S. G. WILDMAN 



arise, the disparity between the huge number of cells present on the surface 

 and the small number that become infected and produce a lesion requires 

 another factor to be taken into account, namely, the concept of the susceptible 

 site. It is the difficulty in making susceptible sites that is considered to limit 

 the extent of initial infection, rather than differences inherent in the capacity 

 of cells to support virus infection. 



20 



10- 



0-5- 



E 0-2- 



0-1 



,? 0-05 - 



002 



2 5 10 20 50 100 200 500 



Concentration of virus (mg/ml-.xlO" ) 



Fig. 1. Relationship between number of lesions and concentration of two strains of 

 TMV. P is a theoretical curve for the expression, F/iV = 1 — e~*", where Yl'N = rela- 

 tive number of lesions, and m = average number of infectious imits per susceptible site, 

 m ranging from 0.28 to 5.6 units per site. Experimental values for strain U2 are close to 

 the theoretical. The greater departure of strain Ul from the theoretical can be explained 

 as resulting from aggregation of the infectious imits (Bald, 1950). 



B. The Susceptible Site and the Initial Act of Infection 



The leaf must be injured before infection with virus is possible. This re- 

 quirement can be illustrated by the fact that a leaf can be caused to take up 

 relatively large amounts of Hquid by the process of vacuum infiltration, so 

 that the entire intercellular space of the interior of the leaf, ordmarily filled 

 with air, will be occupied by liquid. Introducing tremendous concentrations 

 of virus into the interior of a leaf by this means, and thereby placing virus in 

 contact with nearly every cell of the leaf, has never produced a lesion in our 

 experience and that of others (Caldwell, 1932). Yet, gentle rubbing of either 

 Burface of the leaf in the presence of virus will almost invariably produce 

 lesions. Thus, the conclusion seems inescapable that an absolute requirement 

 for infection is injury of the leaf, thereby producing a susceptible site through 

 which the virus can enter the protoplasm of the host cells. 



Returning to the infectivity-dilution curve, we see that the bending of the 

 curve at high virus concentrations finds a reasonable interpretation in terms 



