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

J. Fellay; D. Ge; K.V. Shianna; S. Colombo; B. Ledergerber; E.T. Cirulli; T.J. Urban; K. Zhang; C.E. Gumbs; J.P. Smith; A. Castagna; A. Cozzi-Lepri; Luca A. De; P. Easterbrook; H.F. Gunthard; S. Mallal; C. Mussini; J. Dalmau; J. Martinez-Picado; J.M. Miro; N. Obel; S.M. Wolinsky; J.J. Martinson; R. Detels; J.B. Margolick; L.P. Jacobson; P. Descombes; S.E. Antonarakis; J.S. Beckmann; S.J. O'Brien; N.L. Letvin; A.J. McMichael; B.F. Haynes; M. Carrington; S. Feng; A. Telenti; D.B. Goldstein

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

J. Fellay, D. Ge, K.V. Shianna, S. Colombo, B. Ledergerber, E.T. Cirulli, T.J. Urban, K. Zhang, C.E. Gumbs, J.P. Smith, A. Castagna, A. Cozzi-Lepri, Luca A. De, P. Easterbrook, H.F. Gunthard, S. Mallal, C. Mussini, J. Dalmau, J. Martinez-Picado, J.M. MiroN. Obel, S.M. Wolinsky, J.J. Martinson, R. Detels, J.B. Margolick, L.P. Jacobson, P. Descombes, S.E. Antonarakis, J.S. Beckmann, S.J. O'Brien, N.L. Letvin, A.J. McMichael, B.F. Haynes, M. Carrington, S. Feng, A. Telenti, D.B. Goldstein

304 Citations (Scopus)

Abstract

To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians
Udgivelsesdato: 2009/12

Original language	English
Journal	PLoS Genetics
Volume	5
Issue number	12
Pages (from-to)	e1000791-
ISSN	1553-7390
Publication status	Published - 2009

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Cite this

Fellay, J., Ge, D., Shianna, K. V., Colombo, S., Ledergerber, B., Cirulli, E. T., Urban, T. J., Zhang, K., Gumbs, C. E., Smith, J. P., Castagna, A., Cozzi-Lepri, A., De, L. A., Easterbrook, P., Gunthard, H. F., Mallal, S., Mussini, C., Dalmau, J., Martinez-Picado, J., ... Goldstein, D. B. (2009). Common genetic variation and the control of HIV-1 in humans. PLoS Genetics, 5(12), e1000791-.

Fellay, J, Ge, D, Shianna, KV, Colombo, S, Ledergerber, B, Cirulli, ET, Urban, TJ, Zhang, K, Gumbs, CE, Smith, JP, Castagna, A, Cozzi-Lepri, A, De, LA, Easterbrook, P, Gunthard, HF, Mallal, S, Mussini, C, Dalmau, J, Martinez-Picado, J, Miro, JM, Obel, N, Wolinsky, SM, Martinson, JJ, Detels, R, Margolick, JB, Jacobson, LP, Descombes, P, Antonarakis, SE, Beckmann, JS, O'Brien, SJ, Letvin, NL, McMichael, AJ, Haynes, BF, Carrington, M, Feng, S, Telenti, A & Goldstein, DB 2009, 'Common genetic variation and the control of HIV-1 in humans', PLoS Genetics, vol. 5, no. 12, pp. e1000791-.

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abstract = "To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians Udgivelsesdato: 2009/12",

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AU - Fellay, J.

AU - Ge, D.

AU - Shianna, K.V.

AU - Colombo, S.

AU - Ledergerber, B.

AU - Cirulli, E.T.

AU - Urban, T.J.

AU - Zhang, K.

AU - Gumbs, C.E.

AU - Smith, J.P.

AU - Castagna, A.

AU - Cozzi-Lepri, A.

AU - De, Luca A.

AU - Easterbrook, P.

AU - Gunthard, H.F.

AU - Mallal, S.

AU - Mussini, C.

AU - Dalmau, J.

AU - Martinez-Picado, J.

AU - Miro, J.M.

AU - Obel, N.

AU - Wolinsky, S.M.

AU - Martinson, J.J.

AU - Detels, R.

AU - Margolick, J.B.

AU - Jacobson, L.P.

AU - Descombes, P.

AU - Antonarakis, S.E.

AU - Beckmann, J.S.

AU - O'Brien, S.J.

AU - Letvin, N.L.

AU - McMichael, A.J.

AU - Haynes, B.F.

AU - Carrington, M.

AU - Feng, S.

AU - Telenti, A.

AU - Goldstein, D.B.

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N2 - To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians Udgivelsesdato: 2009/12

AB - To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians Udgivelsesdato: 2009/12

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