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

Artikel i vetenskaplig tidskrift
Författare Magnus Gisslén
Annika Lekman
Pam Fredman
Publicerad i Infection
Volym 28
Nummer/häfte 3
Sidor 143-8
Publiceringsår 2000
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar
Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Institutionen för klinisk neurovetenskap, Sektionen för kliniska nervsjukdomar
Sidor 143-8
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord 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
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

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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