Specific inhibition of tobacco mosaic virus protein and single-stranded RNA synthesis by arabinofuranosyladenine.
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.
D012313:RNA / Q000096:biosynthesis*; D012367:RNA, Viral / Q000096:biosynthesis*; D013997:Time Factors; D014027:Tobacco Mosaic Virus / Q000187:drug effects*; D014740:Vidarabine / Q000494:pharmacology*; D014764:Viral Proteins / Q000096:biosynthesis*; D014779:Virus Replication / Q000187:drug effects*
D012367:RNA, Viral; D014764:Viral Proteins; D012313:RNA; D014740:Vidarabine