Abstract
BackgroundThe Interleukin 28B (IL28B) rs12979860 polymorphisms was recently reported to be associated with the human T-cell leukemia virus type 1 (HTLV-1) proviral load (PvL) and the development of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).MethodsIn an attempt to examine this hypothesis, we assessed the association of the rs12979860 genotypes with HTLV-1 PvL levels and clinical status in 112 unrelated Brazilian subjects (81 HTLV-1 asymptomatic carriers, 24 individuals with HAM/TSP and 7 with Adult T cell Leukemia/Lymphoma (ATLL)).ResultsAll 112 samples were successfully genotyped and their PvLs compared. Neither the homozygote TT nor the heterozygote CT mutations nor the combination genotypes (TT/CT) were associated with a greater PvL. We also observed no significant difference in allele distribution between asymptomatic carriers and patients with HTLV-1 associated HAM/TSP.ConclusionsOur study failed to support the previously reported positive association between the IL28B rs12979860 polymorphisms and an increased risk of developing HAM/TSP in the Brazilian population.
Highlights
The Interleukin 28B (IL28B) rs12979860 polymorphisms was recently reported to be associated with the human T-cell leukemia virus type 1 (HTLV-1) proviral load (PvL) and the development of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP)
Human T-lymphotropic virus type I (HTLV-I) is an oncogenic human retrovirus that was first isolated from a T-cell line, HUT102, that had been obtained from a patient with adult T-cell leukemia/lymphoma (ATLL) [1]
The PvL levels were significantly higher in both HAM/TSP patients and ATLL patients (p < 0.0001, for each), compared to asymptomatic carriers (ACs)
Summary
The Interleukin 28B (IL28B) rs12979860 polymorphisms was recently reported to be associated with the human T-cell leukemia virus type 1 (HTLV-1) proviral load (PvL) and the development of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Genetic variation at site −592 resulted in no association in other study analyzing the impact of these polymorphisms on the risk of HAM/TSP in Brazilian patients [20]. A 857 T polymorphism in tumor necrosis factor α (TNF-α), which is a potent immuno-modulator and proinflammatory cytokine, has been shown to be associated with ATLL patients compared to healthy subjects, suggesting that the genetic alteration that increases the production of TNF-α is associated with a susceptibility to ATLL [13]
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