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Teresita S. Elizan, MD
Department of Neurology

James G. Wetmur, PhD
Department of Microbiology Mount Sinai School of Medicine 1 Gustave L. Levy PI New York, NY 10029

Arch Neurol. 1980;37(4):253.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.—

Dr Openshaw suggests that a better positive control for our experiments with brain material from patients with Parkinson's disease¹ would have been infected with mouse ganglia or human trigeminal ganglia instead of acutely infected mouse brains. This suggestion is based on certain assumptions concerning the state of a latent virus in a chronic neurological disease. We address this point first. He further suggests that the sensitivity limits for the reassociation technique would have been affected by the choice of control material. We also address this point.

If a virus were involved in a chronic neurological disease such as Parkinson's, the nature of its indefinite persistence in the brain is conjectural.² In the case of herpes simplex virus, a prototype of viral latency, the state and activity of the virus or its genome in the latently infected sensory ganglia of experimental animals and man remain unsettled.^3-5 Viral latency . . . [Full Text PDF of this Article]

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