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Neurology 2000;55:1398-1401
© 2000 American Academy of Neurology
Brief Communications

Monoclonal antibodies against Epstein–Barr virus cross-react with {alpha}-synuclein in human brain

J. Woulfe, MD, H. Hoogendoorn, M. Tarnopolsky, MD, PhD and D. G. Muñoz, MD

From the Department of Pathology and Molecular Medicine, McMaster University, Hamilton; the Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences Corporation (Dr. Woulfe); Affinity Biologicals (H. Hoogendoorn), HCH Research Centre, Hamilton; the Department of Medicine, Division of Neurology (Dr. Tarnopolsky), McMaster University Medical Centre, Hamilton; and the Departments of Pathology and Clinical Neurological Sciences (Dr. Muñoz), University of Western Ontario, London, Ontario, Canada; and Servicio de Neurologia (Dr. Muñoz), "Doce de Octubre" Hospital, Madrid, Spain.

Address correspondence and reprint requests to Dr. John Woulfe, Anatomic Pathology Division, The Ottawa Hospital–Civic Campus, 1053 Carling Ave., Ottawa, Ontario K1Y 4E9, Canada; e-mail: jwoulfe{at}ottawahospital.on.ca

Using antibodies generated against the latent membrane protein 1 of Epstein–Barr virus, intense immunoreactivity of Lewy bodies (in PD and dementia with Lewy bodies) and glial cytoplasmic inclusions (in multiple system atrophy) was demonstrated. ELISA and Western blotting techniques confirmed that this immunolabeling was due to cross-reactivity of the antiviral antibody with {alpha}-synuclein, a neuronal protein implicated in the pathogenesis of PD. This example of cross-reactivity between Epstein–Barr virus and {alpha}-synuclein may bear implications for further elucidating infectious or autoimmune mechanisms in PD.




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