, M A H, Brouwer, A E, Adams, A, van Erve, R, de Kruijf-van de Wiel, B A F M, Keelan-Phaf, S, van der Ven, B, Buiting, A G M, Murck, J L, de Vries-Sluijs, T E M S, Bax, H I, van Gorp, E C M, de Jong-Peltenburg, N C, de Mendonç A Melo, M, van Nood, E, Nouwen, J L, Rijnders, B J A, Rokx, C, Schurink, C A M, Slobbe, L, Verbon, A, Bassant, N, van Beek, J E A, Vriesde, M, van Zonneveld, L M, de Groot, J, Boucher, C A B, Koopmans, M P G, van Kampen, J J A, Fraaij, P L A, van Rossum, A M C, Vermont, C L, van der Knaap, L C, Visser, E, Branger, J, Douma, R A, Cents-Bosma, A S, Duijf-van de Ven, C J H M, Schippers, E F, van Nieuwkoop, C, van Ijperen, J M, Geilings, J, van der Hut, G, van Burgel, N D, Leyten, E M S, Gelinck, L B S, Mollema, F, Davids-Veldhuis, S, Tearno, C, Wildenbeest, G S, Heikens, E, Groeneveld, P H P, Bouwhuis, J W, Lammers, A J J, Kraan, S, van Hulzen, A G W, Kruiper, M S M, van der Bliek, G L, Bor, P C J, Debast, S B, Wagenvoort, G H J, Kroon, F P, de Boer, M G J, Jolink, H, Lambregts, M M C, Roukens, A H E, Scheper, H, Dorama, W, van Holten, N, Claas, E C J, Wessels, E, den Hollander, J G, El Moussaoui, R, Pogany, K, Smit, J V, Struik-Kalkman, D, van Niekerk, T, Pontesilli, O, Lowe, S H, Oude Lashof, A M L, Posthouwer, D, van Wolfswinkel, M E, Ackens, R P, Burgers, K, Schippers, J, Weijenberg-Maes, B, van Loo, I H M, Havenith, T R A, van Vonderen, M G A, Kampschreur, L M, Faber, S, Steeman-Bouma, R, Al Moujahid, A, Kootstra, G J, Delsing, C E, van der Burg-van de Plas, M, Scheiberlich, L, Kortmann, W, van Twillert, G, Renckens, R, Ruiter-Pronk, D, van Truijen-Oud, F A, Cohen Stuart, J W T, Jansen, E R, Hoogewerf, M, Rozemeijer, W, van der Reijden, W A, Sinnige, J C, Brinkman, K, van den Berk, G E L, Blok, W L, Lettinga, K D, de Regt, M, Schouten, W E M, Stalenhoef, J E, Veenstra, J, Vrouenraets, S M E, Blaauw, H, Geerders, G F, Kleene, M J, Kok, M, Knapen, M, van der Meché, I B, Mulder-Seeleman, E, Toonen, A J M, Wijnands, S, Wttewaal, E, Kwa, D, van Crevel, R, van Aerde, K, Dofferhoff, A S M, Henriet, S S V, Ter Hofstede, H J M, Hoogerwerf, J, Keuter, M, Richel, O, Albers, M, Grintjes-Huisman, K J T, de Haan, M, Marneef, M, Strik-Albers, R, Rahamat-Langendoen, J, Stelma, F F, Burger, D, Gisolf, E H, Hassing, R J, Claassen, M, Ter Beest, G, van Bentum, P H M, Langebeek, N, Tiemessen, R, Swanink, C M A, van Lelyveld, S F L, Soetekouw, R, van der Prijt, L M M, van der Swaluw, J, Bermon, N, Jansen, R, Herpers, B L, Veenendaal, D, Verhagen, D W M, Lauw, F N, van Broekhuizen, M C, van Wijk, M, Bierman, W F W, Bakker, M, Kleinnijenhuis, J, Kloeze, E, Middel, A, Postma, D F, Schölvinck, E H, Stienstra, Y, Verhage, A R, Wouthuyzen-Bakker, M, Boonstra, A, de Groot-de Jonge, H, van der Meulen, P A, de Weerd, D A, Niesters, H G M, van Leer-Buter, C C, Knoester, M, Hoepelman, A I M, Arends, J E, Barth, R E, Bruns, A H W, Ellerbroek, P M, Mudrikova, T, Oosterheert, J J, Schadd, E M, van Welzen, B J, Aarsman, K, Griffioen-van Santen, B M G, de Kroon, I, van Berkel, M, van Rooijen, C S A M, Schuurman, R, Verduyn-Lunel, F, Wensing, A M J, Bont, L J, Geelen, S P M, Loeffen, Y G T, Wolfs, T F W, Nauta, N, Rooijakkers, E O W, Holtsema, H, Voigt, R, van de Wetering, D, Alberto, A, van der Meer, I, Rosingh, A, Halaby, T, Zaheri, S, Boyd, A C, Bezemer, D O, van Sighem, A I, Smit, C, Hillebregt, M, de Jong, A, Woudstra, T, Bergsma, D, Meijering, R, van de Sande, L, Rutkens, T, van der Vliet, S, de Groot, L, van den Akker, M, Bakker, Y, El Berkaoui, A, Bezemer, M, Brétin, N, Djoechro, E, Groters, M, Kruijne, E, Lelivelt, K J, Lodewijk, C, Lucas, E, Munjishvili, L, Paling, F, Peeck, B, Ree, C, Regtop, R, Ruijs, Y, Schoorl, M, Schnörr, P, Scheigrond, A, Tuijn, E, Veenenberg, L, Visser, K M, Witte, E C, Van Frankenhuijsen, Maartje, Allegre, Thierry, Makhloufi, Djamila, Livrozet, Jean-Michel, Chiarello, Pierre, Godinot, Mathieu, Brunel-Dalmas, Florence, Gibert, Sylvie, Trepo, Christian, Peyramond, Dominique, Miailhes, Patrick, Koffi, Joseph, Thoirain, Valérie, Brochier, Corinne, Baudry, Thomas, Pailhes, Sylvie, Lafeuillade, Alain, Philip, Gisèle, Hittinger, Gilles, Assi, Assi, Lambry, Véronique, Rosenthal, Eric, Naqvi, Alissa, Dunais, Brigitte, Cua, Eric, Pradier, Christian, Durant, Jacques, Joulie, Aline, Quinsat, Denis, Tempesta, Serge, Ravaux, Isabelle, Martin, Isabelle Poizot, Faucher, Olivia, Cloarec, Nicolas, Champagne, Hélène, Pichancourt, Gilles, Morlat, Philippe, Pistone, Thierry, Bonnet, Fabrice, Mercie, Patrick, Faure, Isabelle, Hessamfar, Mojgan, Malvy, Denis, Lacoste, Denis, Pertusa, Marie-Carmen, Vandenhende, Marie-Anne, Bernard, Noëlle, Paccalin, François, Martell, Cédric, Roger-Schmelz, Julien, Receveur, Marie-Catherine, Duffau, Pierre, Dondia, Denis, Ribeiro, Emmanuel, Caltado, Sabrina, Neau, Didier, Dupont, Michel, Dutronc, Hervé, Dauchy, Frédéric, Cazanave, Charles, Vareil, Marc-Olivier, Wirth, Gaétane, Le Puil, Séverine, Pellegrin, Jean-Luc, Raymond, Isabelle, Viallard, Jean-François, Chaigne de Lalande, Severin, Garipuy, Daniel, Delobel, Pierre, Obadia, Martine, Cuzin, Lise, Alvarez, Muriel, Biezunski, Noemie, Porte, Lydie, Massip, Patrice, Debard, Alexa, Balsarin, Florence, Lagarrigue, Myriam, Prevoteau du Clary, François, Aquilina, Christian, Reynes, Jacques, Baillat, Vincent, Merle, Corinne, Lemoing, Vincent, Atoui, Nadine, Makinson, Alain, Jacquet, Jean Marc, Psomas, Christina, Tramoni, Christine, Aumaitre, Hugues, Saada, Mathieu, Medus, Marie, Malet, Martine, Eden, Aurélia, Neuville, Ségolène, Ferreyra, Milagros, Sotto, Albert, Barbuat, Claudine, Rouanet, Isabelle, Leureillard, Didier, Mauboussin, Jean-Marc, Lechiche, Catherine, Donsesco, Régine, Cabie, André, Abel, Sylvie, Pierre-Francois, Sandrine, Batala, Anne-Sophie, Cerland, Christophe, Rangom, Camille, Theresine, Nadine, Hoen, Bruno, Lamaury, Isabelle, Fabre, Isabelle, Schepers, Kinda, Curlier, Elodie, Ouissa, Rachida, Gaud, Catherine, Ricaud, Carole, Rodet, Roland, Wartel, Guillaume, Sautron, Carmele, Beck-Wirth, Geneviève, Michel, Catherine, Beck, Charles, Halna, Jean-Michel, Kowalczyk, Jakub, Benomar, Meryem, Drobacheff-Thiebaut, Christine, Chirouze, Catherine, Faucher, Jean-François, Parcelier, François, Foltzer, Adeline, Haffner-Mauvais, Cécile, Hustache Mathieu, Mathieu, Proust, Aurélie, Piroth, Lionel, Chavanet, Pascal, Duong, Michel, Buisson, Marielle, Waldner, Anne, Mahy, Sophie, Gohier, Sandrine, Croisier, Delphine, May, Thierry, Delestan, Mikael, Andre, Marie, Zadeh, Mahsa Mohseni, Martinot, Martin, Rosolen, Béatrice, Pachart, Anne, Martha, Benoît, Jeunet, Noëlle, Rey, David, Cheneau, Christine, Partisani, Maria, Priester, Michèle, Bernard-Henry, Claudine, Batard, Marie-Laure, Fischer, Patricia, Berger, Jean-Luc, Kmiec, Isabelle, Robineau, Olivier, Huleux, Thomas, Ajana, Faïza, Alcaraz, Isabelle, Allienne, Christophe, Baclet, Véronique, Meybeck, Agnès, Valette, Michel, Viget, Nathalie, Aissi, Emmanuelle, Biekre, Raphael, Cornavin, Pauline, Merrien, Dominique, Seghezzi, Jean-Christophe, Machado, Moise, Diab, Georges, Raffi, François, Bonnet, Bénédicte, Allavena, Clotilde, Grossi, Olivier, Reliquet, Véronique, Billaud, Eric, Brunet, Cecile, Bouchez, Sabelline, Morineau-Le Houssine, Pascale, Sauser, Fabienne, Boutoille, David, Besnier, Michel, Hue, Hervé, Hall, Nolwenn, Brosseau, Delphine, Souala, Faouzi, Michelet, Christian, Tattevin, Pierre, Arvieux, Cédric, Revest, Matthieu, Leroy, Helene, Chapplain, Jean-Marc, Dupont, Matthieu, Fily, Fabien, Patra-Delo, Solène, Lefeuvre, Céline, Bernard, Louis, Bastides, Frédéric, Nau, Pascale, Verdon, Renaud, de la Blanchardiere, Arnaud, Martin, Anne, Feret, Philippe, Geffray, Loïk, Daniel, Corinne, Rohan, Jennifer, Fialaire, Pascale, Chennebault, Jean Marie, Rabier, Valérie, Abgueguen, Pierre, Rehaiem, Sami, Luycx, Odile, Niault, Mathilde, Moreau, Philippe, Poinsignon, Yves, Goussef, Marie, Mouton-Rioux, Virginie, Houlbert, Dominique, Alvarez-Huve, Sandrine, Barbe, Frédérique, Haret, Sophie, Perre, Philippe, Leantez-Nainville, Sophie, Esnault, Jean-Luc, Guimard, Thomas, Suaud, Isabelle, Girard, Jean-Jacques, Simonet, Véronique, Debab, Yasmine, Schmit, Jean-Luc, Jacomet, Christine, Weinberck, Pierre, Genet, Claire, Pinet, Pauline, Ducroix, Sophie, Durox, Hélène, Denes, Éric, Abraham, Bruno, Gourdon, Florence, Antoniotti, Odile, Molina, Jean-Michel, Ferret, Samuel, Lascoux-Combe, Caroline, Lafaurie, Matthieu, Colin de Verdiere, Nathalie, Ponscarme, Diane, De Castro, Nathalie, Aslan, Alexandre, Rozenbaum, Willy, Pintado, Claire, Clavel, François, Taulera, Olivier, Gatey, Caroline, Munier, Anne-Lise, Gazaigne, Sandrine, Penot, Pauline, Conort, Guillaume, Lerolle, Nathalie, Leplatois, Anne, Balausine, Stéphanie, Delgado, Jeannine, Timsit, Julie, Tabet, Magda, Gerard, Laurence, Girard, Pierre-Marie, Picard, Odile, Tredup, Jürgen, Bollens, Diane, Valin, Nadia, Campa, Pauline, Bottero, Julie, Lefebvre, Benedicte, Tourneur, Muriel, Fonquernie, Laurent, Wemmert, Charlotte, Lagneau, Jean-Luc, Yazdanpanah, Yazdan, Phung, Bao, Pinto, Adriana, Vallois, Dorothée, Cabras, Ornella, Louni, Françoise, Pialoux, Gilles, Lyavanc, Thomas, Berrebi, Valérie, Chas, Julie, Lenagat, Sophie, Rami, Agathe, Diemer, Myriam, Parrinello, Maguy, Depond, Audrey, Salmon, Dominique, Guillevin, Loïc, Tahi, Tassadit, Belarbi, Linda, Loulergue, Pierre, Zak Dit Zbar, Olivier, Launay, Odile, Silbermann, Benjamin, Leport, Catherine, Alagna, Laura, Pietri, Marie-Pierre, Simon, Anne, Bonmarchand, Manuela, Amirat, Naouel, Pichon, François, Kirstetter, Myriam, Katlama, Christine, Valantin, Marc Antoine, Tubiana, Roland, Caby, Fabienne, Schneider, Luminita, Ktorza, Nadine, Calin, Ruxandra, Merlet, Audrey, Ben Abdallah, Saadia, Weiss, Laurence, Buisson, Martin, Batisse, Dominique, Karmochine, Marina, Pavie, Juliette, Minozzi, Catherine, Jayle, Didier, Castel, Philippe, Derouineau, Jean, Kousignan, Pascale, Eliazevitch, Murielle, Pierre, Isabelle, Collias, Lio, Viard, Jean-Paul, Gilquin, Jacques, Sobel, Alain, Slama, Laurence, Ghosn, Jade, Hadacek, Blanka, Thu-Huyn, Nugyen, Nait-Ighil, Lella, Cros, Agnes, Maignan, Aline, Duvivier, Claudine, Consigny, Paul Henri, Lanternier, Fanny, Shoai-Tehrani, Michka, Touam, Fatima, Jerbi, Saadia, Bodard, Loïc, Jung, Corinne, Goujard, Cécile, Quertainmont, Yann, Duracinsky, Martin, Segeral, Olivier, Blanc, Arnaud, Peretti, Delphine, Cheret, Antoine, Chantalat, Christelle, Dulucq, Marie Josée, Levy, Yves, Lelievre, Jean Daniel, Lascaux, Anne Sophie, Dumont, Cécile, Boue, François, Chambrin, Véronique, Abgrall, Sophie, Kansau, Imad, Raho-Moussa, Mariem, De Truchis, Pierre, Dinh, Aurélien, Davido, Benjamin, Marigot, Dhiba, Berthe, Huguette, Devidas, Alain, Chevojon, Pierre, Chabrol, Amélie, Agher, Nouara, Lemercier, Yvon, Chaix, Fabrice, Turpault, Isabelle, Bouchaud, Olivier, Honore, Patricia, Rouveix, Elisabeth, Reimann, Evelyne, Belan, Alix Greder, Godin Collet, Claire, Souak, Safia, Mortier, Emmanuel, Bloch, Martine, Simonpoli, Anne-Marie, Manceron, Véronique, Cahitte, Isabelle, Hiraux, Emmanuel, Lafon, Erik, Cordonnier, François, Zeng, Ai-Feng, Zucman, David, Majerholc, Catherine, Bornarel, Dominique, Uludag, Agnès, Gellen-Dautremer, Justine, Lefort, Agnès, Bazin, Christine, Daneluzzi, Vincent, Gerbe, Juliette, Jeantils, Vincent, Coupard, Mélissa, Patey, Olivier, Bantsimba, Jonas, Delllion, Sophie, Paz, Pauline Caraux, Cazenave, Benoit, Richier, Laurent, Garrait, Valérie, Delacroix, Isabelle, Elharrar, Brigitte, Vittecoq, Daniel, Bolliot, Claudine, Lepretre, Annie, Genet, Philippe, Masse, Virginie, Perrone, Véronique, Boussard, Jean-Luc, Chardon, Patricia, Froguel, Eric, Simon, Philippe, Tassi, Sylvie, Avettand Fenoel, Véronique, Barin, Francis, Bourgeois, Christine, Cardon, Fanny, Chaix, Marie-Laure, Delfraissy, Jean François, Essat, Asma, Fischer, Hugues, Lecuroux, Camille, Petrov-Sanchez, Ventzislava, Rouzioux, Christine, Saez-Cirion, Asier, Seng, Rémonie, Kuldanek, Kristin, Mullaney, Scott, Young, Carmel, Zucchetti, Antonella, Bevan, Margaret-Ann, McKernan, Sinead, Wandolo, Emily, Richardson, Celia, Youssef, Elaney, Green, Pippa, Faulkner, Sue, Faville, Rebecca, Herman, Sandra, Care, Christine, Blackman, Helen, Bellenger, Katharine, Fairbrother, Keith, Phillips, Andrew, Babiker, Abdel, Delpech, Valerie, Fidler, S, Clarke, Mindy, Fox, Julie, Gilson, R, Goldberg, David, Hawkins, David, Johnson, Anne, Johnson, Margaret, McLean, Ken, Nastouli, Eleni, Post, Frank, Kennedy, N, Pritchard, J, Andrady, U, Rajda, N, Donnelly, C, McKernan, S, Drake, S, Gilleran, G, White, D, Ross, J, Harding, J, Faville, R, Sweeney, J, Flegg, P, Toomer, S, Wilding, H, Woodward, R, Dean, G, Richardson, C, Perry, N, Gompels, M, Jennings, L, Bansaal, D, Browing, M, Connolly, L, Stanley, B, Estreich, S, Magdy, A, O'Mahony, C, Fraser, P, Jebakumar, S P R, David, L, Mette, R, Summerfield, H, Evans, M, White, C, Robertson, R, Lean, C, Morris, S, Winter, A, Faulkner, S, Goorney, B, Howard, L, Fairley, I, Stemp, C, Short, L, Gomez, M, Young, F, Roberts, M, Green, S, Sivakumar, K, Minton, J, Siminoni, A, Calderwood, J, Greenhough, D, DeSouza, C, Muthern, Lisa, Orkin, C, Murphy, S, Truvedi, M, McLean, K, Hawkins, D, Higgs, C, Moyes, A, Antonucci, S, McCormack, S, Lynn, W, Bevan, M, Fox, J, Teague, A, Anderson, J, Mguni, S, Post, F, Campbell, L, Mazhude, C, Russell, H, Carrick, G, Ainsworth, J, Waters, A, Byrne, P, Johnson, M, Kuldanek, K, Mullaney, S, Lawlor, V, Melville, R, Sukthankar, A, Thorpe, S, Murphy, C, Wilkins, E, Ahmad, S, Green, P, Tayal, S, Ong, E, Meaden, J, Riddell, L, Loay, D, Peacock, K, Blackman, H, Harindra, V, Saeed, A M, Allen, S, Natarajan, U, Williams, O, Lacey, H, Care, C, Bowman, C, Herman, S, Devendra, S V, Wither, J, Bridgwood, A, Singh, G, Bushby, S, Kellock, D, Young, S, Rooney, G, Snart, B, Currie, J, Fitzgerald, M, Arumainayyagam, J, Chandramani, S, Rajamanoharan, S, Robinson, T, Taylor, B, Brewer, C, Mayr, Christoph, Schmidt, Wolfgang, Speidel, Andrea, Strohbach, Frank, Arastéh, Keikawus, Cordes, Christiane, Stündel, Manfred, Claus, Jörg, Baumgarten, Axel, Carganico, Andreas, Ingiliz, Patrick, Dupke, Stephan, Freiwald, Matthias, Rausch, Michael, Moll, Arend, Schleehauf, Dorothea, Hintsche, Bettina, Klausen, Gerd, Jessen, Heiko, Jessen, Arne, Köppe, Siegfried, Kreckel, Peter, Schranz, Dietmar, Fischer, Klaus, Schulbin, Hubert, Speer, Miriam, Glaunsinger, Tobias, Wicke, Thomas, Bieniek, Bernhard, Hillenbrand, Heribert, Schlote, Frank, Lauenroth-Mai, Elke, Schuler, Christoph, Schürmann, Dirk, Wesselmann, Hans, Brockmeyer, Norbert, Gehring, Peter, Schmalöer, Dirk, Hower, Martin, Spornraft-Ragaller, Petra, Häussinger, Dieter, Reuter, Stefan, Esser, Stefan, Markus, Rudolf, Kreft, Burkhard, Berzow, Dirk, Christl, Andreas, Meyer, Andreas, Plettenberg, Andreas, Stoehr, Albrecht, Graefe, Katrin, Lorenzen, Thore, Adam, Axel, Schewe, Knut, Weitner, Lutwin, Fenske, Stefan, Hansen, Stefan, Stellbrink, Hans-Jürgen, Wiemer, Dorothea, Hertling, Sandra, Schmidt, Reinhold, Arbter, Peter, Claus, Bernd, Galle, Peter, Jäger, Hans, Jä Gel-Guedes, Eva, Postel, Nils, Fröschl, Monika, Spinner, Christoph, Bogner, Johannes, Salzberger, Bernd, Schölmerich, Jürgen, Audebert, Franz, Marquardt, Ties, Schaffert, Andreas, Schnaitmann, Eiko, Trein, Andreas, Frietsch, Bernhard, Müller, Marcus, Ulmer, Albrecht, Detering-Hübner, Barbara, Kern, Peter, Schubert, Franz, Dehn, Günther, Schreiber, Maria, Güler, Cengiz, Schmidt, Daniel, Meixenberger, Karolin, Medical Microbiology & Infectious Diseases, Internal Medicine, Virology, Pediatrics, Medical Microbiology and Infection Prevention, AII - Infectious diseases, Global Health, Infectious diseases, APH - Aging & Later Life, Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Internal medicine, VU University medical center, Surgery, AMS - Rehabilitation & Development, APH - Quality of Care, Psychiatry, Pediatric surgery, Neurology, Public and occupational health, APH - Mental Health, Pathology, Cardiology, ACS - Heart failure & arrhythmias, Anesthesiology, IOO, Rehabilitation medicine, Obstetrics and gynaecology, General practice, Gastroenterology and hepatology, Pulmonary medicine, ACS - Pulmonary hypertension & thrombosis, Medical oncology laboratory, Hematology, Epidemiology and Data Science, Physiology, Microbes in Health and Disease (MHD), University of Oxford, Stichting HIV Monitoring [Amsterdam], Universiteit van Amsterdam (UvA), European Bioinformatics Institute [Hinxton] (EMBL-EBI), EMBL Heidelberg, Amsterdam UMC - Amsterdam University Medical Center, The Wellcome Trust Sanger Institute [Cambridge], Karolinska Institutet [Stockholm], Robert Koch Institute [Berlin] (RKI), Ecole Polytechnique Fédérale de Lausanne (EPFL), Johns Hopkins University (JHU), Universität Zürich [Zürich] = University of Zurich (UZH), Helsinki University Hospital [Helsinki, Finlande], Helsingin yliopisto = Helsingfors universitet = University of Helsinki, National Institute of Allergy and Infectious Diseases [Bethesda] (NIAID-NIH), National Institutes of Health [Bethesda] (NIH), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, University College of London [London] (UCL), Kymab Ltd, Cambridge, England, Institut Pasteur [Paris] (IP), This study was funded by ERC Advanced Grant PBDR-339251 and a Li Ka Shing Foundation grant, both awarded to C.F. The ATHENA Cohort is managed by Stichting HIV Monitoring and supported by a grant from the Dutch Ministry of Health, Welfare and Sport through the Centre for Infectious Disease Control of the National Institute for Public Health and the Environment., We thank K. Fransen and G. Vanham for help with the Belgian data, O. Ratmann for help in identifying the Dutch clusters, K. Kusejko for testing for additional VB individuals in the SHCS, B. Foley for help with genome sharing, B. Dearlove and L. Thomson for help with software, and J. Herbeck and three other reviewers for helpful suggestions., Contributors and affiliations are listed in the supplementary materials., Department of Medicine, University of Helsinki, Infektiosairauksien yksikkö, HUS Inflammation Center, and Clinicum
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Adult ,Male ,HIV-1/genetics ,Genotype ,Anti-HIV Agents ,Evolution ,[SDV]Life Sciences [q-bio] ,lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4] ,HIV Infections/drug therapy ,selection ,HIV Infections ,Genome, Viral ,heritability ,epidemic ,human-immunodeficiency-virus ,Evolution, Molecular ,SDG 3 - Good Health and Well-being ,[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases ,Humans ,Viral ,Phylogeny ,Netherlands ,Multidisciplinary ,Genome ,model ,Virulence ,transmission ,Molecular ,setpoint viral load ,reverse-transcriptase ,dynamics ,Viral Load ,CD4 Lymphocyte Count ,lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4] ,3121 General medicine, internal medicine and other clinical medicine ,Anti-HIV Agents/therapeutic use ,Mutation ,HIV-1 ,Female ,progression - Abstract
Comment in Does HIV-1 virulence matter in the ART era? Lewitus E, Rolland M. Med (N Y). 2022 Apr 8;3(4):217-219. doi: 10.1016/j.medj.2022.03.003. PMID: 35590149; International audience; We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log 10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.
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- 2022
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21. Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium
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Colom, Bartomeu, Alcolea, Maria P, Piedrafita, Gabriel, Hall, Michael WJ, Wabik, Agnieszka, Dentro, Stefan C, Fowler, Joanna C, Herms, Albert, King, Charlotte, Ong, Swee Hoe, Sood, Roshan K, Gerstung, Moritz, Martincorena, Inigo, Hall, Benjamin A, Jones, Philip H, Colom, Bartomeu [0000-0001-6256-6462], Piedrafita, Gabriel [0000-0001-8701-1084], Ong, Swee Hoe [0000-0002-3629-5387], Sood, Roshan K [0000-0002-1318-7025], Gerstung, Moritz [0000-0001-6709-963X], Hall, Benjamin A [0000-0003-0355-2946], Jones, Philip H [0000-0002-5904-795X], and Apollo - University of Cambridge Repository
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Male ,High-Throughput Nucleotide Sequencing ,Membrane Proteins ,Reproducibility of Results ,Mice, Transgenic ,Epithelium ,Mice, Inbred C57BL ,ADAM10 Protein ,Esophagus ,Mutation ,Animals ,Cell Lineage ,Diethylnitrosamine ,Female ,Receptor, Notch2 ,Amyloid Precursor Protein Secretases ,Receptor, Notch1 ,Tumor Suppressor Protein p53 ,health care economics and organizations - Abstract
During aging, progenitor cells acquire mutations, which may generate clones that colonize the surrounding tissue. By middle age, normal human tissues, including the esophageal epithelium (EE), become a patchwork of mutant clones. Despite their relevance for understanding aging and cancer, the processes that underpin mutational selection in normal tissues remain poorly understood. Here, we investigated this issue in the esophageal epithelium of mutagen-treated mice. Deep sequencing identified numerous mutant clones with multiple genes under positive selection, including Notch1, Notch2 and Trp53, which are also selected in human esophageal epithelium. Transgenic lineage tracing revealed strong clonal competition that evolved over time. Clone dynamics were consistent with a simple model in which the proliferative advantage conferred by positively selected mutations depends on the nature of the neighboring cells. When clones with similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constraint that explains how selection operates in normal-appearing epithelium.
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- 2020
22. p53 mutation in normal esophagus promotes multiple stages of carcinogenesis but is constrained by clonal competition
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Murai, Kasumi, primary, Dentro, Stefan, additional, Ong, Swee Hoe, additional, Sood, Roshan, additional, Fernandez-Antoran, David, additional, Herms, Albert, additional, Kostiou, Vasiliki, additional, Hall, Benjamin A, additional, Gerstung, Moritz, additional, and Jones, Philip H, additional
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- 2022
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23. Periodic re-emergence of endemic strains with strong epidemic potential—A proposed explanation for the 2004 Indonesian dengue epidemic
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Ong, Swee Hoe, Yip, Jin Teen, Chen, Yen Liang, Liu, Wei, Harun, Syahrial, Lystiyaningsih, Erlin, Heriyanto, Bambang, Beckett, Charmagne G., Mitchell, Wayne P., Hibberd, Martin L., Suwandono, Agus, Vasudevan, Subhash G., and Schreiber, Mark J.
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- 2008
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24. Notch1mutation drives clonal expansion in normal esophageal epithelium but impairs tumor growth
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Abby, Emilie, primary, Dentro, Stefan C, additional, Hall, Michael W J, additional, Fowler, Joanna C, additional, Ong, Swee Hoe, additional, Sood, Roshan, additional, Siebel, Christian W, additional, Gerstung, Moritz, additional, Hall, Benjamin A, additional, and Jones, Philip H, additional
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- 2021
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25. Levelling out differences in aerobic glycolysis neutralizes the competitive advantage of oncogenicPIK3CAmutant progenitors in the esophagus
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Herms, Albert, primary, Colom, Bartomeu, additional, Piedrafita, Gabriel, additional, Murai, Kasumi, additional, Ong, Swee Hoe, additional, Fernandez-Antoran, David, additional, Bryant, Christopher, additional, Frezza, Christian, additional, Vanhaesebroeck, Bart, additional, and Jones, Philip H., additional
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- 2021
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26. Notch1mutations drive clonal expansion in normal esophageal epithelium but impair tumor growth
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Abby, Emilie, Dentro, Stefan C., Hall, Michael W. J., Fowler, Joanna C., Ong, Swee Hoe, Sood, Roshan, Herms, Albert, Piedrafita, Gabriel, Abnizova, Irina, Siebel, Christian W., Gerstung, Moritz, Hall, Benjamin A., and Jones, Philip H.
- Abstract
NOTCH1mutant clones occupy the majority of normal human esophagus by middle age but are comparatively rare in esophageal cancers, suggesting NOTCH1mutations drive clonal expansion but impede carcinogenesis. Here we test this hypothesis. Sequencing NOTCH1mutant clones in aging human esophagus reveals frequent biallelic mutations that block NOTCH1signaling. In mouse esophagus, heterozygous Notch1mutation confers a competitive advantage over wild-type cells, an effect enhanced by loss of the second allele. Widespread Notch1loss alters transcription but has minimal effects on the epithelial structure and cell dynamics. In a carcinogenesis model, Notch1mutations were less prevalent in tumors than normal epithelium. Deletion of Notch1reduced tumor growth, an effect recapitulated by anti-NOTCH1 antibody treatment. Notch1null tumors showed reduced proliferation. We conclude that Notch1mutations in normal epithelium are beneficial as wild-type Notch1favors tumor expansion. NOTCH1 blockade may have therapeutic potential in preventing esophageal squamous cancer.
- Published
- 2023
- Full Text
- View/download PDF
27. LoFreq: a sequence-quality aware, ultra-sensitive variant caller for uncovering cell-population heterogeneity from high-throughput sequencing datasets
- Author
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Wilm, Andreas, Aw, Pauline Poh Kim, Bertrand, Denis, Yeo, Grace Hui Ting, Ong, Swee Hoe, Wong, Chang Hua, Khor, Chiea Chuen, Petric, Rosemary, Hibberd, Martin Lloyd, and Nagarajan, Niranjan
- Published
- 2012
- Full Text
- View/download PDF
28. Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site
- Author
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Fowler, Joanna C., primary, King, Charlotte, additional, Bryant, Christopher, additional, Hall, Michael W.J., additional, Sood, Roshan, additional, Ong, Swee Hoe, additional, Earp, Eleanor, additional, Fernandez-Antoran, David, additional, Koeppel, Jonas, additional, Dentro, Stefan C., additional, Shorthouse, David, additional, Durrani, Amer, additional, Fife, Kate, additional, Rytina, Edward, additional, Milne, Doreen, additional, Roshan, Amit, additional, Mahububani, Krishnaa, additional, Saeb-Parsy, Kourosh, additional, Hall, Benjamin A., additional, Gerstung, Moritz, additional, and Jones, Philip H., additional
- Published
- 2021
- Full Text
- View/download PDF
29. A Genomics Approach to Understanding Host Response during Dengue Infection
- Author
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Hibberd, Martin L., primary, Ling, Ling, additional, Tolfvenstam, Thomas, additional, Mitchell, Wayne, additional, Wong, Chris, additional, Kuznetsov, Vladimir A., additional, George, Joshy, additional, Ong, Swee-Hoe, additional, Ruan, Yijun, additional, Wei, Chia L., additional, Gu, Feng, additional, Fink, Joshua, additional, Yip, Andy, additional, Liu, Wei, additional, Schreiber, Mark, additional, and Vasudevan, Subhash G., additional
- Published
- 2008
- Full Text
- View/download PDF
30. KAT7 is a genetic vulnerability of acute myeloid leukemias driven by MLL rearrangements
- Author
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Au, Yan Zi, primary, Gu, Muxin, additional, De Braekeleer, Etienne, additional, Gozdecka, Malgorzata, additional, Aspris, Demetrios, additional, Tarumoto, Yusuke, additional, Cooper, Jonathan, additional, Yu, Jason, additional, Ong, Swee Hoe, additional, Chen, Xi, additional, Tzelepis, Konstantinos, additional, Huntly, Brian J. P., additional, Vassiliou, George, additional, and Yusa, Kosuke, additional
- Published
- 2020
- Full Text
- View/download PDF
31. Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium
- Author
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Colom, Bartomeu, primary, Alcolea, Maria P., additional, Piedrafita, Gabriel, additional, Hall, Michael W. J., additional, Wabik, Agnieszka, additional, Dentro, Stefan C., additional, Fowler, Joanna C., additional, Herms, Albert, additional, King, Charlotte, additional, Ong, Swee Hoe, additional, Sood, Roshan K., additional, Gerstung, Moritz, additional, Martincorena, Inigo, additional, Hall, Benjamin A., additional, and Jones, Philip H., additional
- Published
- 2020
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- View/download PDF
32. KAT7 is a therapeutic vulnerability of MLL-rearranged acute myeloid leukemia
- Author
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Au, Yan Zi, primary, Gu, Muxin, additional, De Braekeleer, Etienne, additional, Yu, Jason, additional, Ong, Swee Hoe, additional, Gozdecka, Malgorzata, additional, Chen, Xi, additional, Tzelepis, Konstantinos, additional, Huntly, Brian J.P, additional, Vassiliou, George, additional, and Yusa, Kosuke, additional
- Published
- 2020
- Full Text
- View/download PDF
33. IDBD: Infectious Disease Biomarker Database
- Author
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Yang, In Seok, Ryu, Chunsun, Cho, Ki Joon, Kim, Jin Kwang, Ong, Swee Hoe, Mitchell, Wayne P., Kim, Bong Su, Oh, Hee-Bok, and Kim, Kyung Hyun
- Published
- 2008
34. KAT7 is a genetic vulnerability of acute myeloid leukemias driven by MLL rearrangements
- Author
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70551381, 00813180, Au, Yan Zi, Gu, Muxin, De Braekeleer, Etienne, Gozdecka, Malgorzata, Aspris, Demetrios, Tarumoto, Yusuke, Cooper, Jonathan, Yu, Jason, Ong, Swee Hoe, Chen, Xi, Tzelepis, Konstantinos, Huntly, Brian J. P., Vassiliou, George, Yusa, Kosuke, 70551381, 00813180, Au, Yan Zi, Gu, Muxin, De Braekeleer, Etienne, Gozdecka, Malgorzata, Aspris, Demetrios, Tarumoto, Yusuke, Cooper, Jonathan, Yu, Jason, Ong, Swee Hoe, Chen, Xi, Tzelepis, Konstantinos, Huntly, Brian J. P., Vassiliou, George, and Yusa, Kosuke
- Abstract
Histone acetyltransferases (HATs) catalyze the transfer of an acetyl group from acetyl-CoA to lysine residues of histones and play a central role in transcriptional regulation in diverse biological processes. Dysregulation of HAT activity can lead to human diseases including developmental disorders and cancer. Through genome-wide CRISPR-Cas9 screens, we identified several HATs of the MYST family as fitness genes for acute myeloid leukemia (AML). Here we investigate the essentiality of lysine acetyltransferase KAT7 in AMLs driven by the MLL-X gene fusions. We found that KAT7 loss leads to a rapid and complete loss of both H3K14ac and H4K12ac marks, in association with reduced proliferation, increased apoptosis, and differentiation of AML cells. Acetyltransferase activity of KAT7 is essential for the proliferation of these cells. Mechanistically, our data propose that acetylated histones provide a platform for the recruitment of MLL-fusion-associated adaptor proteins such as BRD4 and AF4 to gene promoters. Upon KAT7 loss, these factors together with RNA polymerase II rapidly dissociate from several MLL-fusion target genes that are essential for AML cell proliferation, including MEIS1, PBX3, and SENP6. Our findings reveal that KAT7 is a plausible therapeutic target for this poor prognosis AML subtype.
- Published
- 2020
35. Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load.
- Author
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Zhao, Lele, Wymant, Chris, Blanquart, François, Golubchik, Tanya, Gall, Astrid, Bakker, Margreet, Bezemer, Daniela, Hall, Matthew, Ong, Swee Hoe, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Grabowski, M Kate, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych F, Kivelä, Pia, Kouyos, Roger D, Laeyendecker, Oliver, Meyer, Laurence, and Porter, Kholoud
- Subjects
VIRAL load ,HIV ,ANTIRETROVIRAL agents - Abstract
Set-point viral load (SPVL), a common measure of human immunodeficiency virus (HIV)-1 virulence, is partially determined by viral genotype. Epidemiological evidence suggests that this viral property has been under stabilising selection, with a typical optimum for the virus between 10
4 and 105 copies of viral RNA per ml. Here we aimed to detect transmission fitness differences between viruses from individuals with different SPVLs directly from phylogenetic trees inferred from whole-genome sequences. We used the local branching index (LBI) as a proxy for transmission fitness. We found that LBI is more sensitive to differences in infectiousness than to differences in the duration of the infectious state. By analysing subtype-B samples from the Bridging the Evolution and Epidemiology of HIV in Europe project, we inferred a significant positive relationship between SPVL and LBI up to approximately 105 copies/ml, with some evidence for a peak around this value of SPVL. This is evidence of selection against low values of SPVL in HIV-1 subtype-B strains, likely related to lower infectiousness, and perhaps a peak in the transmission fitness in the expected range of SPVL. The less prominent signatures of selection against higher SPVL could be explained by an inherent limit of the method or the deployment of antiretroviral therapy. [ABSTRACT FROM AUTHOR]- Published
- 2022
- Full Text
- View/download PDF
36. RNAmut: robust identification of somatic mutations in acute myeloid leukemia using RNA-sequencing
- Author
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Gu, Muxin, primary, Zwiebel, Maximillian, additional, Ong, Swee Hoe, additional, Boughton, Nick, additional, Nomdedeu, Josep, additional, Basheer, Faisal, additional, Nannya, Yasuhito, additional, Quiros, Pedro M., additional, Ogawa, Seishi, additional, Cazzola, Mario, additional, Rad, Roland, additional, Butler, Adam P., additional, Vijayabaskar, MS, additional, and Vassiliou, George S., additional
- Published
- 2019
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- View/download PDF
37. Abstract 321: Genome-wide CRISPR screens identify combination strategies for Capivasertib (AZD5363; AKT) and AZD8186 (PI3Kβ/δ) in PTEN-null breast cancer
- Author
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Dunn, Shanade, primary, Yu, Jason, additional, Gris-Oliver, Albert, additional, Pilling, James, additional, Hopcroft, Philip, additional, Yelland, Urs, additional, Cureton, Natalie, additional, Staniszewsla, Anna, additional, Au, Yan Zi, additional, Ong, Swee Hoe, additional, Isherwood, Beverley, additional, Serra, Violeta, additional, Barry, Simon, additional, Davies, Barry R., additional, Lynch, James T., additional, and Yusa, Kosuke, additional
- Published
- 2019
- Full Text
- View/download PDF
38. Easy and accurate reconstruction of whole HIV genomes from short-read sequence data with shiver
- Author
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BEEHIVE Collaboration, Wymant, Chris, Blanquart, Francois, Golubchik, Tanya, Gall, Astrid, Bakker, Margreet, Bezemer, Daniela, Croucher, Nicholas J., Hall, Matthew, Hillebregt, Mariska, Ong, Swee Hoe, Ratmann, Oliver, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Fransen, Katrien, Gourlay, Annabelle, Grabowski, M. Kate, Gunsenheimer-Bartmeyer, Barbara, Gunthard, Huldrych F., Kivelä, Pia, Kouyos, Roger, Laeyendecker, Oliver, Liitsola, Kirsi, Meyer, Laurence, Porter, Kholoud, Ristola, Matti, van Sighem, Ard, Berkhout, Ben, Cornelissen, Marion, Kellam, Paul, Reiss, Peter, Fraser, Christophe, Institute for Particle Physics Phenomenology (IPPP), Durham University, Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Stichting HIV Monitoring [Amsterdam], Universiteit van Amsterdam (UvA), Evolution and Ecology Research Center, University of New South Wales [Sydney] (UNSW), Department of Infectious Disease Epidemiology [London] (DIDE), Imperial College London, Ecole Polytechnique Fédérale de Lausanne (EPFL), University College of London [London] (UCL), Universität Zürich [Zürich] = University of Zurich (UZH), Department of Infectious Diseases and Hospital Epidemiology [Zurich], University hospital of Zurich [Zurich], Department of Medicine, The Johns Hopkins University School of Medicine-Division of Infectious Diseases, Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Center for Infection and Immunity Amsterdam (CINIMA), Wellcome Trust Genome Campus, Structures et propriétés d'architectures moléculaire (SPRAM - UMR 5819), Institut Nanosciences et Cryogénie (INAC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Big Data Institute, University of Oxford, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), University of Cambridge [UK] (CAM), Laboratory of Experimental Virology - Department of Medical Microbiology [Amsterdam, The Netherlands], Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA)-University of Amsterdam [Amsterdam] (UvA)-Center for Infection and Immunity Amsterdam - CINIMA [Amsterdam, The Netherlands], The Wellcome Trust Sanger Institute [Cambridge], Karolinska Institutet [Stockholm], Robert Koch Institute [Berlin] (RKI), Johns Hopkins University (JHU), Helsinki University Hospital [Finland] (HUS), Division of Intramural Research [Bethesda, MD, USA] (Cardiovascular Branch), National Institutes of Health [Bethesda] (NIH)-National Heart, Lung, and Blood Institute [Bethesda] (NHLBI), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris-Saclay, THe BEEHIVE Collaboration, European Project: 339251,EC:FP7:ERC,ERC-2013-ADG,BEEHIVE(2014), AII - Infectious diseases, Medical Microbiology, APH - Aging & Later Life, Infectious diseases, Global Health, Clinicum, Infektiosairauksien yksikkö, HUS Inflammation Center, HUS Internal Medicine and Rehabilitation, and Bill & Melinda Gates Foundation
- Subjects
0301 basic medicine ,PROTEASE ,Computer science ,Sequence assembly ,RECOMBINATION ,Computational biology ,Microbiology ,Genome ,DNA sequencing ,diversity ,Set (abstract data type) ,03 medical and health sciences ,Virology ,[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN] ,ddc:610 ,mapping ,TYPE-1 ,ComputingMilieux_MISCELLANEOUS ,Sequence (medicine) ,Contig ,IDENTIFICATION ,[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE] ,BEEHIVE Collaboration ,HIV ,INSERTIONS ,food and beverages ,bioinformatics ,TRANSFORM ,GENE ,Resources ,3. Good health ,Identification (information) ,ALIGNMENT ,030104 developmental biology ,3121 General medicine, internal medicine and other clinical medicine ,HUMAN-IMMUNODEFICIENCY-VIRUS ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,genome assembly ,next-generation sequencing ,3111 Biomedicine ,610 Medizin und Gesundheit ,INHIBITORS ,Reference genome - Abstract
International audience; Studying the evolution of viruses and their molecular epidemiology relies on accurate viral sequence data, so that small differences between similar viruses can be meaningfully interpreted. Despite its higher throughput and more detailed minority variant data, next-generation sequencing has yet to be widely adopted for HIV. The difficulty of accurately reconstructing the consensus sequence of a quasispecies from reads (short fragments of DNA) in the presence of large betweenand within-host diversity, including frequent indels, may have presented a barrier. In particular, mapping (aligning) reads to a reference sequence leads to biased loss of information; this bias can distort epidemiological and evolutionary conclusions. De novo assembly avoids this bias by aligning the reads to themselves, producing a set of sequences called contigs. However contigs provide only a partial summary of the reads, misassembly may result in their having an incorrect structure, and no information is available at parts of the genome where contigs could not be assembled. To address these problems we developed the tool shiver to pre-process reads for quality and contamination, then map them to a reference tailored to the sample using corrected contigs supplemented with the user’s choice of existing reference sequences. Run with two commands per sample, it can easily be used for large heterogeneous data sets. We used shiver to reconstruct the consensus sequence and minority variant information from paired-end short-read whole-genome data produced with the Illumina platform, for sixty-five existing publicly available samples and fifty new samples. We show the systematic superiority of mapping to shiver’s constructed reference compared with mapping the same reads to the closest of 3,249 real references: median values of 13 bases called differently and more accurately, 0 bases called differently and less accurately, and 205 bases of missing sequence recovered. We also successfully applied shiver to whole-genome samples of Hepatitis C Virus and Respiratory Syncytial Virus. shiver is publicly available from https://github.com/ChrisHIV/shiver.
- Published
- 2018
- Full Text
- View/download PDF
39. Author Correction: Optimised metrics for CRISPR-KO screens with second-generation gRNA libraries
- Author
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Ong, Swee Hoe, primary, Li, Yilong, additional, Koike-Yusa, Hiroko, additional, and Yusa, Kosuke, additional
- Published
- 2018
- Full Text
- View/download PDF
40. Optimised metrics for CRISPR-KO screens with second-generation gRNA libraries
- Author
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Ong, Swee Hoe, primary, Li, Yilong, additional, Koike-Yusa, Hiroko, additional, and Yusa, Kosuke, additional
- Published
- 2017
- Full Text
- View/download PDF
41. Accurate characterization of the IFITM locus using MiSeq and PacBio sequencing shows genetic variation in Galliformes
- Author
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Bassano, Irene, primary, Ong, Swee Hoe, additional, Lawless, Nathan, additional, Whitehead, Thomas, additional, Fife, Mark, additional, and Kellam, Paul, additional
- Published
- 2017
- Full Text
- View/download PDF
42. Molecular epidemiology of dengue viruses from complete genome sequences
- Author
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Ong, Swee Hoe, Tanner, Marcel, Beck, Hans-Peter, and Schreiber, Mark J.
- Subjects
viruses - Abstract
The availability of the complete genetic blueprint of the dengue virus is essential in molecular epidemiological studies to uncover the role of the virus in dengue pathogenesis. During the course of this project, over two hundred complete genomes of the dengue virus were generated from clinical samples collected in three dengue-endemic Southeast Asian countries. In addition, a bioinformatics platform integrating a sequence database, sequence retrieval tools, sequence annotation data and a variety of analysis tools was developed for easy management, manipulation and analysis of dengue virus sequence data. Whereas previous studies have mostly focused on epidemiological events in the Americas and Thailand, sequence data recovered from dengue epidemics in Indonesia, Malaysia and Singapore in this study have uncovered some of the dengue virus diversity circulating in the region. The three countries appear to share similar pool of dengue viruses, with some viral lineages in sustained circulation since at least the 1970s. Sequencing of historical virus isolates prior to the 2004/2005 epidemics in Indonesia and Singapore revealed that adaptive viral evolution played little or no role in triggering those epidemics. Lastly, a method that utilised all available sequence data from Malaysia was devised to reconstruct the history of dengue virus in that country since the 1960s.
- Published
- 2010
43. Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe.
- Author
-
Blanquart, François, Wymant, Chris, Cornelissen, Marion, Gall, Astrid, Bakker, Margreet, Bezemer, Daniela, Hall, Matthew, Hillebregt, Mariska, Ong, Swee Hoe, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Fransen, Katrien, Gourlay, Annabelle J., Grabowski, M. Kate, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych F., Kivelä, Pia, Kouyos, Roger, and Laeyendecker, Oliver
- Subjects
VIRAL genetics ,HIV ,BIOLOGICAL evolution ,GENETICS ,VIRAL transmission ,RNA viruses - Abstract
HIV-1 set-point viral load—the approximately stable value of viraemia in the first years of chronic infection—is a strong predictor of clinical outcome and is highly variable across infected individuals. To better understand HIV-1 pathogenesis and the evolution of the viral population, we must quantify the heritability of set-point viral load, which is the fraction of variation in this phenotype attributable to viral genetic variation. However, current estimates of heritability vary widely, from 6% to 59%. Here we used a dataset of 2,028 seroconverters infected between 1985 and 2013 from 5 European countries (Belgium, Switzerland, France, the Netherlands and the United Kingdom) and estimated the heritability of set-point viral load at 31% (CI 15%–43%). Specifically, heritability was measured using models of character evolution describing how viral load evolves on the phylogeny of whole-genome viral sequences. In contrast to previous studies, (i) we measured viral loads using standardized assays on a sample collected in a strict time window of 6 to 24 months after infection, from which the viral genome was also sequenced; (ii) we compared 2 models of character evolution, the classical “Brownian motion” model and another model (“Ornstein–Uhlenbeck”) that includes stabilising selection on viral load; (iii) we controlled for covariates, including age and sex, which may inflate estimates of heritability; and (iv) we developed a goodness of fit test based on the correlation of viral loads in cherries of the phylogenetic tree, showing that both models of character evolution fit the data well. An overall heritability of 31% (CI 15%–43%) is consistent with other studies based on regression of viral load in donor–recipient pairs. Thus, about a third of variation in HIV-1 virulence is attributable to viral genetic variation. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
44. A method for full genome sequencing of all four serotypes of the dengue virus
- Author
-
Christenbury, Joseph G., Aw, Pauline P.K., Ong, Swee Hoe, Schreiber, Mark J., Chow, Angelia, Gubler, Duane J., Vasudevan, Subhash G., Ooi, Eng Eong, and Hibberd, Martin L.
- Published
- 2010
- Full Text
- View/download PDF
45. IVA: accurate de novo assembly of RNA virus genomes
- Author
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Hunt, Martin, primary, Gall, Astrid, additional, Ong, Swee Hoe, additional, Brener, Jacqui, additional, Ferns, Bridget, additional, Goulder, Philip, additional, Nastouli, Eleni, additional, Keane, Jacqueline A., additional, Kellam, Paul, additional, and Otto, Thomas D., additional
- Published
- 2015
- Full Text
- View/download PDF
46. Systems consequences of amplicon formation in human breast cancer
- Author
-
Massachusetts Institute of Technology. Department of Biological Engineering, Wagner, Joel Patrick, Inaki, Koichiro, Menghi, Francesca, Woo, Xing Yi, Jacques, Pierre-Étienne, Lee, Yi Fang, Shreckengast, Phung Trang, Soon, Wendy WeiJia, Malhotra, Ankit, Teo, Audrey S.M., Hillmer, Axel M., Khng, Alexis Jiaying, Ruan, Xiaoan, Ong, Swee Hoe, Bertrand, Denis, Nagarajan, Niranjan, Karuturi, R. Krishna Murthy, Miranda, Alfredo Hidalgo, Liu, Edison T., Massachusetts Institute of Technology. Department of Biological Engineering, Wagner, Joel Patrick, Inaki, Koichiro, Menghi, Francesca, Woo, Xing Yi, Jacques, Pierre-Étienne, Lee, Yi Fang, Shreckengast, Phung Trang, Soon, Wendy WeiJia, Malhotra, Ankit, Teo, Audrey S.M., Hillmer, Axel M., Khng, Alexis Jiaying, Ruan, Xiaoan, Ong, Swee Hoe, Bertrand, Denis, Nagarajan, Niranjan, Karuturi, R. Krishna Murthy, Miranda, Alfredo Hidalgo, and Liu, Edison T.
- Abstract
Chromosomal structural variations play an important role in determining the transcriptional landscape of human breast cancers. To assess the nature of these structural variations, we analyzed eight breast tumor samples with a focus on regions of gene amplification using mate-pair sequencing of long-insert genomic DNA with matched transcriptome profiling. We found that tandem duplications appear to be early events in tumor evolution, especially in the genesis of amplicons. In a detailed reconstruction of events on chromosome 17, we found large unpaired inversions and deletions connect a tandemly duplicated ERBB2 with neighboring 17q21.3 amplicons while simultaneously deleting the intervening BRCA1 tumor suppressor locus. This series of events appeared to be unusually common when examined in larger genomic data sets of breast cancers albeit using approaches with lesser resolution. Using siRNAs in breast cancer cell lines, we showed that the 17q21.3 amplicon harbored a significant number of weak oncogenes that appeared consistently coamplified in primary tumors. Down-regulation of BRCA1 expression augmented the cell proliferation in ERBB2-transfected human normal mammary epithelial cells. Coamplification of other functionally tested oncogenic elements in other breast tumors examined, such as RIPK2 and MYC on chromosome 8, also parallel these findings. Our analyses suggest that structural variations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously and that such oncogenic cassettes are favored during the evolution of a cancer., Singapore. Agency for Science, Technology and Research, National Science Foundation (U.S.) (East Asia and Pacific Summer Institutes (OISE-1108282))
- Published
- 2014
47. Patient-Based Transcriptome-Wide Analysis Identify Interferon and Ubiquination Pathways as Potential Predictors of Influenza A Disease Severity
- Author
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Hoang, Long Truong, primary, Tolfvenstam, Thomas, additional, Ooi, Eng Eong, additional, Khor, Chiea Chuen, additional, Naim, Ahmand Nazri Mohamed, additional, Ho, Eliza Xin Pei, additional, Ong, Swee Hoe, additional, Wertheim, Heiman F., additional, Fox, Annette, additional, Van Vinh Nguyen, Chau, additional, Nghiem, Ngoc My, additional, Ha, Tuan Manh, additional, Thi Ngoc Tran, Anh, additional, Tambayah, Paul, additional, Lin, Raymond, additional, Sangsajja, Chariya, additional, Manosuthi, Weerawat, additional, Chuchottaworn, Chareon, additional, Sansayunh, Piamlarp, additional, Chotpitayasunondh, Tawee, additional, Suntarattiwong, Piyarat, additional, Chokephaibulkit, Kulkanya, additional, Puthavathana, Pilaipan, additional, de Jong, Menno D., additional, Farrar, Jeremy, additional, van Doorn, H. Rogier, additional, and Hibberd, Martin Lloyd, additional
- Published
- 2014
- Full Text
- View/download PDF
48. Deep Sequencing of Norovirus Genomes Defines Evolutionary Patterns in an Urban Tropical Setting
- Author
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Cotten, Matthew, primary, Petrova, Velislava, additional, Phan, My V. T., additional, Rabaa, Maia A., additional, Watson, Simon J., additional, Ong, Swee Hoe, additional, Kellam, Paul, additional, and Baker, Stephen, additional
- Published
- 2014
- Full Text
- View/download PDF
49. Systems consequences of amplicon formation in human breast cancer
- Author
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Inaki, Koichiro, primary, Menghi, Francesca, additional, Woo, Xing Yi, additional, Wagner, Joel P., additional, Jacques, Pierre-Étienne, additional, Lee, Yi Fang, additional, Shreckengast, Phung Trang, additional, Soon, Wendy WeiJia, additional, Malhotra, Ankit, additional, Teo, Audrey S.M., additional, Hillmer, Axel M., additional, Khng, Alexis Jiaying, additional, Ruan, Xiaoan, additional, Ong, Swee Hoe, additional, Bertrand, Denis, additional, Nagarajan, Niranjan, additional, Karuturi, R. Krishna Murthy, additional, Hidalgo Miranda, Alfredo, additional, and Liu, Edison T., additional
- Published
- 2014
- Full Text
- View/download PDF
50. Spread, Circulation, and Evolution of the Middle East Respiratory Syndrome Coronavirus
- Author
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Cotten, Matthew, primary, Watson, Simon J., additional, Zumla, Alimuddin I., additional, Makhdoom, Hatem Q., additional, Palser, Anne L., additional, Ong, Swee Hoe, additional, Al Rabeeah, Abdullah A., additional, Alhakeem, Rafat F., additional, Assiri, Abdullah, additional, Al-Tawfiq, Jaffar A., additional, Albarrak, Ali, additional, Barry, Mazin, additional, Shibl, Atef, additional, Alrabiah, Fahad A., additional, Hajjar, Sami, additional, Balkhy, Hanan H., additional, Flemban, Hesham, additional, Rambaut, Andrew, additional, Kellam, Paul, additional, and Memish, Ziad A., additional
- Published
- 2014
- Full Text
- View/download PDF
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