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Department of Neurology (Dr. Elovaara and Ms. Poutiainen), and the Department of Bacteriology and Immunology (Drs. Elovaara and Seppälä), University of Helsinki, and Aurora Hospital (Drs. Elovaara, Suni, and Valle), Helsinki, Finland.
We analyzed the intrathecal humoral immunologic response in 42 human immunodeficiency virus (HIV)-infected patients. Eighteen patients had clinical neurologic abnormalities, while the remaining 24 patients were neurologically symptom-free. Nine of the neurologically symptomatic patients at early infection had slight neurologic dysfunction; in nine other subjects at late infection, the neurologic impairment was moderate or severe. When compared with symptom-free patients, neurologically symptomatic patients had increased intra-blood-brain barrier (BBB) HIV-specific IgG (p < 0.001) and total IgG synthesis (p < 0.01) with oligoclonal bands (OCBs) in the CSF and/or serum (11/18 versus 3/24). At early stages of the infection, neurologically symptomatic patients showed increased total intrathecal IgG synthesis (9/9) coincident with OCBs in the CSF and serum (7/9) and slight mononuclear pleocytosis (7/9), but less frequent HIV-specific IgG production within the CNS (6/9). In advanced infection, the number of neurologically symptomatic patients with intrathecal HIV-specific IgG synthesis (8/9) was higher, while the number of those with increased total intra-BBB IgG synthesis (5/9;p < 0.01), OCBs (4/9), and increased CSF leukocyte count (1/9; p < 0.001) was lower than at early infection. Our data suggest humoral intra-BBB immunoactivation at early stages of HIV infection followed by declining B cell response within the CNS at advanced infection.
Address correspondence and reprint requests to Dr. Elovaara, Department of Neurology, University of Helsinki, Haartmaninkatu 4, 00290 Helsinki, Finland.
Supported by the Finnish Academy of Sciences and the Finnish Cultural Foundation.
Received November 20, 1987. Accepted for publication in final form February 1, 1988.
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