94 S. E. LURIA 



ing to various conceivable mechanisms of multiplication of the virus inside the 

 bacterial cell, thus proving or disproving the correctness of each of these mech- 

 anisms. This comparison, however, is hampered by the low efficiency of plating 

 of both the mutant viruses a' and y' . Some of the theoretical distributions are 

 not completely known, and the effect on them of the low efficiency of plating 

 cannot be predicted. This is true, for instance, of the distribution encountered 

 in the study of bacterial mutations (Luria and Dele-ruck 1943), which would 

 apply with some modifications to our case if the virus multiplied in the cell as 

 bacteria multiply in a culture. Besides, the efficiency of plating may not be ex- 

 actly constant even within each experiment, and its variations may affect any 

 distribution. Further discussion of this point is postponed until experimental 

 data obtained under conditions in which the efficiency of plating is equal to 

 one will be available. Experiments in this direction are now in progress. 



Similar considerations make it pointless to attempt figuring values for the 

 rates of mutation from the data in tables 3 and 4. Obviously, the correct mode 

 of calculating mutation rates depends on the unknown mechanism of virus 

 multiplication. 



Antigenic relation of normal and mutant viruses 



Bacterial viruses injected into the animal body stimulate the production of 

 antibodies, of which the best known property is their specific virus-neutralizing 

 power. Antisera against viruses a, 7, and 7' were prepared by repeated injec- 

 tions into white rabbits, until the homologous titer had reached a satisfactory 

 level. Cross-inactivation tests were then performed. It was found that, within 

 the experimental precision, a serum neutralized virus a and virus a', or virus 7 

 and virus 7', with the same titer and at the same rate. As an example, we give 

 the values of the fractional rate of neutralization (Hershey et al. 1943) ob- 

 tained by testing the same dilutions of various sera on normal and mutant 

 viruses: 



Serum anti-7 :k r =i.3; k y ' = i.o. 



Serum anti-7 / :k 7 = o.8; ky = o.8 (approximate values). 



Serum anti-a :k a = o.3; ^ = 0.35. 



No cross-inactivation was found between viruses a and a' on the one hand 

 and viruses 7 and 7' on the other hand. For virus 7', it was found that both its 

 activities on B and on B7 were neutralized at the same rate. 



These results clearly show that, whatever structural differences exist be- 

 tween a virus and a mutant derived from it, they are not revealed by serologi- 

 cal tests, at least of this rather simple nature. 



rhe virus mutations in relation to the bacterial mutations 



Arising by mutation from viruses a and 7, viruses a' and 7' acquire the abil- 

 ity to attack bacterial strains that by mutation have lost their sensitivity to 

 the original virus. The virus mutations compensate for the bacterial muta- 

 tions. The mutation 7-^7' is complementary to the mutation B—^By; the mu- 

 tation a->a' is complementary to the mutation B-»Ba 2 . That the compensation 



232 



