PROCESS OF INFECTION AND VIRUS SYNTHESIS 5 



give the same type of symptom as in Turkish Samsuii, but U2, more often 

 than not, will not spread from the inoculated leaf to produce a symptom in 

 other leaves; instead, it will produce necrotic spots on the inoculated leaf. 

 Symptom development arises from the systemic invasion of all parts of the 

 plant, in contrast to the local lesion response, which reveals the presence of 

 the virus when cells become necrotic and die as the result of virus infection. 



III. Behavior of Plant Viruses in a Local Lesion Host 

 A. Local Lesion Assay for Infectivity 



When TMV is rubbed over the surface of N. glutinosa leaves, discrete 

 necrotic spots wiU appear on the rubbed leaf in about 2 days. Production of 

 local lesions can be induced by TMV in other hosts, such as pinto bean. 

 Datura, etc. Local lesions can also be induced by other plant viruses as well. 

 Li 1929, Holmes made the important observation that the number of lesions 

 induced by TMV is a function of the concentration of the virus applied. His 

 discovery thereby gave rise to the local lesion assay for measuring plant 

 virus iiifectivity. Mathematical analysis of the infectivity-dilution curve by 

 numerous workers (Bald, 1937, 1950; Lauffer and Price, 1945; Kleczkowski, 

 1950; Youden et al., 1935) has led to the general acceptance of the concept 

 that lesions can arise from infection of single cells by single virus particles. 



Estimating plant virus activity is not as straightforward as might be 

 desired, because the test plants vary so markedly in sensitivity in terms of 

 absolute numbers of lesions arising from the same concentration of virus. 

 Sensitivity changes can be very great on a day-to-day basis. Smaller changes 

 in sensitivity appear on an hourly basis (Matthews, 1953), as well as on a leaf 

 level and plant-to-plant basis. Efforts to level out changing sensitivity 

 by more precise environmental control suggest that nothing less than a 

 Phytotron would produce plants with a significant reduction in sensitivity 

 differences. 



While sensitivity differences represent a hurdle of no mean proportions, it 

 does appear that the relative nmnber of lesions produced as a function of 

 virus concentration is a constant within limits of experimental error. With 

 sufficient repetition and adequate randomization, virus dilution curves, such 

 as that shown in Fig. 1, can be produced. Furthermore, the experimental 

 points fit rather well a theoretical curve calculated from the Poisson distribu- 

 tion on the expectation that each infection would arise from a single infec- 

 tious unit of virus activity. The curve is linear over a fairly wide range of 

 virus concentrations, but bends toward the abcissa as virus concentration is 

 increased. Since the surface of the leaf contams many millions of cells, and 

 the curve bends when only hmidreds, or, at the most, thousands of lesions 



