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Human T-cell lymphotropic virus type 1 (HTLV-1) is involved with two well-described clinical conditions: HTLV-1-associated myelopathy/ tropical spastic paraparesis (HAM/TSP) and adult T cell leukemia. The neurological disease affects predominantly the spinal cord. Although unusual, the brain as well as other organs may be involved by inflammatory reaction associated with HTLV-1 infection. This condition was recently described in our report “Temporal lesions and widespread involvement of white matter associated with multi-organ inflammatory disease in human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP)”. The development of HTLV-1-associated diseases seems to be regulated by viral, host and environmental determinants. High proviral load (PVL) is the best predictor of HAM/TSP. Proviral integration into transcriptionally active units in host genomes and genotypes HLA-B*5401 and HLA-DRB1*0101 are associated with high PVL and consequently linked to HAM/TSP. The increased proliferation and migration of HTLV-1 infected lymphocytes to central nervous system and a resulting strong pro-inflammatory reaction play a crucial role in the neuropathogenesis of the disease. In general, increasing in HTLV-1 PVL in both peripheral blood mononuclear cells and in cerebrospinal fluid (CSF) cells coincides with the exacerbation of neurological symptoms. Analysis of CSF in HAM/TSP shows an inflammatory response characterized by lymphocytic pleocytosis, raised protein content, intrathecal synthesis of oligoclonal IgG bands and of specific IgG, and increased concentration of pro-inflammatory markers. Here, it will be discussed the pathogenesis and the inflammatory mechanisms leading to injury of the central nervous system in HTLV-1 infection.

Inflammation Inducing Central Nervous System Damage in HTLV-1 Infection