Abstract

9-beta-D-Arabinofuranosyladenine (ara A) was shown to inhibit a specific step of tobacco mosaic virus (TMV) multiplication. The time course of the ara A-sensitive function occurred 'late' coinciding with the period of viral RNA and protein synthesis. When treatment began after viral RNA synthesis was established, 1.0 mM ara A inhibited viral single-stranded RNA and viral protein synthesis, but not viral double-stranded RNA synthesis. Viral double-stranded RNA synthesis was inhibited totally only when treatment with ara A began within the first 4 h (before any RNA synthesis was detected), and the degree of inhibition decreased rapidly when treatments began at later times. In contrast, single-stranded TMV RNA synthesis and viral protein synthesis were inhibited throughout the infection. The mode of action of ara A against TMV involves selective inhibition of a function required for single-stranded RNA synthesis and viral protein synthesis without detectable inhibition of RNA or protein synthesis of the host or ongoing viral double-stranded RNA synthesis.

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