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PubMed1989

Tropical spastic paraparesis: a model of virus-induced, cytotoxic T-cell-mediated demyelination?

Tropical spastic paraparesis is a neurological disorder that is most commonly seen in certain tropical (mainly Caribbean) areas and that presents as a progressive spastic paraparesis and urinary dysfunction. Recent studies have revealed an association between tropical spastic paraparesis and human T-cell lymphotropic virus type I (HTLV-I) infection. We report the results of a detailed morphological and immunocytochemical study of a patient with tropical spastic paraparesis. Lesions were restricted to the spinal cord and optic nerve, where demyelination, inflammation, and fiber loss were common features. Lymphocytes were seen closely applied to nerve fibers within which were changes resembling those seen in myelinated central nervous system cultures exposed to cytokines. Immunocytochemically, HTLV-I p19 core protein and a predominance of CD8+ (suppressor/cytotoxic) T cells and expression of class I major histocompatibility antigen were demonstrated in spinal cord lesions. It is postulated that cytotoxic T cells, either directly or via cytokines, induce lysis of the myelin sheath and subsequently the axon, resulting in a mixed picture of demyelination and axonal loss with secondary tractal degeneration. Despite this destruction, extensive remyelination was evident within affected areas of spinal cord.

Female↗
PubMed1988

HTLV-1 infection in tropical spastic paraparesis: lymphocyte culture and serologic response.

All 17 patients with tropical spastic paraparesis (TSP) in a series seen in the United Kingdom have antibodies to the human T cell leukemia virus type 1 (HTLV-1). Cultured peripheral blood lymphocytes from these patients formed multinucleated giant cells and reacted with sera and monoclonal antibodies to HTLV-1 in a manner identical to adult T cell leukemia-lymphoma (ATLL) patient lymphocytes. Western blot analysis failed to reveal any marked difference in the antigens recognized by sera from TSP and ATLL patients. The sera from TSP patients, their asymptomatic relatives and ATLL patients were titrated using the following assays: enzyme-linked immunosorbent assays (ELISA), particle agglutination, antibody-dependent cell-mediated cytotoxicity, and pseudotype neutralization. There were significantly stronger serologic responses in the TSP patients than in their relatives or ATLL patients. High antibody titers in the presence of replicating virus often reflect the antigen load; however, these data are also consistent with the suggestion that neurologic damage in TSP may be immunologically mediated.

Adult↗
PubMed1996

[Tropical spastic paraparesis: a necessary redefinition].

The author disserts on the definition of Tropical Spastic Paraparesis since its first description up to the etiological involvement of HTLV-1 in part of the cases. According to him the basic nucleus of the syndrome consists of a paraparesis with pyramidal signs (spasticity and hyperreflexia) with variable sensory and sphincter symptoms. The retroviral etiology by HTLV-1 is one of the variable elements of the condition. He aims at preventing conceptual distortions in the description of this condition.

Humans↗
PubMed1998

[Familial form of tropical spastic paraparesis. Report of 4 families].

We report eight patients with familial tropical spastic paraparesis belonging to four families. The diagnosis was reached by clinical, radiological and electrophysiological studies. Human lymphotropic virus type I infection was confirmed by ELISA, immunofluorescence essays. Western blot and polymerase chain reaction in DNA of peripheral blood mononuclear cells, using primers for tax and 5'ltr genes. In all these families there was a vertical transmission of the disease from the first to the second generation. All patients improved their spastic gait after prednisone treatment. Among patients of the second generation, all had dacrysialoadenitis, three had leukemia like lymphocytes in the blood smear, two had mycosis fungoides and one had hepatic cirrhosis.

Adolescent↗
PubMedDate not supplied

HTLV-1 and tropical spastic paraparesis. 1. Clinical features, pathology and epidemiology.

The clinical profile of tropical spastic paraparesis (TSP), described in scattered tropical and subtropical territories over the past 30 years, has been more clearly defined since the discovery of its direct association with human T lymphotropic virus type 1 (HTLV-1). A chronic disease of adults, commoner in women, it usually presents as a progressive spastic paraparesis with sphincter disturbance, sometimes with backache and lower limb sensory disorder. Most cases are chair-bound within 10 years. Histology reveals a chronic lymphocytic meningomyelopathy, predominantly in the spinal cord, together with long tract demyelination and hyalinoid thickening of the media and adventitia of small blood vessels. Geographical areas of high prevalence of TSP are known in the Caribbean, South America, South Africa, southern Japan, the Seychelles and probably in India, and it is sparsely endemic elsewhere. The virus appears to exist within lymphocytes for long periods. Vertical transmission occurs postnatally, and sexual and transfusion infection are also recognized, but much remains to be clarified regarding its pathogenesis and epidemiology.

Brain Stem↗
PubMed1994

[Tropical spastic paraparesis (HAM/TSP) in different regions of the world. Subclinical and geographic differences in neurophysiologic studies].

Tropical spastic paraparesis is the same clinical entity all over the world. It has been suggested that some clinical presentation differences are due to not well defined environmental factors that act along with the virus, modifying the start and progression of the disease. We analyzed 25 publications on the disease coming from different parts of the world, aiming to unravel regional differences. In these reports, we found different degrees of subclinical abnormalities in visual and somatosensory evoked potentials, nerve conduction studies, superior and inferior limb F wave and electromyography. It is concluded that genetic, environmental and even cultural factors may influence the clinical presentation of tropical spastic paraparesis and explain the detected differences in the reports analyzed in this study.

Electromyography↗
PubMed1992

Activated, HTLV-1-specific cytotoxic T-lymphocytes are found in healthy seropositives as well as in patients with tropical spastic paraparesis.

In human T cell lymphoma/leukemia virus (HTLV-1)-infected people with tropical spastic paraparesis (TSP), there are activated HTLV-1-specific cytotoxic T lymphocytes (CTL) in the circulation and lymphocytic infiltrates in spinal cord lesions that are rich in CD8+ T cells. These observations suggest a role for virus-specific CTL in the pathogenesis of TSP. We have examined the anti-HTLV-1 cytotoxic activity of freshly isolated CD8+ T cells from peripheral blood lymphocytes of eight subjects seropositive for HTLV-1. Four of five subjects with TSP had circulating activated anti-Tax CTL. However, two of three seropositive subjects without TSP also had activated anti-Tax CTL. These observations show that such activated CTL are not confined to patients with TSP and raise some uncertainty about their significance in the pathogenesis of the disease. In cultures of CD8+ T cells from two TSP subjects, we detected CTL with other HTLV-1 specificities, without exogenous antigenic stimulation. A CTL epitope in the middle region of Tax and one in the C terminus of Pol have been mapped at the peptide level and the HLA Class 1 molecules restricting their recognition have been defined.

Amino Acid Sequence↗
PubMed1985

Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis.

10 out of 17 (59%) patients with tropical spastic paraparesis (TSP) had antibodies to human T-lymphotropic virus-I (HTLV-I), as did 5 out of 5 TSP patients with systemic symptoms. Only 13 out of 303 (4%) controls, made up of blood donors, medical personnel, and other neurological patients, had such antibodies. These findings suggest either that HTLV-I is neurotropic or that the virus or a related one contributes to the pathogenesis of TSP.

Adolescent↗
PubMed1993

Spirochetal antibodies in tropical spastic paraparesis: their significance.

The prevalence of antibodies to Treponema pallidum and Borrelia burgdorferi was investigated in Jamaicans with tropical spastic paraparesis (TSP). A significantly higher prevalence of reactive serologic tests for syphilis (STS) was found in TSP patients (35.0%) when compared with controls (14.5%; P < .001). Venereal Disease Research Laboratory (VDRL) test titers less than 1:8 were obtained in 88.4% of reactive sera from patients and in all reactive sera of controls. The biologic false-positive rate was also significantly higher in TSP patients (P < .05). A higher frequency of a reactive STS was observed in TSP patients (P < .01) and controls (P < .001) more than 40 years of age. The prevalence of reactive serologic tests for syphilis in TSP patients younger than 40 years was also higher than in controls in this age group (P < .1). The prevalence of positive immunofluorescent antibody tests and enzyme immunoassay for antibodies to B burgdorferi was similar in sera of TSP patients (12.5%) and healthy controls (10%). However, none of the sera was positive by Western immunoblot. Leptospiral antibodies were not present in any serum tested. This study's data do not support an etiologic role for treponemal disease in tropical spastic paraparesis, but rather suggest that the high prevalence of reactive STS in Jamaicans is multifactorial.

Adolescent↗
PubMed2004

Clinical characteristics of patients in Peru with human T cell lymphotropic virus type 1-associated tropical spastic paraparesis.

BACKGROUND: Human T cell lymphotropic virus type 1 (HTLV-1) is associated with tropical spastic paraparesis (TSP). Peru is an area of endemicity for HTLV-1. METHODS: All patients with suspected cases of TSP referred to our institute (Institute of Tropical Medicine Alexander von Humboldt, Lima, Peru) from 1989 through 2002 were interviewed and tested for HTLV-1. All patients with positive results were evaluated by an expert physician. Disease progression was defined as "rapid" if the time between TSP onset and inability to walk unaided was <2 years. RESULTS: Among 165 patients enrolled, the symptoms and signs most frequently found were spasticity (in 97.5% of patients), hyperreflexia (95.4%), lower limb paresthesia (90.2%), pyramidal signs (82.6%), urinary complaints (82.0%), and lumbar pain (79.0%). Rapid progression was present in 21.5% of patients; mean age at TSP onset was higher among these patients than among slow progressors (P<.001). Severe spasticity, diminished vibratory sensation, and tremor were found more frequently among rapid progressors, compared with slow progressors. CONCLUSIONS: HTLV-1--associated TSP is frequently diagnosed in areas of HTLV-1-endemicity. A subgroup of patients experiences rapid disease progression.

Adolescent↗
PubMed2000

[Increased activity of metalloproteinases and their inhibitors in cerebrospinal fluid of patients with tropical spastic paraparesis].

BACKGROUND: Proteolytic modifications of neuronal surfaces and the surrounding extracellular matrix are very important in neuronal development and regeneration. Increased activity of matrix metalloproteinases (MMPs) and their tissue inhibitors, due to secretion by macrophages and lymphocytes, occur in inflammatory processes that disrupt the blood brain barrier. However, neurons and microglia can also secrete these enzymes. AIM: To identify the type of MMP present in the cerebrospinal fluid (CSF) and changes in the expression of tissue inhibitors of metalloproteinases (TIMPs) in patients with HTLV-1 associated tropical spastic paraparesis. PATIENTS AND METHODS: CSF samples from 12 patients with HTLV-1 associated tropical spastic paraparesis and 12 healthy controls were obtained by an atraumatic lumbar puncture. The presence of MMPs was measured by zymography and the relative amounts of TIMPs were measured by immunowestern blot. RESULTS: In the CSF of both controls and patients, a similar gelatinolytic band corresponding to proMMP-2 (latent form) was observed. In 83.3% of patients with HTLV 1 associated tropical spastic paraparesis, the MMP-9 was also present. TIMP-1, TIMP-2 and TIMP-3 were elevated 2.24 +/- 0.72, 3.85 +/- 1.38 and 5.89 +/- 3.4 fold, respectively, in the CSF of patients as compared to controls. CONCLUSIONS: Patients with HTLV-1 associated tropical spastic paraparesis have elevated activity of MMP-9 and levels of TIMPs in the CSF, when compared to healthy controls.

Adult↗
PubMed1988

Tropical spastic paraparesis in Colombia.

A high-incidence focus of tropical spastic paraparesis (TSP) occurs on the South Pacific coast of Colombia. Of 55 patients studied, 52 (94.5%) had IgG antibodies to the human T-cell lymphotropic virus type I (HTLV-I) in serum and/or cerebrospinal fluid. Control groups did not show similar high positivity. Our results suggest that HTLV-I or other antigenically related retroviruses may be the cause of TSP in Colombia. Similar clinical, laboratory, and epidemiological findings have been reported in widely remote geographical regions of the world, with very similar clinical pictures of TSP in all high-incidence regions. The demonstration of IgG antibodies in serum and cerebrospinal fluid of patients with TSP in the Caribbean and Seychelles Islands, southern Japan, and the Ivory Coast indicate that the HTLV-I retrovirus could be the cause of this "tropical" myeloneuropathy.

Adolescent↗
PubMed1989

Viral specific IgG and IgM antibodies in the CSF of patients with tropical spastic paraparesis.

The cerebrospinal fluid (CSF) from seven West Indian migrants to the United Kingdom with tropical spastic paraparesis were studied by antigen immunoblotting for specific anti-HTLV1 oligoclonal IgG and IgM. Eight CSFs from five patients were positive for specific IgG and negative for IgM; three CSFs from two patients were positive for IgM and negative for IgG. No patient had both IgG- and IgM-positive CSF. Those patients with IgM only had disease of the shortest duration. When looking for evidence that neurological damage is caused by HTLV1, both IgM and IgG should be examined.

Adult↗
PubMed1989

Characterization of HTLV-I isolates and T lymphoid cell lines derived from French West Indian patients with tropical spastic paraparesis.

Lymphoid cell lines derived from the peripheral blood of French West Indian patients with HTLV-I sero-positive Tropical Spastic Paraparesis and HTLV-I isolates were characterized. While patients' peripheral blood lymphocytes did not express detectable HTLV-I antigens when uncultured, they did so after short-term culture. Established cell lines were of T-cell lineage: CD2+, CD3+, CD4+, CD7+, WT31+ with activated T-cell markers CD25+, DR+ and a clonal rearrangement of the beta and gamma genes of the T-cell receptor. HTLV-I antigens were detected in cell lines by indirect immunofluorescence, Western blot and radio-immunoprecipitation assays. After 4 months in culture, low levels of Mg2+ dependent reverse transcriptase activity were detected and electron microscopy revealed numerous type-C retroviral particles similar to HTLV-I virions. Western blot and radio-immunoprecipitation analysis of purified viruses revealed gp46, p24, p19 and Pr53gag proteins similar to those detected in HUT 102 and MT2 cell lines. Deep analysis of env-coded precursor of one TSP versus ATL isolates revealed minor differences in their molecular weights. Southern blot analysis using 32P HTLV-I env gene as a probe showed the presence of HTLV-I proviral fragments clonally integrated into the genome of the cell lines. Our data suggest that HTLV-I isolated from Tropical Spastic Paraparesis does not differ significantly from the leukemogenic prototypes. Does HTLV-I induce either acute lymphoproliferative diseases or chronic neuromyelopathies depending upon as yet unknown co-factors? This question remains to be determined.

Blotting, Southern↗
PubMed1988

Intrathecal synthesis of IgG antibodies to HTLV-I supports an etiological role for HTLV-I in tropical spastic paraparesis.

High titers of antibody to human T-lymphotropic virus type I (HTLV-I) have been reported in the sera and cerebrospinal fluids of patients with tropical spastic paraparesis. By means of agarose isoelectric focusing and selective immunoblotting, we demonstrated oligoclonal bands of immunoglobulin G antibodies to HTLV-I in the serum and cerebrospinal fluid of patients with tropical spastic paraparesis. Such cerebrospinal fluid-specific immunoglobulin bands indicate intrathecal synthesis of specific antibodies to HTLV-I. These findings mimic the antibody response to measles virus in subacute sclerosing panencephalitis and support an etiological role for HTLV-I in the pathogenesis of tropical spastic paraparesis.

Antibodies, Anti-Idiotypic↗
PubMed1988

HTLV-I-associated tropical spastic paraparesis in Martinique: a reappraisal.

Human T-lymphotropic virus type I (HTLV-I)-associated tropical spastic paraparesis in Martinique has been identified in 54 patients, 49 women and 5 men. This myelopathy represents an endemic problem on this island and the earliest documented case dates from 1952. A blood transfusion history was obtained in 7 of the 54 patients (13%). There was a preponderance of cases from the northern Atlantic coast of Martinique, the most humid region on the island. The prevalence in this region reached 49.5 per 100,000, compared with the global prevalence of 11.9 cases per 100,000 for the island. An immune-mediated mechanism may be important in the pathogenesis of HTLV-I-associated tropical spastic paraparesis.

Adult↗