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Abstract
Methyl benzimidazol-2yl-carbamate inhibited the accumulation of tobacco mosaic virus in actively growing parts of infected tobacco plants. It also prevented the inhibition of leaf growth by the virus. In expanding leaves, phytotoxic effects of methyl benzimidazol-2ylcarbamate were seen only at levels 50 to 100 times those required to inhibit viral multiplication. No direct inhibition of tobacco mosaic virus ribonucleic acid synthesis was found when the effects of methyl benzimidazol-2yl-carbamate on incorporation of 32P-orthophosphate into nucleic acid were studied. From experiments on time of application, dose level and leaf age, it is suggested that methyl benzimidazol-2yl-carbamate inhibits viral ribonucleic acid synthesis indirectly, by maintaining the host in a state unsuitable for viral multiplication. This may occur through the known cytokinin activity of the compound. In some circumstances, higher concentrations of tobacco mosiac virus were found to result from treatment with methyl benzimidazol-2yl-carbamate. The relationships between leaf growth, symptom formation and viral multiplication are discussed.
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