PHYSIOLOGICAL TRIGGERS 



beginning infection to cell death, may be observed under the microscope within 

 a perimeter of a few cells at the edge of the necrosis. 



The primary act of infection begins with the entry of a single virus particle 

 into a susceptible cell. This initial act of host-virus combination occurs with 

 great rapidity, and corresponds to an all-or-none physiological response. As far 

 as can be ascertained, the infection is either instantaneously successful or it does 

 not occur at all. For example, when the leaf is thoroughly washed immediately 

 after rubbing with virus, no reduction in lesion count is usually observed, com- 

 pared to an unwashed leaf. However, those infectious virus particles which 

 failed to make the appropriate cellular connections can be recovered from the 

 wash water, and made to infect another leaf. 



The events which immediately follow the successful union of virus and host 

 cells have been studied, using a technique developed by Luria and Laterjet for 



4 5 6 



DOSE (minutes) '"""^ Mr . tr. INOCULATION 



Fig. I. In vitro and in vivo ultraviolet survival curves for TMV. Numbers on curves repre- 

 sent hours after inoculation {Virology 2: 69, 1956). 



Fig. 2. Ultraviolet survival of infectious centers as a function of time in hours after inocula- 

 tion. Numbers on curves indicate phases of sensitivity (Virology 2: 69, 1956). 



demonstrating bacteriophage multiplication within living Escherichia coli cells. 

 The procedure consists of irradiating the infected leaf cells with an appropriate 

 dose of ultraviolet light; that is, one which kills the infectious agents but causes 

 no undue harm to the host. 



The ultraviolet (UV) survival curves for TINIV-infected leaf cells suggest that 

 a regular sequence of events preparatory to multiplication takes place within 

 the cell. The data from a number of experiments carried out at increasing times 

 after inoculation are shown in figure i. They describe the survival of TMV as a 

 function of UV dose, both before and after cellular attachment. The /;/ vitro 

 inactivation is steep and exponential; characteristic of a single target or 'one- 

 hit' type of curve. Irradiating the leaves immediately after the union of virus 

 and cell cytoplasm shows only a slight difference in the survival of what are now 

 the infectious centers. This similaritv in the inactivation of infectious centers 



