Polymorphism in the Interleukin-10 Promoter Affects Both Provirus Load and the Risk of Human T Lymphotropic Virus Type I-Associated Myelopathy/Tropical Spastic Paraparesis
To investigate non-human leukocyte antigen candidate genes that influence the outcome of human T cell lymphotropic virus (HTLV) type I infection, we analyzed 6 single-nucleotide polymorphisms in the interleukin (IL)-10 promoter region in 280 patients with HTLV-I-associated myelopathy/tropical spasti...
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Published in | The Journal of infectious diseases Vol. 190; no. 7; pp. 1279 - 1285 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Chicago, IL
The University of Chicago Press
01.10.2004
University of Chicago Press Oxford University Press |
Subjects | |
Online Access | Get full text |
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Summary: | To investigate non-human leukocyte antigen candidate genes that influence the outcome of human T cell lymphotropic virus (HTLV) type I infection, we analyzed 6 single-nucleotide polymorphisms in the interleukin (IL)-10 promoter region in 280 patients with HTLV-I-associated myelopathy/tropical spastic paraparesis(HAM/ TSP) and 255 HTLV-I-seropositive asymptomatic carriers from an area where HTLV-I is endemic. The IL-10 −592 A allele, which shows lower HTLV-I Tax-induced transcriptional activity than the C allele in the Jurkat T cell line, was associated with a >2-fold reduction in the odds of developing HAM/TSP (P = .011; odds ratio [OR], 0.50 [95% confidence interval, 0.30–0.86]) by reducing the provirus load in the whole cohort (P = .009, analysis of variance). Given the OR and the observed frequency of IL-10 −592 A, we demonstrate that this allele prevents ∼44.7% (standard deviation, ±13.1%) of potential cases of HAM/TSP, which indicates that it defines one component of the genetic susceptibility to HAM/TSP in the cohort. |
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Bibliography: | istex:3921B6EA67614A2D4A5CA79E92A0D48DEA2C779C ark:/67375/HXZ-NQTHV6BF-H Present affiliation: Department of Immunology, Imperial College, London, United Kingdom. ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-1899 1537-6613 |
DOI: | 10.1086/423942 |