16 



S. G. WILDMAN 



interest to know the answers to such questions as to whether some enzymatic 

 action of the host uncovers the nucleic acid, or whether this can be accomphshed 

 by the virus itself, when placed in the proper en^oronment. But further 

 progress must await new ideas on how to locate the small proportion of cells 

 that are sustaining virus activity out of the mjrriad that are as yet uninfected. 



lOr 



4 6 8 10 12 



Hours after inoculation 



14 



Fig. 5. UV survival of infective centers as a function of time after inoculation. Dose 

 of UV: intact U2 and nucleic acids, 90 sec; Ul, 5 min. Note four phases in changing 

 resistance of intact U2. From Siegel et al. (1957). 



Key: •, Ul nucleic acid; Q, U2 nucleic acid; V, iiitact U2; O and X , intact Ul. 



J. Spread of Infectivity from Focus of Infection 



The radiation inactivation experiments so far discussed provide informa- 

 tion on the behaviour of TMV in presumably the first cell that is invaded by 

 the virus, and which serves as the focus for infection of the many thousands 

 of cells that comprise a visible lesion. A kinetic analysis of the spread of virus 

 activity contained within lesions has presented further information on the 

 behavior of TMV during its active period of reproduction (Rappaport and 

 Wildman, 1957). 



The essence of the experiments on lesion growth has been to maintam 

 N. glutinosa plants, infected with TMV, under standard environmental 

 conditions during the time that lesion growth measurements are being made. 

 At 25°C., with 18 hours of hght at 1500-foot candles during each 24-hour 

 period, measurable lesions appear on a still expanding leaf about 40 

 hours after the leaf is rubbed with virus. The area of necrotic cells which 

 distinguishes the lesion from surrounding healthy, green tissue continues to 

 increase with time. While measurements reveal the lesions to be more in the 

 shape of elhpses, rather than circles, the ratio of the major to the minor 



