oo S. E. LURIA 



plaques are identical, and so is the growth in liquid medium: constant period 

 13 minutes, burst size 1 10-130 in broth at 37°C. Plated with bacteria of strain 

 Ba 2 , a suspension of virus a' gives a smaller number of plaques than with B. 

 The efficiency of plating is 0.25-0.7. The plaques are of smaller and more varia- 

 ble size. In liquid medium, bacteria Ba 2 adsorb virus a' extremely slowly, so 

 that reliable adsorption measurements are difficult to obtain. The constant 

 period for growth in broth at 37°C is 13 minutes, similar to the growth on B. 

 The burst size is difficult to determine with any degree of accuracy, because the 

 presence of large amounts of unadsorbed virus disturbs the calculation of the 

 number of infected bacteria. From an experiment in which at least a great part 

 of the free virus was eliminated by means of anti-serum, we obtained for the 

 burst size a minimum value of 55. 



There are some indications that strains of virus a' independently isolated 

 may differ from one another. The size of the plaques produced on the same 

 bacterial strain is sometimes different. This point has not yet been further in- 

 vestigated. 



The mutational origin of viruses a' and y' 



The presence of virus a' in suspensions of virus a and that of virus y' in sus- 

 pensions of virus 7 are demonstrated by plating a large amount of the suspen- 

 sions with bacteria resistant to the normal virus. We observe only the end re- 

 sult — that is, the appearance of a few plaques containing a new type of virus. 

 Several alternative modes of origin of the new virus are a priori conceivable. 

 Hypothesis 1: There is a small finite probability that, when plated with re- 

 sistant bacteria, a normal virus particle succeeds in attacking one of the re- 

 sistant cells; when this happens, then the particle will give rise to a virus strain 

 capable of attacking the bacteria resistant to the original virus. Hypothesis 2 : 

 There is a small finite probability that a normal virus particle in a culture of 

 virus growing on sensitive bacteria mutates, becoming hereditarily capable of 

 attacking the resistant bacteria. Hypothesis 3: There are in a sensitive bac- 

 terial culture some exceptional, abnormal bacteria which, when infected by a 

 normal virus particle, produce virus of the new type instead of the normal 

 type. 



As far as hypotheses 1 and 2 are concerned, the situation is similar to that 

 encountered in the study of virus-resistant bacteria from virus-sensitive bac- 

 terial strains, and analogous considerations apply (Lurta and Delbruck 



1943)- 



According to hypothesis 1, on the one hand, the number of virus particles 

 that succeed in giving plaques on the resistant bacteria should be proportional 

 to the number of virus particles tested. This will be true whether these par- 

 ticles come from the same virus culture or from different cultures, since the 

 particles that produce plaques on the resistant bacteria are normal particles 

 at the time of plating, and the probability of producing a plaque is assumed to 

 be uniform for all particles. If we test a large number of samples each contain- 

 ing the same amount of normal virus, the numbers of plaques produced on the 

 resistant bacteria should show only the fluctuations due to the sampling er- 



228 



