All PCR-positive cases were seropositive, including 4 cases of tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM) (4/4), and one case each of myasthenia gravis (1/7) and multiple sclerosis (1/8).
Therefore, it is unlikely that the central nervous system tissue damage in HAM/TSP is a consequence of productive infection of HTLV-I in the CNS tissue.
Human T cell lymphotrophic virus type I (HTLV-I) is the etiologic agent of adult T cell lymphoma/leukemia (ATLL) and tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM).
Human T lymphotropic virus type-1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is endemic in tropical areas and in southwestern Japan, and has now been identified among risk groups in the United States and some European countries.
The central nervous system (CNS) pathology of HTLV-I associated myelopathy or tropical spastic paraparesis (HAM/TSP) is reviewed, based mainly on 12 autopsy cases of Japanese HAM/TSP with a serological confirmation of HTLV-I infection.
Higher absorbance values were obtained with sera from TSP/HAM patients than from asymptomatic carriers, but the difference between the two groups was not statistically significant.
The sequence of a 522-bp fragment corresponding to the carboxy terminus of gp46 and the majority of gp21 were determined for five HTLV-I-seropositive individuals, including the TSP/HAM patient.
Molecular variants of human T-cell lymphotropic virus type I (HTLV-I) have been isolated recently from lifelong residents of remote Melanesian populations, including a Solomon Islander with tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) or HTLV-I myeloneuropathy.
In contrast, viral RNA was found occasionally by in situ hybridization in muscle lesions of some patients with polymyositis, but was never found in central nervous system lesions of TSP/HAM patients.
Human T-lymphotropic virus, type 1 (HTLV-1) infection was detected in two unrelated Kuwaiti patients with tropical spastic paraparesis (HAM/TSP) and in the asymptomatic mother of one of them.
Cases of adult T-cell leukemia/lymphoma as well as tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) have already been described in Brazil.
We have identified a mutation in nucleotide 7959 of the tax gene of 14 Tumaco HTLV-I isolates (14 positive of 14 tested) that was present in 5 of 14 (35%) TSP/HAM patients from Japan and in 8 of 11 (72%) TSP/HAM patients from other geographic locations.
We cloned and sequenced a complete HTLV-I provirus (HTLV-IBoi) derived from the uncultured lymphocytes of a sub-acute post-transfusional TSP/HAM patient with clonal integration of HTLV-I.
We have investigated the expression of these molecules in human and rat glial cells infected with retrovirus HTLV-I, the causative agent of HTLV-I associated myelopathy (TSP/HAM).
Analysis of RNA from HTLV-I-infected cells established from patients with adult T cell leukemia (ATL) as well as tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) and both IL-2-dependent and IL-2-independent HTLV-I-infected cell lines by RNase protection has confirmed the existence of all of the alternatively spliced messages in each cell line analyzed.
Patients with human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) typically have a high HTLV-1 proviral load in peripheral blood mononuclear cells and abundant, activated HTLV-1-specific cytotoxic T lymphocytes (CTLs).
Human T-cell lymphotropic virus type I (HTLV-I) is associated with adult T-cell leukemia (ATL) and tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM).
To explore mechanisms of tax/rex expression in the lung, tax/rex mRNA expression and proviral DNA load were compared between peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage cells (BALC) from four patients with HTLV-1-associated myelopathy (HAM/TSP) and 13 carriers with various pulmonary symptoms.