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Impact of Heterozygosity for the Chemokine Receptor CCR5 32-bp-Deleted Allele on Plasma Virus Load and CD4 T Lymphocytes in Perinatally Human Immunodeficiency Virus-Infected Children at 8 Years of Age

F. Buseyne, G. Janvier, J. P. Teglas, S. Ivanoff, M. Burgard, E. Bui, M.-J. Mayaux, S. Blanche, C. Rouzioux and Y. Rivière
The Journal of Infectious Diseases
Vol. 178, No. 4 (Oct., 1998), pp. 1019-1023
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30117172
Page Count: 5
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Impact of Heterozygosity for the Chemokine Receptor CCR5 32-bp-Deleted Allele on Plasma Virus Load and CD4 T Lymphocytes in Perinatally Human Immunodeficiency Virus-Infected Children at 8 Years of Age
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Abstract

The CCR5 gene encodes one of the major human immunodeficiency virus type 1 (HIV-1) coreceptors. A 32-bp deletion in this gene (Δ-ccr5) is associated with relative resistance to disease progression in heterozygous HIV-1-infected persons. The effect of this mutation on virologie and immunologic parameters was determined in a cohort of 45 perinatally HIV-1-infected children prospectively followed after 5 years of age. At a median age of 8.3 years, heterozygous children had significantly lower virus load than homozygous children (median, 3.3 vs. 4.1 log copies/mL, P <.009) and higher percentages of CD4 T cells (median, 26% vs. 17%, P < .07). However, there was no discernible influence of the CCR5 genotype on the percentages of CD8 T cells (P <.27) or on HIV-specific cytotoxic T lymphocyte activities (P < .65). There was a trend for lower rates of progression to AIDS (CDC stage C) in heterozygous children. These data confirm a major role for the CCR5 coreceptor in HIV-1 pathogenesis in children.

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