Abstract

Multiplication of tobacco mosaic virus within the inoculated leaves of four local lesion hosts and the quality of necrotic lesions on the leaves of these hosts were compared.First recovery of virus from the inoculated leaves preceded the lesion appearance in all hosts used: Nicotiana glutinosa, Datura stramonium, Nicotiana tabacum var. Samsun NN, and Phaseolus vulgaris. It is concluded that virus multiplication occurred first in leaf cells to which virus was introduced and then necrotization of these cells followed. This confirmed the idea of Dr. Yoshii that necroic reaction in local lesion host to virus infection was completely different from the “hypersensitive reaction” that was given first to the phenomenon of cell death of hypersensitive wheat variety against incompatible race of Puccinia graminis.From the interval between first virus recovery and lesion appearance, these hosts were divided into two groups. In N. glutinosa, D. stramonium, and N. tabacum var. Samsun NN the interval was long, while it was short in P. vulgaris.Virus multiplication curve within the inoculated leaves of these hosts was divided into 2 types. Type A has no plateau after lesion appearance but simply shows a sigmoid curve, which is similar to the case in the systemic host, N. tabacum var. Samsun. Type B has a clear plateau after lesion appearance. N. tabacum var. Samsun NN and D. stramonium showed type B or sometimes type A in replicated trials. N. glutinosa and P. vulgaris always showed type B. The plateau in virus multiplication curve was seen during 20-40 hours after lesion appearance, while number and size of lesions were. still increasing. It was supposed that the limiting mechanism of virus multiplication and movement connected with the browning of infected cells is intensively operating during this period.After this period, virus multiplication still continues for a while. This seems to proceed with the increase of lesion size, especially in the case of N. tabacum var. Samsun NN and D. stramonium. Necrotization of infected cells then overcomes the spread of virus, and eventually virus multiplication ceases.The intervals between first virus recovery and lesion appearance and the type of virus multiplication curve within the inoculated leaves correspond with the color, size, and shape of lesions on different local lesion hosts. The lesion color, size, and shape also reflect on maximum yield of virus 100 hours after inoculation.

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