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13. Contribution of genetic background, traditional risk factors, and HIV-related factors to coronary artery disease events in HIV-positive persons

Author

Rotger, M, Glass, Tr, Junier, T, Lundgren, J, Neaton, Jd, Poloni, Es, van 't Wout AB, Lubomirov, R, Colombo, S, Martinez, R, Rauch, A, Günthard, Hf, Neuhaus, J, Wentworth, D, van Manen, D, Gras, La, Schuitemaker, H, Albini, L, Torti, C, Jacobson, Lp, Li, X, Kingsley, La, Carli, F, Guaraldi, G, Ford, Es, Sereti, I, Hadigan, C, Martinez, E, Arnedo, M, Egaña-Gorroño, L, Gatell, Jm, Law, M, Bendall, C, Petoumenos, K, Rockstroh, J, Wasmuth, Jc, Kabamba, K, Delforge, M, De Wit, S, Berger, F, Mauss, S, de Paz Sierra, M, Losso, M, Belloso, Wh, Leyes, M, Campins, A, Mondi, A, De Luca, A, Bernardino, I, Barriuso-Iglesias, M, Torrecilla-Rodriguez, A, Gonzalez-Garcia, J, Arribas, Jr, Fanti, I, Gel, S, Puig, J, Negredo, E, Gutierrez, M, Domingo, P, Fischer, J, Fätkenheuer, G, Alonso-Villaverde, C, Macken, A, Woo, J, Mcginty, T, Mallon, P, Mangili, A, Skinner, S, Wanke, Ca, Reiss, P, Weber, R, Bucher, Hc, Fellay, J, Telenti, A, Tarr, Pe, Vullo, V, Magnificent, Consortium, Insight, Swiss HIV Cohort Study, Mastroianni, C, MAGNIFICENT Consortium, Swiss HIV Cohort Study, INSIGHT, Rotger, M., Glass, TR., Lubomirov, R., Bucher, HC., Telenti, A., Tarr, PE., Junier, T., Poloni, ES., Fellay, J., Colombo, S., Martinez, R., Rauch, A., Weber, R., Günthard, HF., Neuhaus, J., Wentworth, D., Lundgren, J., Neaton, JD., van Manen, D., Gras, AL., Schuitemaker, H., van Wout AB., Reiss, P., Albini, L., Torti, C., Jacobson, LP., Li, X., Kingsley, LA., Carli, F., Guaraldi, G., Ford, ES., Sereti, I., Hadigan, C., Martinez, E., Arnedo-Valero, M., Egaña-Gorroño, L., Gatell, JM., Law, M., Bendall, C., Petoumenos, K., Rockstroh, J., Wasmuth, JC., Kabamba, K., Delforge, M., De Wit, S., Berger, F., Mauss, S., Sierra Mde, P., Losso, M., Belloso, WH., Leyes, M., Campins, A., Mondi, A., De Luca, A., Bernardino, I., Barriuso-Iglesias£££Mónica£££ M., Rodriguez, AT., Garcia, JG., Arribas, JR., Fanti, I., Gel, S., Puig, J., Negredo, E., Gutierrez, M., Domingo, P., Fischer, J., Fätkenheuer, G., Alonso-Villaverde, C., Macken, A., Woo, J., McGinty, T., Mallon, P., Mangili, A., Skinner, S., Wanke, CA., Aubert, V., Barth, J., Battegay, M., Bernasconi, E., Böni, J., Burton-Jeangros, C., Calmy, A., Cavassini, M., Egger, M., Elzi, L., Fehr, J., Francioli, P., Furrer, H., Fux, CA., Gorgievski, M., Günthard, H., Haerry, D., Hasse, B., Hirsch, HH., Hirschel, B., Hösli, I., Kahlert, C., Kaiser, L., Keiser, O., Kind, C., Klimkait, T., Kovari, H., Ledergerber, B., Martinetti, G., Martinez de Tejada, B., Metzner, K., Müller, N., Nadal, D., Pantaleo, G., Regenass, S., Rickenbach, M., Rudin, C., Schmid, P., Schultze, D., Schöni-Affolter, F., Schüpbach, J., Speck, R., Taffé, P., Tarr, P., Trkola, A., Vernazza, P., Prins, YS., Kuijpers, TW., Scherpbier, HJ., Boer, K., van der Meer JT., Wit, FW., Godfried, MH., van der Poll, T., Nellen, FJ., Lange, JM., Geerlings, SE., van Vugt, M., Vrouenraets, SM., Pajkrt, D., Bos, JC., van der Valk, M., Schreij, G., Lowe, S., Lashof, AO., Pronk, MJ., Bravenboer, B., van der Ende ME., de Vries-Sluijs TE., Schurink, CA., van der Feltz, M., Nouwen, JL., Gelinck, LB., Verbon, A., Rijnders, BJ., van de Ven-de Ruiter ED., Slobbe, L., Haag, D., Kauffmann, RH., Schippers, EF., Groeneveld, PH., Alleman, MA., Bouwhuis, JW., ten Kate RW., Soetekouw, R., Kroon, FP., van den Broek PJ., van Dissel JT., Arend, SM., van Nieuwkoop, C., de Boer MJ., Jolink, H., den Hollander JG., Pogany, K., Bronsveld, W., Kortmann, W., van Twillert, G., van Houte DP., Polée, MB., van Vonderen MG., ten Napel CH., Kootstra, GJ., Brinkman, K., Blok, WL., Frissen, PH., Schouten, WE., van den Berk GE., Juttmann, JR., van Kasteren ME., Brouwer, AE., Mulder, JW., van Gorp EC., Smit, PM., Weijer, S., van Eeden, A., Verhagen, DW., Sprenger, HG., Doedens, R., Scholvinck, EH., van Assen, S., Stek, CJ., Hoepelman, IM., Mudrikova, T., Schneider, MM., Jaspers, CA., Ellerbroek, PM., Peters, EJ., Maarschalk-Ellerbroek, LJ., Oosterheert, JJ., Arends, JE., Wassenberg, MW., van der Hilst JC., Richter, C., van der Berg JP., Gisolf, EH., Margolick, JB., Plankey, M., Crain, B., Dobs, A., Farzadegan, H., Gallant, J., Johnson-Hill, L., Sacktor, N., Selnes, O., Shepard, J., Thio, C., Phair, JP., Wolinsky, SM., Badri, S., Conover, C., O'Gorman, M., Ostrow, D., Palella, F., Ragin, A., Detels, R., Martínez-Maza, O., Aronow, A., Bolan, R., Breen, E., Butch, A., Fahey, J., Jamieson, B., Miller, EN., Oishi, J., Vinters, H., Visscher, BR., Wiley, D., Witt, M., Yang, O., Young, S., Zhang, ZF., Rinaldo, CR., Becker, JT., Cranston, RD., Martinson, JJ., Mellors, JW., Silvestre, AJ., Stall, RD., Muñoz, A., Abraham, A., Althoff, K., Cox, C., D'Souza, G., Gange, SJ., Golub, E., Schollenberger, J., Seaberg, EC., Su, S., Huebner, RE., Dominguez, G., Moroni, M., Angarano, G., Antinori, A., Carosi, G., Cauda, R., Monforte£££A d'Arminio£££ A., Di Perri, G., Galli, M., Iardino, R., Ippolito, G., Lazzarin, A., Perno, CF., Sagnelli, E., Viale, PL., Von Schlosser, F., d'Arminio Monforte, A., Ammassari, A., Andreoni, M., Balotta, C., Bonfanti, P., Bonora, S., Borderi, M., Capobianchi, MR., Castagna, A., Ceccherini-Silberstein, F., Cozzi-Lepri, A., Gargiulo, M., Gervasoni, C., Girardi, E., Lichtner, M., Lo Caputo, S., Madeddu, G., Maggiolo, F., Marcotullio, S., Monno, L., Murri, R., Mussini, C., Puoti, M., Formenti, T., Galli, L., Lorenzini, P., Montroni, M., Giacometti, A., Costantini, A., Riva, A., Tirelli, U., Martellotta, F., Ladisa, N., Lazzari, G., Verucchi, G., Castelli, F., Scalzini, A., Minardi, C., Bertelli, D., Quirino, T., Abeli, C., Manconi, PE., Piano, P., Vecchiet, J., Falasca, K., Carnevale, G., Lorenzotti, S., Sighinolfi, L., Segala, D., Leoncini, F., Mazzotta, F., Pozzi, M., Cassola, G., Viscoli, G., Viscoli, A., Piscopo, R., Mazzarello, G., Mastroianni, C., Belvisi, V., Caramma, I., Chiodera, A., Castelli, P., Rizzardini, G., Ridolfo, AL., Foschi, A., Salpietro, S., Galli, A., Bigoloni, A., Spagnuolo, V., Merli, S., Carenzi, L., Moioli, MC., Cicconi, P., Bisio, L., Gori, A., Lapadula, G., Abrescia, N., Chirianni, A., De Marco, M., Ferrari, C., Borghi, R., Baldelli, F., Belfiori, B., Parruti, G., Ursini, T., Magnani, G., Ursitti, MA., Narciso, P., Tozzi, V., Vullo, V., d'Avino, A., Zaccarelli, M., Gallo, L., Acinapura, R., Capozzi, M., Libertone, R., Trotta, MP., Tebano, G., Cattelan, AM., Mura, MS., Caramello, P., Orofino, GC., Sciandra, M., Raise, Ebo, F., Pellizzer, G., Manfrin, V., McManus, H., Wright, S., Moore, R., Edwards, S., Medische Microbiologie, RS: CAPHRI School for Public Health and Primary Care, AII - Amsterdam institute for Infection and Immunity, Experimental Immunology, Other departments, Graduate School, APH - Amsterdam Public Health, Global Health, Medical Microbiology and Infection Prevention, Paediatric Infectious Diseases / Rheumatology / Immunology, Other Research, Obstetrics and Gynaecology, Infectious diseases, General Internal Medicine, Center of Experimental and Molecular Medicine, University of Zurich, Tarr, Philip E, Rotger, M, Glass, T, Junier, T, Lundgren, J, Neaton, J, Poloni, E, Van 'T Wout, A, Lubomirov, R, Colombo, S, Martinez, R, Rauch, A, Günthard, H, Neuhaus, J, Wentworth, D, Van Manen, D, Gras, L, Schuitemaker, H, Albini, L, Torti, C, Jacobson, L, Li, X, Kingsley, L, Carli, F, Guaraldi, G, Ford, E, Sereti, I, Hadigan, C, Martinez, E, Arnedo, M, Egaña Gorroño, L, Gatell, J, Law, M, Bendall, C, Petoumenos, K, Rockstroh, J, Wasmuth, J, Kabamba, K, Delforge, M, De Wit, S, Berger, F, Mauss, S, De Paz Sierra, M, Losso, M, Belloso, W, Leyes, M, Campins, A, Mondi, A, De Luca, A, Bernardino, I, Barriuso Iglesias, M, Torrecilla Rodriguez, A, Gonzalez Garcia, J, Arribas, J, Fanti, I, Gel, S, Puig, J, Negredo, E, Gutierrez, M, Domingo, P, Fischer, J, Fätkenheuer, G, Alonso Villaverde, C, Macken, A, Woo, J, Mcginty, T, Mallon, P, Mangili, A, Skinner, S, Wanke, C, Reiss, P, Weber, R, Bucher, H, Fellay, J, Telenti, A, Tarr, P, Gori, A, Junier, Thomas, Poloni, Estella S., Rotger, Margalida, Glass, Tracy R., Junier, Thoma, Lundgren, Jen, Neaton, James D., Van 't Wout, Angã©lique B., Lubomirov, Rubin, Colombo, Sara, Martinez, Raquel, Rauch, Andri, Gã¼nthard, Huldrych F., Neuhaus, Jacqueline, Wentworth, Deborah, Van Manen, Danielle, Gras, Luuk A., Schuitemaker, Hanneke, Albini, Laura, Torti, Carlo, Jacobson, Lisa P., Li, Xiuhong, Kingsley, Lawrence A., Carli, Federica, Guaraldi, Giovanni, Ford, Emily S., Sereti, Irini, Hadigan, Colleen, Martinez, Esteban, Arnedo, Mireia, Egaã±a gorroã±o, Lander, Gatell, Jose M., Law, Matthew, Bendall, Courtney, Petoumenos, Kathy, Rockstroh, Jã¼rgen, Wasmuth, Jan christian, Kabamba, Kabeya, Delforge, Marc, De Wit, Stephane, Berger, Florian, Mauss, Stefan, De Paz Sierra, Mariana, Losso, Marcelo, Belloso, Waldo H., Leyes, Maria, Campins, Antoni, Mondi, Annalisa, De Luca, Andrea, Bernardino, Ignacio, Barriuso iglesias, Mã³nica, Torrecilla rodriguez, Ana, Gonzalez garcia, Juan, Arribas, Josã© R., Fanti, Iuri, Gel, Silvia, Puig, Jordi, Negredo, Eugenia, Gutierrez, Mar, Domingo, Pere, Fischer, Julia, Fã¤tkenheuer, Gerd, Alonso villaverde, Carlo, Macken, Alan, Woo, Jame, Mcginty, Tara, Mallon, Patrick, Mangili, Alexandra, Skinner, Sally, Wanke, Christine A., Reiss, Peter, Weber, Rainer, Bucher, Heiner C., Fellay, Jacque, Telenti, Amalio, Tarr, Philip E. Swiss Hiv Cohort, and Castagna, Antonella

Subjects
Male, HIV Infections, Genome-wide association study, 030204 cardiovascular system & hematology, 2726 Microbiology (medical), 10234 Clinic for Infectious Diseases, Coronary artery disease, 0302 clinical medicine, ddc:590, Risk Factors, Abacavir, 80 and over, genetics, 030212 general & internal medicine, Family history, Articles and Commentaries, Aged, 80 and over, education.field_of_study, medicine.diagnostic_test, traditional risk factor, Single Nucleotide, Middle Aged, 3. Good health, Infectious Diseases, traditional risk factors, Cohort, Female, HIV infection, antiretroviral therapy, coronary artery disease, Human, medicine.drug, Adult, Microbiology (medical), medicine.medical_specialty, Adolescent, Population, Infectious Disease, 610 Medicine & health, Polymorphism, Single Nucleotide, Genetic Predisposition to Disease, Aged, Coronary Artery Disease, Humans, Polymorphism, Young Adult, 03 medical and health sciences, Internal medicine, medicine, education, Genetic testing, business.industry, Risk Factor, 2725 Infectious Diseases, Odds ratio, medicine.disease, Immunology, genetic, business
Abstract

BACKGROUND: Persons infected with human immunodeficiency virus (HIV) have increased rates of coronary artery disease (CAD). The relative contribution of genetic background, HIV-related factors, antiretroviral medications, and traditional risk factors to CAD has not been fully evaluated in the setting of HIV infection.METHODS: In the general population, 23 common single-nucleotide polymorphisms (SNPs) were shown to be associated with CAD through genome-wide association analysis. Using the Metabochip, we genotyped 1875 HIV-positive, white individuals enrolled in 24 HIV observational studies, including 571 participants with a first CAD event during the 9-year study period and 1304 controls matched on sex and cohort.RESULTS: A genetic risk score built from 23 CAD-associated SNPs contributed significantly to CAD (P = 2.9 × 10(-4)). In the final multivariable model, participants with an unfavorable genetic background (top genetic score quartile) had a CAD odds ratio (OR) of 1.47 (95% confidence interval [CI], 1.05-2.04). This effect was similar to hypertension (OR = 1.36; 95% CI, 1.06-1.73), hypercholesterolemia (OR = 1.51; 95% CI, 1.16-1.96), diabetes (OR = 1.66; 95% CI, 1.10-2.49), ≥ 1 year lopinavir exposure (OR = 1.36; 95% CI, 1.06-1.73), and current abacavir treatment (OR = 1.56; 95% CI, 1.17-2.07). The effect of the genetic risk score was additive to the effect of nongenetic CAD risk factors, and did not change after adjustment for family history of CAD.CONCLUSIONS: In the setting of HIV infection, the effect of an unfavorable genetic background was similar to traditional CAD risk factors and certain adverse antiretroviral exposures. Genetic testing may provide prognostic information complementary to family history of CAD.

Published
2013
Full Text
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19. Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load

Author

Mclaren, Pj, Coulonges, C, Bartha, I, Lenz, Tl, Deutsch, Aj, Bashirova, A, Buchbinder, S, Carrington, Mn, Cossarizza, A, Dalmau, J, De Luca, Andrea, Goedert, Jj, Gurdasani, D, Haas, Dw, Herbeck, Jt, Johnson, Eo, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, Van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, Poli, G, Sandhu, M, Schuitemaker, H, Shea, Pr, Theodorou, I, Walker, Bd, Weintrob, Ac, Winkler, Ca, Wolinsky, Sm, Raychaudhuri, S, Goldstein, Db, Telenti, A, De Bakker, Piw, Zagury, J, Fellay, J., De Luca, Andrea (ORCID:0000-0002-8311-6935), Mclaren, Pj, Coulonges, C, Bartha, I, Lenz, Tl, Deutsch, Aj, Bashirova, A, Buchbinder, S, Carrington, Mn, Cossarizza, A, Dalmau, J, De Luca, Andrea, Goedert, Jj, Gurdasani, D, Haas, Dw, Herbeck, Jt, Johnson, Eo, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, Van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, Poli, G, Sandhu, M, Schuitemaker, H, Shea, Pr, Theodorou, I, Walker, Bd, Weintrob, Ac, Winkler, Ca, Wolinsky, Sm, Raychaudhuri, S, Goldstein, Db, Telenti, A, De Bakker, Piw, Zagury, J, Fellay, J., and De Luca, Andrea (ORCID:0000-0002-8311-6935)

Published
2015

20. Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load

Author

McLaren, P.J., Coulonges, C., Bartha, I., Lenz, T.L., Deutsch, A.J., Bashirova, A., Buchbinder, S., Carrington, M.N., Cossarizza, A., Dalmau, J., De Luca, A., Goedert, J.J., Gurdasani, D., Haas, D.W., Herbeck, J.T., Johnson, E.O., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., Poli, G., Sandhu, M.S., Schuitemaker, H., Shea, P.R., Theodorou, I., Walker, B.D., Weintrob, A.C., Winkler, C.A., Wolinsky, S.M., Raychaudhuri, S., Goldstein, D.B., Telenti, A., de Bakker, P.I.W., Zagury, J-F, Fellay, J., McLaren, P.J., Coulonges, C., Bartha, I., Lenz, T.L., Deutsch, A.J., Bashirova, A., Buchbinder, S., Carrington, M.N., Cossarizza, A., Dalmau, J., De Luca, A., Goedert, J.J., Gurdasani, D., Haas, D.W., Herbeck, J.T., Johnson, E.O., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., Poli, G., Sandhu, M.S., Schuitemaker, H., Shea, P.R., Theodorou, I., Walker, B.D., Weintrob, A.C., Winkler, C.A., Wolinsky, S.M., Raychaudhuri, S., Goldstein, D.B., Telenti, A., de Bakker, P.I.W., Zagury, J-F, and Fellay, J.

Abstract

Previous genome-wide association studies (GWAS) of HIV-1–infected populations have been underpowered to detect common variants with moderate impact on disease outcome and have not assessed the phenotypic variance explained by genome-wide additive effects. By combining the majority of available genome-wide genotyping data in HIV-infected populations, we tested for association between ∼8 million variants and viral load (HIV RNA copies per milliliter of plasma) in 6,315 individuals of European ancestry. The strongest signal of association was observed in the HLA class I region that was fully explained by independent effects mapping to five variable amino acid positions in the peptide binding grooves of the HLA-B and HLA-A proteins. We observed a second genome-wide significant association signal in the chemokine (C-C motif) receptor (CCR) gene cluster on chromosome 3. Conditional analysis showed that this signal could not be fully attributed to the known protective CCR5Δ32 allele and the risk P1 haplotype, suggesting further causal variants in this region. Heritability analysis demonstrated that common human genetic variation—mostly in the HLA and CCR5 regions—explains 25% of the variability in viral load. This study suggests that analyses in non-European populations and of variant classes not assessed by GWAS should be priorities for the field going forward.

Published
2015

21. Phosphatidylinositol transfer protein α regulates growth and apoptosis of NIH3T3 cells: involvement of a cannabinoid 1-like receptor

Author

Schenning, M., van Tiel, C.M., van Manen, D., Stam, J.C., Gadella, B.M., Wirtz, K.W.A., Snoek, G.T., Cell Cycle Regulation, Lipide chemie op enkel-cel-niveau, Universiteit Utrecht, Dep Scheikunde, Dep Biologie, Faculteit Diergeneeskunde, and Sub Membrane Enzymology begr. 01-06-12

Subjects
Biologie/Milieukunde (BIOL), Diergeneeskunde (DGNK)
Published
2004

22. Association study of common genetic variants and HIV-1 acquisition in 6,300 infected cases and 7,200 controls

Author

Mclaren, Pj, Coulonges, C, Ripke, S, Van Den Berg, L, Buchbinder, S, Carrington, M, Cossarizza, A, Dalmau, J, Deeks, Sg, Delaneau, O, De Luca, Andrea, Goedert, Jj, Haas, D, Herbeck, Jt, Kathiresan, S, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, Van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, O'Brien, Sj, Pereyra, F, Plummer, Fa, Poli, G, Qi, Y, Rucart, P, Sandhu, M, Shea, Pr, Schuitemaker, H, Theodorou, I, Vannberg, F, Veldink, J, Walker, Bd, Weintrob, A, Winkler, Ca, Wolinsky, S, Telenti, A, Goldstein, Db, De Bakker, Piw, Zagury, J, Fellay, J., De Luca, Andrea (ORCID:0000-0002-8311-6935), Mclaren, Pj, Coulonges, C, Ripke, S, Van Den Berg, L, Buchbinder, S, Carrington, M, Cossarizza, A, Dalmau, J, Deeks, Sg, Delaneau, O, De Luca, Andrea, Goedert, Jj, Haas, D, Herbeck, Jt, Kathiresan, S, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, Van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, O'Brien, Sj, Pereyra, F, Plummer, Fa, Poli, G, Qi, Y, Rucart, P, Sandhu, M, Shea, Pr, Schuitemaker, H, Theodorou, I, Vannberg, F, Veldink, J, Walker, Bd, Weintrob, A, Winkler, Ca, Wolinsky, S, Telenti, A, Goldstein, Db, De Bakker, Piw, Zagury, J, Fellay, J., and De Luca, Andrea (ORCID:0000-0002-8311-6935)

Published
2013

23. Association study of common genetic variants and HIV-1 acquisition in 6,300 infected cases and 7,200 controls

Author

Balloux, F., McLaren, P.J., Coulonges, C., Ripke, S., van den Berg, L., Buchbinder, S., Carrington, M., Cossarizza, A., Dalmau, J., Deeks, S.G., Delaneau, O., De Luca, A., Goedert, J.J., Haas, D., Herbeck, J.T., Kathiresan, S., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., O'Brien, S.J., Pereyra, F., Plummer, F.A., Poli, G., Qi, Y., Rucart, P., Sandhu, M.S., Shea, P.R., Schuitemaker, H., Theodorou, I., Vannberg, F., Veldink, J., Walker, B.D., Weintrob, A., Winkler, C.A., Wolinsky, S., Telenti, A., Goldstein, D.B., de Bakker, P.I.W., Zagury, J-F, Fellay, J., Balloux, F., McLaren, P.J., Coulonges, C., Ripke, S., van den Berg, L., Buchbinder, S., Carrington, M., Cossarizza, A., Dalmau, J., Deeks, S.G., Delaneau, O., De Luca, A., Goedert, J.J., Haas, D., Herbeck, J.T., Kathiresan, S., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., O'Brien, S.J., Pereyra, F., Plummer, F.A., Poli, G., Qi, Y., Rucart, P., Sandhu, M.S., Shea, P.R., Schuitemaker, H., Theodorou, I., Vannberg, F., Veldink, J., Walker, B.D., Weintrob, A., Winkler, C.A., Wolinsky, S., Telenti, A., Goldstein, D.B., de Bakker, P.I.W., Zagury, J-F, and Fellay, J.

Abstract

Multiple genome-wide association studies (GWAS) have been performed in HIV-1 infected individuals, identifying common genetic influences on viral control and disease course. Similarly, common genetic correlates of acquisition of HIV-1 after exposure have been interrogated using GWAS, although in generally small samples. Under the auspices of the International Collaboration for the Genomics of HIV, we have combined the genome-wide single nucleotide polymorphism (SNP) data collected by 25 cohorts, studies, or institutions on HIV-1 infected individuals and compared them to carefully matched population-level data sets (a list of all collaborators appears in Note S1 in Text S1). After imputation using the 1,000 Genomes Project reference panel, we tested approximately 8 million common DNA variants (SNPs and indels) for association with HIV-1 acquisition in 6,334 infected patients and 7,247 population samples of European ancestry. Initial association testing identified the SNP rs4418214, the C allele of which is known to tag the HLA-B*57:01 and B*27:05 alleles, as genome-wide significant (p = 3.6×10−11). However, restricting analysis to individuals with a known date of seroconversion suggested that this association was due to the frailty bias in studies of lethal diseases. Further analyses including testing recessive genetic models, testing for bulk effects of non-genome-wide significant variants, stratifying by sexual or parenteral transmission risk and testing previously reported associations showed no evidence for genetic influence on HIV-1 acquisition (with the exception of CCR5Δ32 homozygosity). Thus, these data suggest that genetic influences on HIV acquisition are either rare or have smaller effects than can be detected by this sample size.

Published
2013

24. Genome-wide association study identifies single nucleotide polymorphism in DYRK1A associated with replication of HIV-1 in monocyte-derived macrophages

Author

Bol, SM, Moerland, PD, Limou, S, van Remmerden, Y, Coulonges, C, van Manen, D, Herbeck, JT, Fellay, J, Sieberer, M, Sietzema, JG, van 't Slot, R, Martinson, J, Zagury, JF, Schuitemaker, H, van 't Wout, AB, Bol, SM, Moerland, PD, Limou, S, van Remmerden, Y, Coulonges, C, van Manen, D, Herbeck, JT, Fellay, J, Sieberer, M, Sietzema, JG, van 't Slot, R, Martinson, J, Zagury, JF, Schuitemaker, H, and van 't Wout, AB

Abstract

Background: HIV-1 infected macrophages play an important role in rendering resting T cells permissive for infection, in spreading HIV-1 to T cells, and in the pathogenesis of AIDS dementia. During highly active anti-retroviral treatment (HAART), macrophages keep producing virus because tissue penetration of antiretrovirals is suboptimal and the efficacy of some is reduced. Thus, to cure HIV-1 infection with antiretrovirals we will also need to efficiently inhibit viral replication in macrophages. The majority of the current drugs block the action of viral enzymes, whereas there is an abundance of yet unidentified host factors that could be targeted. We here present results from a genome-wide association study identifying novel genetic polymorphisms that affect in vitro HIV-1 replication in macrophages. Methodology/Principal Findings: Monocyte-derived macrophages from 393 blood donors were infected with HIV-1 and viral replication was determined using Gag p24 antigen levels. Genomic DNA from individuals with macrophages that had relatively low (n = 96) or high (n = 96) p24 production was used for SNP genotyping with the Illumina 610 Quad beadchip. A total of 494,656 SNPs that passed quality control were tested for association with HIV-1 replication in macrophages, using linear regression. We found a strong association between in vitro HIV-1 replication in monocyte-derived macrophages and SNP rs12483205 in DYRK1A (p = 2.16×10-5). While the association was not genome-wide significant (p<1×10-7), we could replicate this association using monocyte-derived macrophages from an independent group of 31 individuals (p = 0.0034). Combined analysis of the initial and replication cohort increased the strength of the association (p = 4.84×10-6). In addition, we found this SNP to be associated with HIV-1 disease progression in vivo in two independent cohort studies (p = 0.035 and p = 0.0048). Conclusions/Significance: These findings suggest that the kinase DYRK1A is involved in th

Published
2011

33. Multicohort Genomewide Association Study Reveals a New Signal of Protection Against HIV-1 Acquisition

Author

Limou, S., primary, Delaneau, O., additional, van Manen, D., additional, An, P., additional, Sezgin, E., additional, Le Clerc, S., additional, Coulonges, C., additional, Troyer, J. L., additional, Veldink, J. H., additional, van den Berg, L. H., additional, Spadoni, J.-L., additional, Taing, L., additional, Labib, T., additional, Montes, M., additional, Delfraissy, J.-F., additional, Schachter, F., additional, O'Brien, S. J., additional, Buchbinder, S., additional, van Natta, M. L., additional, Jabs, D. A., additional, Froguel, P., additional, Schuitemaker, H., additional, Winkler, C. A., additional, and Zagury, J.-F., additional

Published
2012
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35. This title is unavailable for guests, please login to see more information.

Author

Cell Cycle Regulation, Lipide chemie op enkel-cel-niveau, Universiteit Utrecht, Dep Scheikunde, Dep Biologie, Faculteit Diergeneeskunde, Sub Membrane Enzymology begr. 01-06-12, Schenning, M., van Tiel, C.M., van Manen, D., Stam, J.C., Gadella, B.M., Wirtz, K.W.A., Snoek, G.T., Cell Cycle Regulation, Lipide chemie op enkel-cel-niveau, Universiteit Utrecht, Dep Scheikunde, Dep Biologie, Faculteit Diergeneeskunde, Sub Membrane Enzymology begr. 01-06-12, Schenning, M., van Tiel, C.M., van Manen, D., Stam, J.C., Gadella, B.M., Wirtz, K.W.A., and Snoek, G.T.

Published
2004

38. Genome-Wide Association Study Implicates PARD3B-Based AIDS Restriction

Author

Troyer, J. L., primary, Nelson, G. W., additional, Lautenberger, J. A., additional, Chinn, L., additional, McIntosh, C., additional, Johnson, R. C., additional, Sezgin, E., additional, Kessing, B., additional, Malasky, M., additional, Hendrickson, S. L., additional, Li, G., additional, Pontius, J., additional, Tang, M., additional, An, P., additional, Winkler, C. A., additional, Limou, S., additional, Le Clerc, S., additional, Delaneau, O., additional, Zagury, J.-F., additional, Schuitemaker, H., additional, van Manen, D., additional, Bream, J. H., additional, Gomperts, E. D., additional, Buchbinder, S., additional, Goedert, J. J., additional, Kirk, G. D., additional, and O'Brien, S. J., additional

Published
2011
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45. Contribution of Genetic Background, Traditional Risk Factors, and HIV-Related Factors to Coronary Artery Disease Events in HIV-Positive Persons

Author

Rotger, M., Glass, T. R., Junier, T., Lundgren, J., Neaton, J. D., Poloni, E. S., Van 'T Wout, A. B., Lubomirov, R., Colombo, S., Martinez, R., Rauch, Andri, Gunthard, H. F., Neuhaus, J., Wentworth, D., Van Manen, D., Gras, L. A., Schuitemaker, H., Albini, L., Torti, C., Jacobson, L. P., Li, X., Kingsley, L. A., Carli, F., Guaraldi, G., Ford, E. S., Sereti, I., Hadigan, C., Martinez, E., Arnedo, M., Egana-Gorrono, L., Gatell, J. M., Law, M., Bendall, C., Petoumenos, K., Rockstroh, J., Wasmuth, J.-C., Kabamba, K., Delforge, M., De Wit, S., Berger, F., Mauss, S., De Paz Sierra, M., Losso, M., Belloso, W. H., Leyes, M., Campins, A., Mondi, A., De Luca, A., Bernardino, I., Barriuso-Iglesias, M., Torrecilla-Rodriguez, A., Gonzalez-Garcia, J., Arribas, J. R., Fanti, I., Gel, S., Puig, J., Negredo, E., Gutierrez, M., Domingo, P., Fischer, J., Fatkenheuer, G., Alonso-Villaverde, C., Macken, A., Woo, J., McGinty, T., Mallon, P., Mangili, A., Skinner, S., Wanke, C. A., Reiss, P., Weber, R., Bucher, H. C., Fellay, J., Telenti, A., and Tarr, P. E.

Subjects
610 Medicine & health, 3. Good health
Abstract

Background Persons infected with human immunodeficiency virus (HIV) have increased rates of coronary artery disease (CAD). The relative contribution of genetic background, HIV-related factors, antiretroviral medications, and traditional risk factors to CAD has not been fully evaluated in the setting of HIV infection. Methods In the general population, 23 common single-nucleotide polymorphisms (SNPs) were shown to be associated with CAD through genome-wide association analysis. Using the Metabochip, we genotyped 1875 HIV-positive, white individuals enrolled in 24 HIV observational studies, including 571 participants with a first CAD event during the 9-year study period and 1304 controls matched on sex and cohort. Results A genetic risk score built from 23 CAD-associated SNPs contributed significantly to CAD (P = 2.9×10−4). In the final multivariable model, participants with an unfavorable genetic background (top genetic score quartile) had a CAD odds ratio (OR) of 1.47 (95% confidence interval [CI], 1.05–2.04). This effect was similar to hypertension (OR = 1.36; 95% CI, 1.06–1.73), hypercholesterolemia (OR = 1.51; 95% CI, 1.16–1.96), diabetes (OR = 1.66; 95% CI, 1.10–2.49), ≥1 year lopinavir exposure (OR = 1.36; 95% CI, 1.06–1.73), and current abacavir treatment (OR = 1.56; 95% CI, 1.17–2.07). The effect of the genetic risk score was additive to the effect of nongenetic CAD risk factors, and did not change after adjustment for family history of CAD. Conclusions In the setting of HIV infection, the effect of an unfavorable genetic background was similar to traditional CAD risk factors and certain adverse antiretroviral exposures. Genetic testing may provide prognostic information complementary to family history of CAD.

46. Genome-wide association studies on HIV susceptibility, pathogenesis and pharmacogenomics

Author

van Manen Daniëlle, van ‘t Wout Angélique B, and Schuitemaker Hanneke

Subjects
Genome-wide association studies, Single-nucleotide polymorphisms, Host genetics, HIV susceptibility, HIV pathogenesis, Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Susceptibility to HIV-1 and the clinical course after infection show a substantial heterogeneity between individuals. Part of this variability can be attributed to host genetic variation. Initial candidate gene studies have revealed interesting host factors that influence HIV infection, replication and pathogenesis. Recently, genome-wide association studies (GWAS) were utilized for unbiased searches at a genome-wide level to discover novel genetic factors and pathways involved in HIV-1 infection. This review gives an overview of findings from the GWAS performed on HIV infection, within different cohorts, with variable patient and phenotype selection. Furthermore, novel techniques and strategies in research that might contribute to the complete understanding of virus-host interactions and its role on the pathogenesis of HIV infection are discussed.

Published
2012
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48. Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load

Author

Andrea De Luca, Aaron J. Deutsch, Deepti Gurdasani, David W. Haas, Jean-François Zagury, Susan Buchbinder, Simon Mallal, Manjinder S. Sandhu, Steven M. Wolinsky, Cédric Coulonges, Laurence Meyer, Paul I.W. de Bakker, James I. Mullins, Daniëlle van Manen, Andrea Cossarizza, José M. Miró, Amy C. Weintrob, Tobias L. Lenz, Judith Dalmau, Olivier Lambotte, Niels Obel, James J. Goedert, Mary Carrington, Ma Luo, Arman Bashirova, David Goldstein, Gregory D. Kirk, Joshua T. Herbeck, Amalio Telenti, Paul J. McLaren, Patrick R. Shea, Javier Martinez-Picado, Cheryl A. Winkler, Bruce D. Walker, Istvan Bartha, Jacques Fellay, Ioannis Theodorou, Hanneke Schuitemaker, Guido Poli, Eric O. Johnson, Soumya Raychaudhuri, Other departments, AII - Amsterdam institute for Infection and Immunity, Experimental Immunology, Mclaren, Pj, Coulonges, C, Bartha, I, Lenz, Tl, Deutsch, Aj, Bashirova, A, Buchbinder, S, Carrington, Mn, Cossarizza, A, Dalmau, J, De Luca, A, Goedert, Jj, Gurdasani, D, Haas, Dw, Herbeck, Jt, Johnson, Eo, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, Poli, Guido, Sandhu, M, Schuitemaker, H, Shea, Pr, Theodorou, I, Walker, Bd, Weintrob, Ac, Winkler, Ca, Wolinsky, Sm, Raychaudhuri, S, Goldstein, Db, Telenti, A, de Bakker, Pi, Zagury, Jf, and Fellay, J.

Subjects
Adult, Receptors, CCR5, infectious disease, Inheritance Patterns, Genome-wide association study, Peptide binding, Human leukocyte antigen, Biology, heritability, Research Support, Settore MED/17 - MALATTIE INFETTIVE, Polymorphism, Single Nucleotide, Genomics, GWAS, Heritability, HIV-1 control, Infectious disease, Journal Article, genomics, Humans, Genetic Predisposition to Disease, Allele, Amino Acids, Non-U.S. Gov't, Genotyping, Alleles, Genetic association, Genetics, Multidisciplinary, Research Support, Non-U.S. Gov't, Haplotype, Viral Load, Biological Sciences, Physical Chromosome Mapping, HLA-B Antigens, Host-Pathogen Interactions, HIV-1, Chromosomes, Human, Pair 3, Viral load, Genome-Wide Association Study
Abstract

Previous genome-wide association studies (GWAS) of HIV-1-infected populations have been underpowered to detect common variants with moderate impact on disease outcome and have not assessed the phenotypic variance explained by genome-wide additive effects. By combining the majority of available genome-wide genotyping data in HIV-infected populations, we tested for association between similar to 8 million variants and viral load (HIV RNA copies per milliliter of plasma) in 6,315 individuals of European ancestry. The strongest signal of association was observed in the HLA class I region that was fully explained by independent effects mapping to five variable amino acid positions in the peptide binding grooves of the HLA-B and HLA-A proteins. We observed a second genome-wide significant association signal in the chemokine (C-C motif) receptor (CCR) gene cluster on chromosome 3. Conditional analysis showed that this signal could not be fully attributed to the known protective CCR5 Delta 32 allele and the risk P1 haplotype, suggesting further causal variants in this region. Heritability analysis demonstrated that common human genetic variation-mostly in the HLA and CCR5 regions-explains 25% of the variability in viral load. This study suggests that analyses in non-European populations and of variant classes not assessed by GWAS should be priorities for the field going forward.

Published
2015

49. Association Study of Common Genetic Variants and HIV-1 Acquisition in 6,300 Infected Cases and 7,200 Controls

Author

David W. Haas, Hanneke Schuitemaker, Steven M. Wolinsky, Paul I.W. de Bakker, Jean-François Zagury, Cédric Coulonges, Olivier Lambotte, Simon Mallal, Sekar Kathiresan, Patrick R. Shea, Pierre Rucart, Jacques Fellay, Niels Obel, Gregory D. Kirk, Joshua T. Herbeck, Fredrik O. Vannberg, David Goldstein, Francis A. Plummer, Ma Luo, Stephan Ripke, M. S. Sandhu, Amalio Telenti, Daniëlle van Manen, Susan Buchbinder, Stephen J. O'Brien, Judith Dalmau, Ying Qi, Mary Carrington, James I. Mullins, Olivier Delaneau, Steven G. Deeks, Florencia Pereyra, Bruce D. Walker, Laurence Meyer, Cheryl A. Winkler, Paul J. McLaren, Ioannis Theodorou, Andrea De Luca, James J. Goedert, Leonard H. van den Berg, Jan H. Veldink, Guido Poli, Javier Martinez-Picado, Andrea Cossarizza, José M. Miró, Amy C. Weintrob, Mclaren, Pj, Coulonges, C, Ripke, S, van den Berg, L, Buchbinder, S, Carrington, M, Cossarizza, A, Dalmau, J, Deeks, Sg, Delaneau, O, De Luca, A, Goedert, Jj, Haas, D, Herbeck, Jt, Kathiresan, S, Kirk, Gd, Lambotte, O, Luo, M, Mallal, S, van Manen, D, Martinez Picado, J, Meyer, L, Miro, Jm, Mullins, Ji, Obel, N, O'Brien, Sj, Pereyra, F, Plummer, Fa, Poli, Guido, Qi, Y, Rucart, P, Sandhu, M, Shea, Pr, Schuitemaker, H, Theodorou, I, Vannberg, F, Veldink, J, Walker, Bd, Weintrob, A, Winkler, Ca, Wolinsky, S, Telenti, A, Goldstein, Db, de Bakker, Piw, Zagury, Jf, Fellay, J., Universitat de Barcelona, Other departments, AII - Amsterdam institute for Infection and Immunity, and Experimental Immunology

Subjects
Viral Diseases, Genome-wide association study, HIV Infections, Communicable diseases, Cohort Studies, 0302 clinical medicine, 030212 general & internal medicine, lcsh:QH301-705.5, Genetics, 0303 health sciences, education.field_of_study, Host-Pathogen Interactions, Polymorphism, Single Nucleotide, Case-Control Studies, European Continental Ancestry Group, Genetic Predisposition to Disease, Genome-Wide Association Study, HIV-1, Humans, Genomics, 3. Good health, Infectious Diseases, Medicine, Research Article, lcsh:Immunologic diseases. Allergy, Immunology, Population, Parenteral transmission, Single-nucleotide polymorphism, Biology, Settore MED/17 - MALATTIE INFETTIVE, Microbiology, Polymorphism, Single Nucleotide, White People, 03 medical and health sciences, Virology, Genetic model, VIH (Virus), Allele, education, Molecular Biology, 030304 developmental biology, Genetic association, HIV (Viruses), HIV, Malalties infeccioses, lcsh:Biology (General), Parasitology, lcsh:RC581-607, Imputation (genetics)
Abstract

Multiple genome-wide association studies (GWAS) have been performed in HIV-1 infected individuals, identifying common genetic influences on viral control and disease course. Similarly, common genetic correlates of acquisition of HIV-1 after exposure have been interrogated using GWAS, although in generally small samples. Under the auspices of the International Collaboration for the Genomics of HIV, we have combined the genome-wide single nucleotide polymorphism (SNP) data collected by 25 cohorts, studies, or institutions on HIV-1 infected individuals and compared them to carefully matched population-level data sets (a list of all collaborators appears in Note S1 in Text S1). After imputation using the 1,000 Genomes Project reference panel, we tested approximately 8 million common DNA variants (SNPs and indels) for association with HIV-1 acquisition in 6,334 infected patients and 7,247 population samples of European ancestry. Initial association testing identified the SNP rs4418214, the C allele of which is known to tag the HLA-B*57:01 and B*27:05 alleles, as genome-wide significant (p = 3.6×10−11). However, restricting analysis to individuals with a known date of seroconversion suggested that this association was due to the frailty bias in studies of lethal diseases. Further analyses including testing recessive genetic models, testing for bulk effects of non-genome-wide significant variants, stratifying by sexual or parenteral transmission risk and testing previously reported associations showed no evidence for genetic influence on HIV-1 acquisition (with the exception of CCR5Δ32 homozygosity). Thus, these data suggest that genetic influences on HIV acquisition are either rare or have smaller effects than can be detected by this sample size., Author Summary Comparing the frequency differences between common DNA variants in disease-affected cases and in unaffected controls has been successful in uncovering the genetic component of multiple diseases. This approach is most effective when large samples of cases and controls are available. Here we combine information from multiple studies of HIV infected patients, including more than 6,300 HIV+ individuals, with data from 7,200 general population samples of European ancestry to test nearly 8 million common DNA variants for an impact on HIV acquisition. With this large sample we did not observe any single common genetic variant that significantly associated with HIV acquisition. We further tested 22 variants previously identified by smaller studies as influencing HIV acquisition. With the exception of a deletion polymorphism in the CCR5 gene (CCR5Δ32) we found no convincing evidence to support these previous associations. Taken together these data suggest that genetic influences on HIV acquisition are either rare or have smaller effects than can be detected by this sample size.

Published
2013

50. CoPoP liposomes displaying stabilized clade C HIV-1 Env elicit tier 2 multiclade neutralization in rabbits.

Author

Koornneef A, Vanshylla K, Hardenberg G, Rutten L, Strokappe NM, Tolboom J, Vreugdenhil J, Boer KF, Perkasa A, Blokland S, Burger JA, Huang WC, Lovell JF, van Manen D, Sanders RW, Zahn RC, Schuitemaker H, Langedijk JPM, and Wegmann F

Subjects
Animals, Female, Rabbits, Antibodies, Neutralizing, HIV Antibodies, HIV Infections, Immunization, Liposomes, Phospholipids, AIDS Vaccines, env Gene Products, Human Immunodeficiency Virus, HIV-1
Abstract

One of the strategies towards an effective HIV-1 vaccine is to elicit broadly neutralizing antibody responses that target the high HIV-1 Env diversity. Here, we present an HIV-1 vaccine candidate that consists of cobalt porphyrin-phospholipid (CoPoP) liposomes decorated with repaired and stabilized clade C HIV-1 Env trimers in a prefusion conformation. These particles exhibit high HIV-1 Env trimer decoration, serum stability and bind broadly neutralizing antibodies. Three sequential immunizations of female rabbits with CoPoP liposomes displaying a different clade C HIV-1 gp140 trimer at each dosing generate high HIV-1 Env-specific antibody responses. Additionally, serum neutralization is detectable against 18 of 20 multiclade tier 2 HIV-1 strains. Furthermore, the peak antibody titers induced by CoPoP liposomes can be recalled by subsequent heterologous immunization with Ad26-encoded membrane-bound stabilized Env antigens. Hence, a CoPoP liposome-based HIV-1 vaccine that can generate cross-clade neutralizing antibody immunity could potentially be a component of an efficacious HIV-1 vaccine., (© 2024. The Author(s).)

Published
2024
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