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ALBIN W. JOHNSON, MD; E. DARRELL JERVEY, MD

Arch Ophthalmol. 1964;72(6):826-828.

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

Introduction

The idea of antimetabolite therapy for virus diseases is not new, but only recently have the first clinically applicable antimetabolites for a "true" (other than the Chlamydozoaceae) virus disease been reported.^1,2 The theoretical basis for the discovery of these agents arose from the observation that herpes simplex virus contains deoxyribonucleic acid (DNA) and after infection the amount of DNA in the cell increases sharply, the DNA being either a part of the virus or a product of its metabolism. It was theorized, therefore, that if DNA production could be impaired with antimetabolites, the reproduction of the virus might be inhibited. The agents that were found to do this effectively in herpetic dendritic keratitis were idoxuridine (5-iodo-2'-deoxyuridine [IDU], also called 5-iodouracil-2'-deoxyriboside [IUDR]), and 5-bromo-2'-deoxyuridine (BDU),² These compounds differ from thymidine, a nucleoside and normal precursor of DNA, only in the substitution of a halogen atom for a methyl . . . [Full Text PDF of this Article]

Author Affiliations
Durham, NC

From the Division of Ophthalmology, Duke University Medical Center.

Footnotes
Submitted for publication May 13, 1964.

This work was supported in part by grant 2B-5232 from the National Institute of Neurological Diseases and Blindness.

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