HTLV-1 indirectly damages the CNS through infecting CD4+ T cells, which cross the blood-brain barrier and activate cytotoxic CD8+ T cells causing neuroglial death and degeneration.8,9 A high proviral load (PVL) and a PVL greater in the CSF than in the blood are risk factors of developing HAM.10 The PVL and the host's immune response are affected by factors such as the host's human leukocyte antigen genotype and single-nucleotide polymorphisms.11 The CSF concentrations of the cytokines neopterin and CXCL10 (IP-10) correlate with the rate of disease progression in HAM. Here, CD8A is linked to tropical spastic paraparesis.