Abstract
Infectious tobacco mosaic virus ribonucleic acid (TMV-RNA) prepared by the salt-heat method and inoculated to Phaseolus vulgaris L. (var. Pinto) or Nicotiana glutinosa L. leaves produces lesions sooner than a tobacco mosaic virus (TMV) control inoculum. Treatment of TMV or one of its strains with high pH or heat and detergent results in inocula which produce lesions on bean delayed in appearance with respect to those produced by the untreated control. This characteristic is maintained after low molecular weight degradation products are removed. The same delayed effect can be produced by adding low molecular weight TMV protein to TMV or TMV-RNA inocula or reconstituted noninfectious TMV to TMV. When small quantities of low molecular weight TMV protein, bovine serum albumin, or reconstituted noninfectious TMV are added to TMV, infectivity is increased with respect to TMV alone; when large quantities are added infectivity is reduced. Addition of low molecular weight TMV protein to infectious TMV-RNA produces similar results, the effect depending on the concentration. Diluted TMV stored at 5° C loses a considerable proportion of its infectivity in the first few days after dilution. It is postulated that these effects are produced in both TMV and TMV-RNA by combination or aggregation with the added protein. Low concentrations of protein protect labile particles from inactivation and increase infectivity. Protection also increases longevity of the infectious particles and permits late infections to be initiated which are reflected in a delay in lesion appearance. High concentrations of protein bring about excessive aggregation which counterbalances protective benefits to infectivity and brings about inhibition.
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