Exhaustive Genotyping of the CEM15 (APOBEC3G) Gene and Absence of Association with AIDS Progression in a French Cohort (original) (raw)

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Équipe Génomique, Bioinformatique et Pathologies du Système Immunitaire, INSERM EMI0355

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Paris

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Centre National de Génotypage

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Evry, France

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Centre National de Génotypage

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Evry, France

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Centre National de Génotypage

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Evry, France

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Centre National de Génotypage

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Evry, France

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Centre National de Génotypage

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Evry, France

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Équipe Génomique, Bioinformatique et Pathologies du Système Immunitaire, INSERM EMI0355

,

Paris

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Center for Neurovirology, Temple University

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Philadelphia, Pennsylvania

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Équipe Génomique, Bioinformatique et Pathologies du Système Immunitaire, INSERM EMI0355

,

Paris

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Centre National de Génotypage

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Evry, France

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Centre National de Génotypage

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Evry, France

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Published:

15 January 2005

Cite

Hervé Do, Alexandre Vasilescu, Gora Diop, Thomas Hirtzig, Simon C. Heath, Cédric Coulonges, Jay Rappaport, Amu Therwath, Mark Lathrop, Fumihiko Matsuda, Jean-François Zagury, Exhaustive Genotyping of the CEM15 (APOBEC3G) Gene and Absence of Association with AIDS Progression in a French Cohort, The Journal of Infectious Diseases, Volume 191, Issue 2, 15 January 2005, Pages 159–163, https://doi.org/10.1086/426826
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Abstract

CEM15 (or APOBEC3G) has recently been identified as an inhibitor of human immunodeficiency virus type 1 (HIV-1) replication in vitro. To evaluate the impact of its genetic variations on the progression of acquired immunodeficiency syndrome (AIDS), we have performed an extensive genetic analysis of CEM15. We have sequenced CEM15 in a cohort of 327 HIV-1-seropositive patients with extreme disease progression phenotypes—either slow progression or rapid progression—and in 446 healthy control subjects, all of white descent. We have identified 29 polymorphisms with allele frequencies >1%, 14 of which were newly characterized. There were no significant associations between the polymorphisms or haplotypes of CEM15 and a disease progression phenotype in our cohort.

© 2005 by the Infectious Diseases Society of America

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