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HTLV-I-associated myelopathy endemic in Texas-born residents and isolation of virus from CSF cells

Departments of Neurology (Drs. McKendall and Oas) and Microbiology (Dr. McKendall), University of Texas Medical Branch, Galveston, TX; and the Clinical Biology Laboratory (Dr. Lairmore), Retrovirus Diseases Branch, the Centers for Disease Control, Atlanta, G A.

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.

Address correspondence and reprint requests to Dr. Robert R. McKendall, Department of Neurology (E39), University of Texas Medical Branch, Galveston, TX 77550.

Received July 19, 1990. Accepted for publication in final form November 20, 1990.

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