24 BALD 



from the horizontal dotted hne in Figure i. They are for experiment 

 lo, 2500; experiment 13, 1250; experiment 14, 590; and experiment 

 15, 350. With these as maxima the more dilute portions of these curves 

 may be fitted, for experiment 10 on the assumption that no aggregation 

 of virus particles occurred, and for the other three on the assumption 

 of aggregation. Experiments 13 and 14 may be fitted with the same 

 value of K but with different values of pv. The results obtained in this 

 way imply that in these two experiments the virus in the inoculum was 

 aggregated in the same degree, but the infectable areas on the leaves of 

 the test plants in experiment 13 were twelve times as susceptible as 

 those in experiment 14. On the other hand, although in experiment 10 

 there was no aggregation and in experiments 14 and 15 the degrees of 

 aggregation were different, the infectable areas on the leaves of the test 

 plants were about equally susceptible. 



For the most part in these four experiments no effects of the virus 

 on the physical properties of the inoculum need be invoked to explain 

 departures from the Poisson relationship at the lower virus concentra- 

 tions, i.e., at levels below the horizontal hatched line in Figure 1. Above 

 this line is a point representing a single virus dilution in experiment 14 

 that is displaced to a position below the upper curve. This may be in- 

 terpreted as the one obvious example of interaction between the physi- 

 cal effects of virus in the inoculum and the effects of infectivity below 

 the maximum needed to present active virus to all infectable areas with 

 which contact is made on the leaf surface. Otherwise, these experiments 

 may be interpreted to indicate only slight interaction between the phys- 

 ical effects of increasing virus in the inoculum and effects arising from 

 the infective capacity of the inoculum. 



These experiments from Kleczkowski's paper have been discussed at 

 some length to show that the original simple explanation of lesion- virus 

 concentration curves based on the Poisson series may still be proved 

 reasonably adequate. Some variability in the susceptibility of infect- 

 able areas is not denied, but it is suggested that this is not the main 

 cause of the heterogeneity of lesion-concentration curves. For the to- 

 bacco mosaic group of viruses and probably for others aggregation of 

 virus particles will explain much of this heterogeneity. It is becoming 

 possible at will to cause aggregation or dispersion of virus in suspen- 

 sions of tobacco mosaic virus and to estimate aggregation by various 

 physical methods. Thus independent experimental evidence of the ef- 

 fects of aggregation on the lesion-virus concentration relationship may 

 be obtained. 



Another postulate which has been used to explain the relationship 



