Association of IL-10 Gene Polymorphisms and Human T Lymphotropic Virus Type I-Associated Myelopathy/tropical Spastic Paraparesis in North-East of Iran (Mashhad)

Document Type: Original Article

Authors

1 Department of Hematology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

2 Neurology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

3 Rheumatic Diseases Research Centre, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

4 Immunology Research Centre, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

5 Immunology Research Group, Faculty of Life Sciences, The University of Manchester, United Kingdom

6 Inflammation and Inflammatory Disease Research Centre, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Abstract

 
The underlying mechanisms leading to the development of human T-cell lymphotropic virus type I (HTLV-I) associated myelopathy/tropical spastic paraparesis (HAM/TSP) in HTLV-I infected individuals are not fully understood. Host genetic factors appear to be involved as risk factors for developing HAM/TSP. We investigated the possible contribution of interleukin-10 (IL-10) as a risk factor to HAM/TSP by comparing frequencies of promoter region single nucleotide polymorphisms in HTLV-I infected Iranian patients who either remained asymptomatic or developed HAM/TSP and asymptomatic HTLV-I carriers. Healthy, uninfected individuals from the same region served as healthy controls. Significant differences were observed in the distribution of IL-10 promoter alleles and genotypes at position -819 and -592 between HAM/TSP patients and healthy controls (P=0.01), and between HTLV-I carriers and healthy controls (P=0.02). The frequency of the low IL-10 producer haplotype (-1082*A, -819*T, -592*A) was significantly associated with HTLV-I carriage or HAM/TSP compared with healthy controls (P=
0.02 and 0.01, respectively). Our results suggest that IL-10 -819*T and -592*A alleles are significant risk factors for developing HTLLV-I infection but do not appear to convey additional risk for developing HAM/TSP
 

Keywords


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