18 



S. G. WILDMAN 



If the reasonable presumption is made that degeneration in the organiza- 

 tion of cells as far removed as 4 cell layers from the necrotic area is a con- 

 sequence of virus iavasion, the entire time course of secondary cell iavasion 

 untn the cell dies can be estimated. For Ul, a necrotic cell is added to the 

 lesion every 4 hours, and since virus activity extends 4 cells beyond the line of 

 necrosis, it appears that 16 hours ensues from the time that a cell is iavaded 

 by Ul until the cell is dead and becomes part of the enlarging lesion. For 

 strain U2, the time period from infection to death is 20 hours, A similar cal- 

 culation leads to a figure of 80 hours for U8, but we are inclined to believe 

 the estimate is unreliable because of the anomolous character of the edge of 

 the U8 lesion, as compared to Ul and U2. 



As shown in Fig. 6, extrapolation of the curves to the day of infection 

 reveals no obvious deviation from a linear relationship during the time that 

 lesions are forming, but are invisible to the eye, until the time that they can 

 be measured. Consequently, we presume that the spread of the virus activity 

 from the initial focus of infection is the same as that encountered during the 

 visible enlargement of lesions. 



10-3 



Lesion area (mm ) 



Fig. 7. Infectivity of three strains of TMV as a function of lesion size on N. glutinosa. 

 From Rappaport and Wildman (1957). 



Key: squares, Ul; circles, U2; triangles. Holmes' rib grass. 



K. Yield of Virus 'per Infected Cell 



As shown by Fig. 7, the amount of extractable infectivity is propor- 

 tional to lesion area for strams Ul and U2. U8, in this respect, behaves 

 differently, since the amoimt of extractable infectivity decreases as the 

 visible lesion area increases. We have no ready explanation to account for 

 the pecuhar behavior of U8, except the reminder that the swoUen cells at the 



