RAPPAPORT, SIEGEL AND WILDMAN 1 5 



only a few the structure necessary to initiate a new infection. Should the latter 

 case be correct, it would leave us in some doubt concerning the true nature of 

 the infectious unit. Once an infection has been established, however, we are con- 

 erned only w^ith particles which are independently capable of maintaining the 

 infection. Any non-viable particles produced in conjunction with the viable ones 

 would not be measured. 



These investigations continue to give us a better perspective and understand- 

 ing of certain aspects of TIMV replication. To date, the data are provocative and 

 lead to a good deal of speculation, which of course is useful in planning future 

 experiments. In some cases, however, our data do not mesh as well as might be 

 desired, particularly the time interA'als for virus spread obtained by lesion 

 growth kinetics as compared with the rate of multiplication derived from irra- 

 diation data. This may be only an expression of different kinds of observations. 

 The irradiation experiments measure what we consider to be the events occur- 



Table I. Virus inactivation and aggreg.ate formation at different 



CONCENTRATIONS OF THE SAME VIRUS-ANTISERUM RATIO* 



I 2 .1 4 5 



ANTISERUM VIRUS CONC, „, % SURVIVAT AFTFR % SURVIVORS 



''""iAr MO/l --'ivAI. ^%r=ofK^o7'' U.C..XRI.UOKI, 



5.57 2.2 19. « 9.0 45 



16.7 6.7 23.2 2.1 9.1 



50.0 20.0 16.5 0.24 1.5 



* J. Imnuowl. 74: 112, 1955. 

 t Top 5 ml. 



ring within the first cell infected, whereas the lesion measurements are con- 

 cerned primarily with virus spread through thousands of cells. 



The primary or initial infection may be uniquely different from the subse- 

 quent cellular infection, for the following reasons. First, an injured cell, which is 

 required to start the infection, may be in quite a different physiological state 

 from an uninjured cell into which the virus spreads after multiplication. Second, 

 if there is a time factor necessary for the penetration of the virus particle from 

 outside to inside the cell, this would be of significance only for the first cell, since 

 further spread of infection from cell to cell probably takes place by infectious 

 units which never leave the cytoplasmic environment. Third, the spread of virus 

 from the initially infected cell is continuous; consequently, adjacent cells become 

 infected before the original cell has produced its total complement of virus 

 particles. 



SUMMARY 



Taken as a whole, the data reveal the following about TMV infection in .V. 

 ghitinosa: One and only one virus particle initiates the infection in a susceptible 

 cell. The infectious unit then passes through three distinct phases of ultraviolet 



