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Cerebrospinal fluid antibodies directed against neuron-associated gangliosides in HIV-1 infection

Journal article
Authors Magnus Gisslén
Annika Lekman
Pam Fredman
Published in Infection
Volume 28
Issue 3
Pages 143-8
Publication year 2000
Published at Institute of Internal Medicine, Dept of Infectious Diseases
Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Institute of Clinical Neurosciences, Section of Neurological Diseases
Pages 143-8
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Adult, Antibodies/blood/*cerebrospinal fluid, Autoantibodies/blood/cerebrospinal fluid, Encephalitis, Viral/*cerebrospinal fluid/etiology, Enzyme-Linked Immunosorbent Assay, Female, G(M1) Ganglioside/immunology, Gangliosides/*immunology, HIV Infections/blood/*cerebrospinal fluid/complications, *Hiv-1, Humans, Immunoglobulin G/blood/cerebrospinal fluid, Immunoglobulin M/blood/cerebrospinal fluid, Lactones/immunology, Male, Middle Aged, Neurons/chemistry
Subject categories Microbiology in the medical area

Abstract

BACKGROUND: Loss of synapses and neurons is a common finding in HIV-1 infection. Since the in vivo infection of neurons by HIV-1 is limited, indirect factors are likely to contribute to the pathogenesis. PATIENTS AND METHODS: We have analyzed cerebrospinal fluid (CSF) and serum samples from 25 HIV-1-infected individuals (nine with and 16 without CNS complications) and 19 HIV-negative controls with aseptic meningitis or viral encephalitis, for the presence of antibodies directed against the neuron-associated gangliosides GM1, GD1a and GD1b. RESULTS: Positive antibody titers to > or =1 of the gangliosides were found in 13/25 HIV-1-infected patients in CSF and in 17/25 in serum. Significant correlations were found between the presence and titers of CSF antibodies against GM1, GD1a, and GD1b. Six out of nine patients with, and 3/16 without neurological complications (p < 0.05) had positive CSF titers of > or = 1 of the ganglioside antibodies combined with negative serum titers, indicating intrathecal antibody production. In contrast, only 1/19 controls had detectable anti-ganglioside antibodies in the CSF. CONCLUSION: The results should be interpreted with caution and CSF anti-ganglioside antibody production might be a part of a non-specific intrathecal polyclonal immunoactivation. Nevertheless, autoantibodies directed against neuron-associated gangliosides might be involved in the neuropathogenesis in HIV-1 disease.

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