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Human Molecular Genetics Advance Access published online on October 6, 2006
Human Molecular Genetics, doi:10.1093/hmg/ddl406
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© The Author 2006. Published by Oxford University Press. All rights reserved
Received June 13, 2006
Revised September 28, 2006
Accepted September 28, 2006

Article

A major susceptibility locus for HTLV-1 infection in childhood maps to chromosome 6q27

Sabine Plancoulaine 1 *, Antoine Gessain 2, Patricia Tortevoye 2, Anne Boland-Auge 3, Alexandre Vasilescu 3, Fumihiko Matsuda 3, and Laurent Abel 1 *

1 Laboratoire de Génétique Humaine des Maladies Infectieuses, Université de Paris René Descartes-INSERM U550, Faculté de Médecine Necker, 156 rue de Vaugirard, 75015 Paris, France, EU
2 Unité d'Epidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, 28 rue du Dr Roux, 75015 Paris, France, EU
3 Centre National de Génotypage, 2 rue Gaston Crémieux, 91057 Cedex Evry, France, EU

* To whom correspondence should be addressed.
Sabine Plancoulaine, E-mail: plancoulaine{at}necker.fr
Laurent Abel, E-mail: abel{at}necker.fr


  Abstract

Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) is a human oncoretrovirus causing adult T-cell leukemia/lymphoma and chronic neuromyelopathy. We previously showed by segregation analysis that a dominant gene controls HTLV-1 infection through breast-feeding in children of African origin. Here, we report the mapping of this locus by a genome-wide linkage analysis based on the genetic model provided by segregation analysis. Five pedigrees of African origin with HTLV-1-seropositive children were included in the study. Significant evidence for linkage (lod-score of 3.36, p = 0.00004) was obtained for chomosomal region 6q27 when using the robust analysis including only HTLV-1-infected subjects. When HTLV-1-seronegative children born to infected mothers were added in the analysis, a maximum lod-score of 2.79 (p = 0.0002) was obtained for chomosome 2p25. This result was entirely due to the largest pedigree of our sample, which alone gave a lod-score of 2.90 (p = 0.00013). We further excluded the role of exonic variants of two candidate genes located in the linked regions, CCR6 (Chemokine receptor 6) in 6q27, and ID2 (inhibitor of DNA binding 2) in 2p25. Our results, mapping a major susceptibility locus to chromosome 6q27 and suggesting genetic heterogeneity with another locus at 2p25, pave the way to determination of the molecular basis of predisposition to HTLV-1 infection in children.


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