Abstract
BackgroundA small fraction of Human T cell Leukemia Virus type-1 (HTLV-I) infected subjects develop a severe form of myelopathy. It has been established that patients with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) show an exaggerated immune response when compared with the immunological response observed in HTLV-I asymptomatic carriers. In this study the immunological responses in HAM/TSP patients and in HTLV-I asymptomatic carriers were compared using several immunological assays to identify immunological markers associated with progression from infection to disease.MethodsImmunoproliferation assays, cytokine levels of unstimulated cultures, and flow cytometry analysis were used to evaluate the studied groups. Nonparametric tests (Mann-Whitney U test and Wilcoxon matched-pairs signed ranks) were used to compare the difference between the groups.ResultsAlthough both groups showed great variability, HAM/TSP patients had higher spontaneous lymphoproliferation as well as higher IFN-γ levels in unstimulated supernatants when compared with asymptomatic carriers. Flow cytometry studies demonstrated a high frequency of inflammatory cytokine (IFN-γ and TNF-α) producing lymphocytes in HAM/TSP as compared to the asymptomatic group. This difference was accounted for mainly by an increase in CD8 cell production of these cytokines. Moreover, the HAM/TSP patients also expressed an increased frequency of CD28-/CD8+ T cells. Since forty percent of the asymptomatic carriers had spontaneous lymphoproliferation and IFN-γ production similar to HAM/TSP patients, IFN-γ levels were measured eight months after the first evaluation in some of these patients to observe if this was a transient or a persistent situation. No significant difference was observed between the means of IFN-γ levels in the first and second evaluation.ConclusionsThe finding that a large proportion of HTLV-I carriers present similar immunological responses to those observed in HAM/TSP, strongly argues for further studies to evaluate these parameters as markers of HAM/TSP progression.
Highlights
A small fraction of Human T cell Leukemia Virus type-1 (HTLV-I) infected subjects develop a severe form of myelopathy
The documentation that some HTLV-I carriers have immunological alteration similar to that observed in HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) suggests that potential markers of disease progression may be determined in HTLV-I infection
To determine if HAM/ TSP patients and asymptomatic subjects produce different levels of secreted cytokines, IFN-γ, TNF-α, IL-10 and IL-5 were measured in supernatants of unstimulated cultures of HTLV-I infected groups and compared with negative controls
Summary
A small fraction of Human T cell Leukemia Virus type-1 (HTLV-I) infected subjects develop a severe form of myelopathy. It has been established that patients with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) show an exaggerated immune response when compared with the immunological response observed in HTLV-I asymptomatic carriers. In this study the immunological responses in HAM/TSP patients and in HTLV-I asymptomatic carriers were compared using several immunological assays to identify immunological markers associated with progression from infection to disease. A small percentage of infected individuals (2 to 5%) develop adult T cell leukemia/lymphoma (ATL) [3,4] or a chronic inflammatory disease, involving the central nervous system, termed HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) [5,6]. The aim of the present study is to compare in HTLV-I asymptomatic carriers, and in HAM/ TSP patients, the spontaneous lymphoproliferative response and cytokine production, the overall ex vivo T cell activation states, and the production of immunoregulatory cytokines by CD4+ and CD8+ T cells. The documentation that some HTLV-I carriers have immunological alteration similar to that observed in HAM/TSP suggests that potential markers of disease progression may be determined in HTLV-I infection
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