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Slow Viruses and Inborn Metabolic ErrorsSummary of a Workshop Sponsored by the National Institutes of Health
John H. Menkes, MD;
Sven G. Eliasson, MD;
Bernard W. Agranoff, PhD
Arch Neurol. 1969;21(6):645-648.
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IN RESPONSE to many requests from individuals working in the area of metabolic and genetic diseases of the central nervous system (CNS), a joint workshop of the National Institutes of Health, Metabolism and Neurology Study Sections was held on April 30, 1969 to assess the current status of two major areas of rapid advance: (1) slow viruses and deoxyribonucleic acid-ribonucleic acid metabolism of the brain, and (2) inborn metabolic errors and amino acid and protein metabolism of the brain.
Slow Viruses
In his introductory summary of the field, Dr. Hilary Koprowski stated that virus and host may interact in the following three different ways: (1) Cellular destruction as seen in the usual forms of viral infection. (2) Proliferation produced by DNA tumor viruses and Rous sarcoma. (3) Cellular dysfunction occurring with rabies, and the slow viruses, scrapie, visna, and Aleutian mink disease. For unknown reasons, neurons show a selective sensitivity
. . . [Full Text PDF of this Article]
Author Affiliations
Los Angeles; St. Louis; Ann Arbor, Mich
From the Department of Pediatrics, UCLA School of Medicine, Los Angeles (Dr. Menkes); the Department of Neurology, Washington University School of Medicine, St. Louis (Dr. Eliasson); and the Department of Biological Chemistry, University of Michigan, Ann Arbor, Mich (Dr. Agranoff).
Footnotes
Submitted for publication June 6, 1969; accepted July 17.
Reprint requests to Department of Pediatrics, UCLA School of Medicine, Los Angeles 90024 (Dr. Menkes).
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