Abstract

An isolate of tomato aspermy virus (TAV) was inactivated both in vivo and in vitro at 36°C. Inactivation took the form of a second or higher order reaction, which indicated that loss of infectivity was not due solely to a direct effect of high temperature on the virus.

The concentration of polyphenoloxidases increased greatly in tobacco plants grown at 36°C, and evidence was obtained to indicate that this enzyme class, either directly or indirectly, enhanced the inactivation of TAV during heat treatment. The concentration of ribonucleases also increased in heat-treated tissues and these may have aided the inactivation, as the infectivity of TAV was shown to be destroyed by RNase in tests in vitro. The pH and ionic strength of the sap decreased in heated plants and these changes may have been significant as TAV had critical requirements of buffer pH and molarity for optimum infectivity.

The alterations in cellular metabolism responsible for these changes result from heat-induced stress. Therefore, the optimum temperature for therapy of many viruses by heat treatment is likely to vary with the host in which it is treated, depending upon the host's heat tolerance.