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PubMed2000

Histopathological analysis of four autopsy cases of HTLV-I-associated myelopathy/tropical spastic paraparesis: inflammatory changes occur simultaneously in the entire central nervous system.

Although brain lesions have been described in some cases with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), little is known about the nature of brain lesion and its relation to the spinal cord lesion. In the present study, we performed histopathological analysis of the brain and the spinal cord of four autopsied cases with HAM/TSP to clarify the relationship between the brain and the spinal cord lesions. In two cases with active-chronic inflammation in the spinal cord, perivascular inflammatory infiltration was also seen in the brain, and the composition of cell subsets was similar both in the spinal cord and in the brain. No active inflammatory change was seen in the brain in two cases with inactive-chronic spinal cord lesions. Inflamed vessels were distributed mainly in the deep white matter and in the area between cerebral cortex and white matter of the brain. In the spinal cord inflamed vessels were mainly seen in the bilateral lateral and the ventral posterior columns. Parenchymal infiltration was diffused in the spinal cord but very sparse in the brain, suggesting the importance of parenchymal infiltration in the destruction of tissues. These results suggest that inflammatory changes occurred simultaneously in the spinal cord and in the brain, and that distribution of inflamed vessels closely correlated with the characteristics of vascular architecture of the brain and the spinal cord, which lead to a slow blood flow. This study may help promote a better understanding of the pathogenesis of HAM/TSP.

Aged↗

PubMed1990

Screening for prolonged incubation of HTLV-I infection in British and Jamaican relatives of British patients with tropical spastic paraparesis.

OBJECTIVE: To compare the prevalence of antibody to and proviral DNA of the retrovirus HTLV-I in relatives of 11 British patients with tropical spastic paraparesis who had migrated from Jamaica before they developed symptoms, and to examine factors possibly related to transmission of HTLV-I. DESIGN: Migrant, family study. Antibody state was determined by several methods and confirmed by western blotting; the polymerase chain reaction was used to detect proviral DNA. SETTING: Britain and Jamaica. SUBJECTS: All available first degree relatives: those born and still resident in Jamaica (group 1); those born in Jamaica who migrated to Britain (group 2); and index patients' children who were born and resident in Britain (group 3). All had been breast fed and none had had blood transfusions. RESULTS: Of the 66 living relatives, 60 were traced. Seroprevalence among those born in Jamaica (irrespective of current residence) was 22% (10/46; 95% confidence limits 9 to 34%) compared with zero among British born offspring (0/14) and was higher in group 2 at 33% (7/21; 12 to 55%) than in group 1 at 12% (3/25; 0 to 25%). (Patients in group 1 had the greatest mean age.) Proviral DNA was not detected in any subject negative for HTLV-I antibody, making prolonged viral incubation in those negative for the antibody unlikely. CONCLUSION: In this sample factors related to place of birth and early residence were more important in transmission of HTLV-I than maternal or age effects. In areas with a low to moderate prevalence policies of preventing mothers who are carriers of the virus from breast feeding would be premature.

Base Sequence↗

PubMed1990

Excessive muscular fatigue in patients with spastic paraparesis.

We used intermittent tetanic contractions and 31P magnetic resonance spectroscopy to investigate human tibialis anterior muscle metabolism and fatigability in a group of patients with spastic paraparesis and in normal controls. During intermittent tetanic stimulation, the decline in tension was significantly greater in patients than in controls, and the half-relaxation time of the tetanus was more prolonged. Moreover, the decline in phosphocreatine and intracellular pH was significantly greater in patients than in controls. These observations suggest that biochemical changes in the muscles of patients with upper motor neuron lesions may contribute to their excessive fatigability.

Action Potentials↗

PubMed1990

The risk of development of HTLV-I-associated myelopathy/tropical spastic paraparesis among persons infected with HTLV-I.

Using data obtained in national surveys of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) conducted in Japan in 1987 and 1988, we estimated the yearly and lifetime risk that HAM/TSP will develop in an HTLV-I-infected person. "Definite" HAM/TSP was defined as slowly progressive myelopathy with antibodies to HTLV-I in both serum and cerebrospinal fluid. Estimates of HTLV-I infection rates in eight endemic prefectures, by age group and sex, were obtained from serologic studies of blood donors; population figures, by age group, sex, and prefecture, were obtained from the census. Of 589 definite cases of HAM/TSP reported nationally, 397 occurred in residents of the eight endemic prefectures; of these, 170 reported onset of illness during the years 1982-1988 (average incidence, 24.3 cases/year). Using the estimated HTLV-I infection rates and the 1985 census figures, we estimated the number of HTLV-I-infected persons in the eight prefectures in 1985 at 794,800. We therefore estimated the incidence of HAM/TSP among HTLV-I-infected persons at 3.1 x 10(-5) cases/year; assuming a lifetime of 75 years, the lifetime incidence is approximately one quarter of 1%. This estimate is important in counseling persons such as blood donors found to be infected with HTLV-I.

Adolescent↗

PubMed2006

Use of intrathecal baclofen in a child with spastic paraparesis related to human immunodeficiency virus infection: A case report.

This case report describes a 2-year treatment course of a 6-year-old with spastic paraparesis due to human immunodeficiency virus (HIV) encephalopathy. She continued to develop worsening musculoskeletal problems and a decline in mobility despite aggressive antispasticity interventions. In addition to meeting the usual clinical criteria for treatment with continuous intrathecal baclofen (ITB), she was believed to be an appropriate candidate for ITB because of adequate treatment of her HIV infection and associated overall low risk of mortality. For over 12 months, she has been successfully treated with ITB and has not developed any complications related to her HIV infection. To my knowledge, this is the first reported successful treatment of spasticity with ITB in a patient with stable HIV infection.

Acquired Immunodeficiency Syndrome↗

PubMed2006

Human T-cell lymphotropic virus type I (HTLV-I) confirmed by PCR-Southern blot and sequencing analysis in a woman with tropical spastic paraparesis.

Human T-cell lymphotropic virus type I (HTLV-I) is a human retrovirus and the aetiological agent of a progressive neurological disease called tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM), as confirmed by evidence accumulated in HTLV-I seroprevalence studies. TSP/HAM is rarely diagnosed in Italy, given the low prevalence of HTLV-I in the population. TSP/HAM begins insidiously in the fourth decade, mainly with spastic paraparesis of the lower extremities and positive Babinski reflex, as well as interfering with bowel and bladder functions. In this study we report the clinical, virological and haemato chemical data of a 54-year-old woman, born in the Ivory Cost, with symptoms suggestive of TSP. The presence of HTLV-I infection was demonstrated by the detection of antibodies in serum and in cerebrospinal fluid by immunoenzymatic assay and Western blot analysis. In addition, viral isolation was carried out in peripheral blood cells, and the presence of HTLV-I proviral DNA was confirmed by polymerase chain reaction/Southern blot and sequencing analysis. According to our results, HTLV-I testing might be useful when TSP/HAM is suspected.

Blotting, Southern↗

PubMed1995

Human T lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis in São Paulo, Brazil.

We conducted a prospective clinical and epidemiologic evaluation of 45 cases of human T lymphotropic virus type I (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in São Paulo, Brazil. All enrolled patients had progressive chronic myelopathy and high titers of HTLV-I and HTLV-II antibodies, as determined by enzyme immunoassay and western blot. In 24 cases, the polymerase chain reaction (PCR) was performed so that HTLV-I could be distinguished from HLTV-II. The clinical and epidemiologic features of the patients from our study were similar to those of patients with HAM/TSP from other areas of endemicity for HTLV-I except that more patients in our study had received a blood transfusion prior to their illness. Despite the presence of HTLV-II virus in Brazil, all patients whose serum was tested by PCR were found to be infected with the HTLV-I virus.

Adult↗

PubMed2006

Levels of serum chemokines discriminate clinical myelopathy associated with human T lymphotropic virus type 1 (HTLV-1)/tropical spastic paraparesis (HAM/TSP) disease from HTLV-1 carrier state.

Approximately 5% of people infected with human T lymphotropic virus type 1 (HTLV-1) develop clinical myelopathy or tropical spastic paraparesis (HAM/TSP) that is associated with high-levels of Th1 cytokines, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. Chemokines are known to induce cytokine secretion and direct the trafficking of immune cells to sites of disease. The present study measured serum chemokines correlated with autonomously released IFN-gamma in cell cultures. HTLV-1 infection was defined by enzyme-linked immunosorbent assay (ELISA) and confirmed by Western blot. Subjects included HTLV-1 carriers (n = 56), patients with HAM/TSP (n = 31) and healthy HTLV-1 seronegative volunteer controls (n = 20). Serum chemokines and IFN-gamma autonomously released by mononuclear cells in culture were quantified by ELISA. Compared to HTLV-1 carriers, serum chemokines in HAM/TSP patients showed significantly increased levels of CXCL9 and CXCL10, significantly diminished levels of CCL2 and similar amounts of CCL11 and CCL24. In contrast, CCL11 and CCL24 were significantly lower in serum of HAM/TSP patients than either control. IFN-gamma was positively correlated with CXCL9 and CXCL10 when HAM/TSP and HTLV-1 carriers were used as a combined group. However, despite a large proportion of HTLV-1 carriers having high IFN-gamma levels, these chemokines were not increased in carriers. This study showed that high levels of CXCL9 and CXCL10 in the systemic circulation and low serum CCL2 levels are features of HAM/TSP. HTLV-1 infection and Tax and/or additional viral encoded factor-mediated pathological processes triggering T cell activation with autogenous IFN-gamma release are probably involved in regulating chemokine release.

Biomarkers↗

PubMed2004

Increased mRNA expression of Th1-cytokine signaling molecules in patients with HTLV-I-associated myelopathy/tropical spastic paraparesis.

Expression of inflammatory cytokines derived from Th1 cell population is increased in patients with human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP). It has been shown that cytokine signaling molecules, including transcription factors T-bet and GATA-3, interleukin-12 receptor beta 2 (IL-12R beta 2) and suppressors of cytokine signaling (SOCS), such as SOCS1, are important in differentiation of naive T cells into Th1 helper T cells. To assess the immunological status from the stand-point of cytokine signaling in patients with HAM/TSP, we analyzed mRNA expression of these cytokine signaling molecules in peripheral blood mononuclear cells using quantitative RT-PCR. Twenty-eight HAM/TSP patients, nine HTLV-I-infected individuals without HAM/TSP and twenty-two HTLV-I-uninfected individuals were included in this study. Expression of T-bet, GATA-3, IL-12R beta 2 and SOCS1 was significantly increased in HAM/TSP patients in comparison with HTLV-I-uninfected individuals. In contrast, expression of SOCS3, a marker for Th2 cells, was significantly decreased in HTLV-I-infected individuals. These results indicate that HAM/TSP patients are associated with increased Th1 and decreased Th2 cytokine signaling activities.

Adult↗

PubMed2002

Presenilin-1 mutation (E280G), spastic paraparesis, and cranial MRI white-matter abnormalities.

The authors report unusual presentations of members of an Irish family with familial AD due to an E280G mutation in exon 8 of presenilin-1. One had spastic paraparesis and white matter abnormalities on cranial MRI. A sibling had an internuclear ophthalmoplegia, spastic-ataxic quadriparesis, and "cotton-wool plaques" with amyloid angiopathy on brain biopsy. Another affected sibling also had MRI white matter abnormalities. The MRI findings may reflect an ischemic leukoencephalopathy due to amyloid angiopathy affecting meningocortical vessels.

Adult↗

PubMed1998

Perivascular T cells are infected with HTLV-I in the spinal cord lesions with HTLV-I-associated myelopathy/tropical spastic paraparesis: double staining of immunohistochemistry and polymerase chain reaction in situ hybridization.

HTLV-I-infected cells play an important role in pathogenesis HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Our previous studies of quantitative polymerase chain reaction (PCR) and in situ PCR suggested that T cells infiltrating in the spinal cord lesion were infected with HTLV-I. To elucidate the localization of HTLV-I proviral DNA directly, we performed double staining using immunohistochemistry and PCR in situ hybridization (PCR-ISH). Fresh frozen sections of the spinal cord from four HAM patients taken at autopsy were first immunostained with antibodies to pan T cells (UCHL-1), macrophages (KP-1) and helper/inducer T cells (OPD4). Then PCR-ISH was carried out with specific primers and probe for the HTLV-I pX region. UCHL-1-positive cells were noted around perivascular areas and, to some extent, in the parenchyma. Of the UCHL-1-positive cells, 9.4% (case 1), 9.6% (case 2), 1.1% (case 3) and 6.7% (case 4) became positive in HTLV-I PCR-ISH. UCHL-1-negative cells were HTLV-I PCR-ISH negative and almost all KP-1-positive cells were HTLV-I negative. HTLV-I was localized to OPD4-positive cells in examined lesions of cases 2 and 4. These data are a direct demonstration of HTLV-I proviral DNA localizing to infiltrated T cells in HAM/TSP spinal cord lesions.

Aged↗

PubMed1995

Folliculitis decalvans and human T cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis.

Human T-cell lymphotropic virus type I (HTLV-I) can be associated with either adult T-cell leukemia or HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic progressive immune-mediated myelopathy. Skin manifestations such as xerosis and erythema may be associated with HAM/TSP. Infective dermatitis due to Staphylococcus aureus or beta-hemolytic Streptococcus has recently been described as a marker for HTLV-I infection and as a probable risk factor for the development of adult T-cell leukemia and lymphoma in Jamaican children. We report a case of folliculitis decalvans, a rare chronic follicular inflammatory process of bacterial origin that is extremely resistant to treatment, in a patient with HAM/TSP. This case suggests the possibility that the disturbance of the immune system that was observed in patients with HAM/TSP can play a role in the persistence of this severe skin lesion. In addition, the findings of our case cast doubt on the hypothesis that the cause of infective dermatitis in persons infected with HTLV-I is immunosuppression due to congenital or perinatal infection of the immature immune system.

Adult↗

PubMed1995

Elevated levels of iC3b and C4d, but not Bb, complement fragments from plasma of persons infected with human T cell leukemia virus (HTLV) with HTLV-I-associated myelopathy/tropical spastic paraparesis.

Plasma levels of complement (C) fragments iC3b, C4d, and Bb from human T cell leukemia virus (HTLV)-positive subjects with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP) were analyzed by EIA. Both iC3b and C4d levels were significantly elevated in persons with HAM/TSP. These levels were similar to those in patients with human immunodeficiency virus (HIV) infection or rheumatoid arthritis (RA), who are known to have increased C fragments. Bb levels in persons with HAM/TSP wer unaffected, suggesting that C activation occurred only via the classical pathway. This differed from findings in HIV-infected or RA patients, who had elevated levels of Bb. The results showed an increase in C activation in persons with HAM/TSP and activation via the classical pathway, likely mediated by virus or immune complexes. It is possible that the C activation observed in these subjects contributed to the inflammatory pathogenesis of HAM/TSP.

Arthritis, Rheumatoid↗

PubMed1999

Transmission of HTLV-I to rats via peripheral blood mononuclear cells and serum from a patient with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) with amyotrophic lateral sclerosis (ALS)-like features.

We tested the possibility that lymphocytes and serum obtained directly from a patient with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) induce infection in rats. Inbred Fischer F344 immunosuppressed rats were inoculated intravenously with 10x10(6) peripheral blood mononuclear cells (PBMC; 3 rats) and serum (3 rats) obtained from a HAM/TSP patient, who was seropositive and polymerase chain reaction (PCR)-positive for the HTLV-I proviral genome. Antibodies to HTLV-I appeared in the rat sera 2 months later; rat peripheral blood lymphocytes, spleen, salivary gland, and spinal cord were found to contain the proviral genome. Control rats inoculated with normal donor PBMC and serum tested negative for the HTLV-I antibodies and for the HTLV-I proviral genome by PCR. The positive control F344 rats inoculated with 5x10(6) cells of a SLB-1 HTLV-I cell line were found to be infected after 2 months. This study demonstrates for the first time that HTLV-I can be transmitted not only by human cellular components but also by human cell-free sera in a rat model.

Adult↗

PubMed1994

Circulating anti-Tax cytotoxic T lymphocytes from human T-cell leukemia virus type I-infected people, with and without tropical spastic paraparesis, recognize multiple epitopes simultaneously.

CD8+ T cells were freshly isolated from a human T-cell leukemia virus type I (HTLV-I)-infected patient with tropical spastic paraparesis. These cells, which were specific for HTLV-I Tax, simultaneously recognized a minimum of five, and possibly as many as seven, distinct peptide epitopes within the protein. A further Tax epitope was recognized after a short period of culture without exogenous peptide stimulation. All but one of these epitopes were clustered in the N-terminal third of Tax, and one of the epitopes was clearly immunodominant on two separate occasions of testing. Recognition of the immunodominant epitope was restricted by human leukocyte antigen (HLA) B15, and recognition of all the others was by HLA A2. Similar patterns of cytotoxic T lymphocyte recognition of the HLA A2-restricted Tax peptides in two healthy HTLV-I-seropositive individuals, each of whom carried the HLA A2 allele, were observed.

Adult↗

PubMed1994

Clonal expansion of CD8+ cytotoxic T lymphocytes against human T cell lymphotropic virus type I (HTLV-I) genome products in HTLV-I-associated myelopathy/tropical spastic paraparesis patients.

Short-term culture of peripheral blood mononuclear cells (PBMC) derived from patients with human T cell lymphotropic virus type I-associated myelopathy (HAM)/tropical spastic paraparesis resulted in dominance by DR+ activated CD8+ T cells. Variations in the T cell receptor (TCR) V alpha and V beta chains in these cells were analyzed, and in all 10 patients examined, 2-3 V gene families were dominant in both TCR V alpha and V beta. In five patients we examined, cultured lymphocytes contained cytotoxic lymphocytes for p40tax (patients HAM2, 3, 7, and 8) or env protein (patient HAM4) of human T lymphotropic virus type I. In patients HAM2 and HAM8, cultured lymphocytes contained a large proportion of V beta 8+ CD8+ and/or V beta 12+ CD8+ cells. The sequence of V beta 8+ and V beta 12+ cDNA revealed that they were oligoclonal with identical or similar sequences in each patient. Elimination experiments with monoclonal antibodies for TCR V beta 8 and V beta 12 showed that they were CD8+ cytotoxic T lymphocytes (CTL) for p40tax. In addition, flow cytometry and sequencing analysis of uncultured PBMC revealed that in HAM2, V beta 8+ CTL and their precursors account for 7% and V beta 12+ CTL and their precursors account for 18% of total CD8+ cells. This indicates the presence of two markedly expanded clones in vivo. No common dominant TCR V alpha or V beta were observed among 10 HAM patients analyzed.

Amino Acid Sequence↗

PubMed1993

The risk of tropical spastic paraparesis differs according to ethnic group among HTLV-I carriers in Inongo, Zaire.

Following the finding in 1990 of six HTLV-I-positive cases of tropical spastic paraparesis (TSP/HAM) is a field survey carried out in the city of Inongo (Bandundu, Zaire), the prevalence of HTLV-I infection has been studied by detection of specific antibodies on a randomized sample of the general population. Among the 1,162 subjects surveyed, 36 (3.1%) were found to be HTLV-I seropositive, giving a seroprevalence of 3.2% (CI: 2.1, 4.3) estimated by direct standardization on age and sex distribution given by the census in the city. Among the five major ethnic groups, the Bolia showed the highest prevalence rate (6.5%) but with no detected TSP/HAM cases, while all six TSP/HAM cases were found among the Ntomba, who showed a prevalence rate of only 2.2%. This finding suggests that besides HTLV-I infection, critical environmental and/or genetic cofactors play a part in the development of TSP/HAM.

Adolescent↗

PubMed2001

Tropical spastic paraparesis.

Human T-cell lymphotropic virus type I (HTLV-I) is the cause of endemic tropical spastic paraparesis (TSP) or HTLV-I-associated myelopathy (HAM). Because TSP/HAM is not a fatal disease, the neuropathology of this disease, albeit relatively well understood, is based on the examination of just a few incidental cases. We summarise our experience with the neuropathology of tropical spastic paraparesis/HTLV-I associated myelopathy (TSP/HAM). We studied three cases of TSP/HAM from different parts of the world. We demonstrated peculiar lamellated structures, called "multilamellar bodies" (MLB). It is tempting to suggest that MLB may represent specific ultrastructural markers of TSP/HAM. The pathology of the anteriorand posterior horns was similar and comprised axonal degeneration, accompanied by extensive astrocytic gliosis. Lymphocytic infiltration, particularly observed as "cuffs" around blood vessels, was scattered among other cellular elements. Ultrastructurally, myelin sheaths were relatively well preserved, and some demyelinated but not remyelinated fibres were observed. Moreover, axons with abnormal accumulations of neurofilaments, suggestive of axonal degeneration, were detected. Several axons contained Hirano bodies. In many samples glial processes replaced most of the remaining neuropil.

Ganglia, Spinal↗