Recent reports have demonstrated that human T lymphotropic virus type 1 (HTLV-1) is associated with other neurological abnormalities in addition to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). It has been well established that high HTLV-1 proviral loads are associated with the development of HAM/TSP. We now demonstrate, for the first time, to our knowledge, that HTLV-1 proviral loads in patients with other neurological abnormalities are also significantly higher than in asymptomatic HTLV-1 carriers.
HIV-individuals are at risk for human T-lymphotropic virus (HTLV) coinfection and neurological diseases. Little is known about the impact of HAART among coinfected patients. In this study, 47 out of 428 HIV individuals were coinfected with HTLV (10.9%). Coinfection was an independent variable associated with neurological outcome (odds ratio 8.73). Coinfection was associated with myelopathy [chi square (X(2)) = 93, P < 0.001], peripheral neuropathy (X(2) = 6.5, P = 0.01), and hepatitis C virus infection (X(2) = 36.5, P < 0.001). HAART did not appear to protect against neurological diseases and had no impact on HTLV proviral load.
Although human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is usually described as a chronic disabling disease, a rapid course over months or even weeks has been reported in some patients. The authors describe the clinical features of HAM/TSP in a Brazilian cohort and evaluate the prevalence of patients with a subacute progression of the disease. This was defined as the requirement of a wheelchair during the first 2 years after the onset of symptoms. Patients with this subacute course and patients with the chronic clinical course were compared in terms of their HTLV-I proviral loads (PLs) using real-time polymerase chain reaction (PCR). Seven out of 88 patients (7.9%) had a subacute progression. All patients were women and 5/7 acquired HTLV-I through sexual contact. There was no significant difference in the real-time PLs between the group with subacute evolution (mean 8.5 copies/100 cells, range 6.03 to 12.09) and those patients with a typical course of disease (mean 11.34 copies/100 cells, range 0.4 to 67.72) (P = .68), suggesting that factors other than the number of infected cells are implicated in the development of such an aggressive course of disease. Early recognition of this subgroup is important because immunosuppressive treatment might be beneficial if instituted promptly.
In Rio de Janeiro (RJ) most cases of paraparesis of obscure origin are associated with the human T‐cell lymphotropic virus type I (HTLV‐I). Thirty‐four consecutive patients with HTLV‐I‐associated myelopathy/tropical spastic paraparesis (HAM/TSP) from RJ were evaluated. Most patients came from low socio‐economic levels. There was no difference in terms of gender. The main affected racial group was white. A history of sexually transmitted diseases was a major risk factor for HAM/TSP and a positive serology for syphilis was found in 26.5% of the patients. The major clinical findings were of a spastic paraparesis with generalized brisk tendon jerks and bilateral Babinki's sign. Sensation was abnormal in 25 patients (73.5%) and five (14.7%) had a sensory level. Three patients (8.8%) had optic atrophy. The cerebrospinal fluid showed a lymphocytic pleocytosis with a mean total protein content of 0.4 g/litre, and an increased intrathecal IgG synthesis in 59.4% of patients. HAM/TSP and multiple sclerosis (MS) occur indigenously in RJ and some HAM/TSP cases can be sometimes confused with MS. Therefore we propose that, in places where MS coexist with HAM/TSP, HTLV‐I antibodies should be sought routinely in those MS suspected cases with prominent spastic paraparesis.
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