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

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Abstract
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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