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Harry Openshaw, MD
Department of Neurology University of California, Davis Medical Center at Sacramento 4301 X Street Sacramento, CA 95817

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.

To the Editor.—

Dr J. G. Wetmur and his co-workers were unable to detect the DNA of herpes simplex virus type 1 (HSV) in the brain tissue of patients with Parkinson's disease (ARCHIVES 36:462-464, 1979). If HSV genomes are present in chronic neurologic disease, it seems probable that the infection would be in a latent stage when the patients died. Therefore, a pertinent question is whether the technique of Wetmur et al was sufficiently sensitive to detect a latent HSV infection.

The authors used infected mouse brains as the positive control. Although details are not given, the mouse brains probably were processed during the productive viral infection (acute encephalitis). This supposition seems likely since latent brain infection has been noted only rarely after intracerebral inoculation of wild-type HSV.¹ A more appropriate positive control would have been mouse ganglia at the latent stage of the infection. Reassociation kinetics in another study . . . [Full Text PDF of this Article]

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