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From the Departments of Neurology (Drs. Ang, Jacobs, van der Meché, and van Doorn), Immunology (Drs. Ang, Jacobs, and Laman), and Virology (Drs. Brandenburg and Osterhaus), Erasmus University Rotterdam, The Netherlands.
Address correspondence and reprint requests to Dr. C.W. Ang, Department of Neurology, Erasmus University Rotterdam, PO Box 1738, 3000 DR Rotterdam, The Netherlands; e-mail: ANG{at}neuro.fgg.eur.nl
OBJECTIVE: To investigate whether anti-GM2 antibodies in patients with Guillain–Barré syndrome (GBS) are induced by molecular mimicry with cytomegalovirus (CMV).
BACKGROUND: Antibodies against ganglioside GM2 are frequently present in the serum from GBS patients with an antecedent infection with CMV.
METHODS: The authors detected inhibition of anti-GM2 reactivity after incubation of GM2-reactive serum samples with fibroblasts infected with a GBS-associated CMV strain. Control sera consisted of GQ1b-reactive samples, and control antigens included uninfected fibroblasts and fibroblasts that were infected with other herpes viruses.
RESULTS: Serum immunoglobulin M reactivity with GM2 was decreased in a dose-dependent manner after incubation with CMV-infected fibroblasts. Incubation of anti-GM2-positive serum samples with uninfected fibroblasts and fibroblasts infected with varicella zoster virus did not inhibit anti-GM2 reactivity, whereas this reactivity was slightly decreased after incubation with herpes simplex virus type 1 in one patient. Antibodies against ganglioside GQ1b did not react with CMV-infected fibroblasts.
CONCLUSIONS: CMV-infected fibroblasts express gangliosidelike epitopes that recognize specifically anti-GM2 antibodies. These results support the hypothesis that antiganglioside antibodies in CMV-infected GBS patients are induced by molecular mimicry between GM2 and antigens that are induced by a CMV infection.
Key words: Guillain–Barré syndrome—Herpesviruses—Gangliosides—Molecular mimicry—Fibroblasts
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