Increased risk for developing HAM is associated with blood-borne viral transmission, increased proviral DNA loads and anti-HTLV antibodies, polymorphisms in the IL-10 promoter and IL-28B gene, HLA-A*02- and HLA-DRB1*0101 alleles, and impaired anti-HTLV cytotoxic T-cell responses [7,15-19]. This evidence concerns the gene HLA-DRB1 and tropical spastic paraparesis.