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HTLV-I-associated myelopathy endemic in Texas-born residents and isolation of virus from CSF cells
R R McKendall1, J Oas, M D Lairmore
1Department of Neurology, University of Texas Medical Branch, Galveston 77550.
Abstract:
We report three Texas-born patients with spastic paraparesis and well-documented infection with HTLV-I. CSF examination showed moderate pleocytosis, protein elevation, and elevated IgG index. Oligoclonal bands were present in two patients. On MRI, one patient had frontal lobe lesions that were low intensity on T1- and high intensity on T2-weighted images. HTLV-I immunoblot studies of serum and CSF revealed reactivity to p19, p24, p53, gp46, or gp68 from all three patients. Titration studies of serum and CSF antibodies on ELISA and immunoblot assays indicated an intrathecal virus-specific response. HTLV-I-specific p19 antigen capture assay and polymerase chain reaction (PCR) demonstrated HTLV-I in lymphocyte cultures derived from each patient's peripheral blood mononuclear cells (PBMC) or CSF cells. Using HTLV-I- and HTLV-II-specific pol and gag primers, PCR studies of PBMC cells obtained directly from the patients demonstrated that the patients were infected with HTLV-I and not HTLV-II. These three cases are to our knowledge the only US cases in whom virus isolation from the CSF has been accomplished. Importantly, two patients may be the first US cases of myelopathy arising from endemic infection.
Insights
This study details three US cases of Human T-lymphotropic virus type I (HTLV-I) infection causing spastic paraparesis. Researchers successfully isolated HTLV-I from cerebrospinal fluid (CSF), confirming endemic myelopathy.
Area of Science:
- Neurology
- Virology
- Immunology
Background:
- Human T-lymphotropic virus type I (HTLV-I) is a retrovirus known to cause neurological diseases, including HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
- Diagnosis of HAM/TSP typically involves clinical presentation, serological evidence of HTLV-I infection, and detection of HTLV-I proviral DNA or RNA in peripheral blood or cerebrospinal fluid (CSF).
Observation:
- Three Texas-born patients presented with spastic paraparesis and confirmed HTLV-I infection.
- Cerebrospinal fluid (CSF) analysis revealed moderate pleocytosis, elevated protein levels, and an increased IgG index, with oligoclonal bands present in two patients.
- Magnetic resonance imaging (MRI) showed frontal lobe lesions in one patient, characterized by low T1 and high T2 signal intensities.
Findings:
- Immunoblot studies of serum and CSF confirmed HTLV-I reactivity to specific viral proteins (p19, p24, p53, gp46, gp68) in all three patients.
- ELISA and immunoblot assays indicated a significant intrathecal, virus-specific antibody response.
- Polymerase chain reaction (PCR) and antigen capture assays successfully detected HTLV-I in peripheral blood mononuclear cells (PBMC) and CSF cells, differentiating it from HTLV-II infection.
Implications:
- These cases represent the first documented instances of HTLV-I isolation from CSF in US patients.
- Two of the patients may be the first reported US cases of myelopathy resulting from endemic HTLV-I infection.
- The findings underscore the importance of considering HTLV-I in the differential diagnosis of myelopathy, particularly in endemic regions within the US.