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Increased reactivity to HTLV‐I in inflammatory nervous system diseases
Author(s) -
Lolli Francesco,
Fredrikson Sten,
KamHansen Slavenka,
Link Hans
Publication year - 1987
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410220115
Subject(s) - antibody , cerebrospinal fluid , multiple sclerosis , immunology , meningoencephalitis , medicine , western blot , antigen , aseptic meningitis , virology , pathology , biology , biochemistry , gene
The presence of IgG antibodies reacting with purified and disrupted human T‐lymphotropic virus type I (HTLV‐I) was examined by an indirect enzyme‐linked immunosorbent assay (ELISA) in sera from 49 patients with multiple sclerosis (MS), 21 patients with aseptic meningoencephalitis (AM), 12 patients with Guillain‐Barré syndrome (GB), and 30 patients with tension headache (TH). This was also assessed in the concentrated cerebrospinal fluid (CSF) of most of these patients, as well as in sera of 60 blood donors (BD). Standardized amounts of serum IgG and CSF IgG were used in ELISA. For sera, higher reactivity with HTLV‐I was found in all four patient groups compared with the BD group, but no significant differences were observed among the four groups. There was higher reactivity with HTLV‐I in the CSF of patients with MS, AM, and GB compared to findings in patients with TH. Ten serum (2 MS, 3 GB, 3 TH, 2 BD) and 3 CSF (1 MS, 1 GB, 1 TH) specimens considered positive by ELISA for HTLV‐I were found negative on confirmatory Western blot analysis. We extended this study to analyze the in vitro production of anti‐HTLV‐I–IgG antibodies by the 24‐hour cultivation of unstimulated lymphocytes from peripheral blood and CSF of 6 additional patients with MS directly in HTLV‐I antigen–coated wells of microtiter plates. This was followed by determination of specific antibodies by ELISA in the same wells. No antibody production was measurable. Our data do not favor the hypothesis of an HTLV‐I–related human retrovirus in the etiology of MS.