MUTATIONS OF BACTERIAL VIRUSES 97 



ample, B— »Bai), the virus mutations occur with a frequency too low to make 

 them detectable in virus suspensions of the usual titers. 



It is clear from the results obtained with viruses a and a' that loss of sensi- 

 tivity to a given virus can be brought about, in the same bacterial strain, by 

 different mutations, leading to differences in sensitivity to another virus closely 

 related to the first. 



DISCUSSION 



The results described above demonstrate that, whereas bacteria can be 

 altered by mutation in their susceptibility to bacterial viruses, the latter can 

 in turn acquire by mutation the ability to attack new bacterial strains. The re- 

 verse change, by which a virus particle would lose by mutation the capacity of 

 attacking a certain bacterium, might conceivably occur, but would be difficult 

 to demonstrate, except in cases where it occurred very frequently. 



The changes in virus properties are here called "mutations" because of their 

 apparently spontaneous and random occurrence, of their transmission to the 

 offspring, and of their stability. The same may be said of the bacterial muta- 

 tions affecting virus-sensitivity. In making any analogy with the process of 

 gene mutation in plants and animals, we should not forget the lack of any di- 

 rect evidence of the presence, in bacteria or viruses, of "genes" in the sense of 

 discrete material units, whose existence in higher organisms is proved by link- 

 age studies. 



As for the structural changes involved in the virus mutations, we have seen 

 that the serological tests failed to reveal any difference between original and 

 mutant strains. For the time being, our only basis for attempting to under- 

 stand the structural changes involved in the mutations is the infectivity of the 

 viruses for different bacterial strains. 



The virus-host interaction involves as first step a process of specific adsorp- 

 tion. The specificity of the adsorption of a virus by a bacterium is generally 

 conceived as due to the presence of "receptors" for the virus on the bacterial 

 surface (see Burnet 1930). Adsorption is conditioned by complementarity of 

 the surface structures of the receptor and of the virus, which enables them to 

 fit together. Since the mutant bacteria resistant to a virus do not adsorb that 

 virus, we may assume that the bacterial mutation causes a change in the re- 

 ceptors. It has long been known (Burnet 1930) that changes in virus-sensitiv- 

 ity of bacterial strains are often accompanied by changes in the antigenic 

 make-up of their surface, and some of the antigens have been supposed to be 

 responsible for virus adsorption. 



The fact that a change in the surface structure of a bacterium can be com- 

 pensated for by an independent change in the virus particle suggests that the 

 changes involved are relatively small, possibly limited to simple stereochemical 

 rearrangements, suppressing or restoring the complementarity of the surface 

 structures. The fact that normal and mutant viruses are serologically indis- 

 tinguishable speaks in favor of this conception. It is interesting to recall that 

 Stanley (1943) and his collaborators found that strains of tobacco mosaic 

 virus, supposed to be closely related to each other, showed serological relation- 



235 



