LURIA 



actions. The replication of specific biological units must involve the 

 building of complex specific molecules or molecular aggregates, the 

 only permissible limitation to identity of model and replica being the 

 production of "mutated" structures, that is, of modified elements rep- 

 Hcated in the modified form. The indispensable presence of the initial 

 model (gene, virus) indicates that this model plays a role in replication, 

 but this role is by no means an obvious one. The model might carry 

 within itself all the enzymes needed for its own synthesis from specif- 

 ic building blocks, or it might act as a directive pattern for synthesis, 

 according to which building blocks are assembled by synthetic enzymes 

 not pertaining to the model itself [this may require a two-dimensional 

 unfolding of the model, to allow point-to-point replication followed by 

 separation of the newly formed unit (33)], or it might function as a 

 directive pattern for folding a pluripotential macromolecule into a 

 specific tridimensional replica, possibly with the intervention of a nega- 

 tive template, by analogy with Pauling's theory of antibody forma- 

 tion (31). 



The study of virus reproduction constitutes one of the best ap- 

 proaches to bridging the gap between growth and replication. I shall 

 deal primarily with the study of bacterial viruses as exemplified by 

 the system of the "T" phages (T1-T7) active on Escherichia coli strain 

 B (5). Reproduction takes place in a short "latent period" (13 to 45 

 minutes for different viruses under standard conditions) between the 

 infection of a bacterial cell and its dissolution or lysis, with a rise in 

 phage activity traceable to liberation upon lysis of large numbers of 

 specific phage particles. The number of infected cells, the number of 

 phage particles infecting each cell ("multiplicity of infection"), the 

 time between infection and liberation and the amount of virus liberated 

 by each cell can be determined accurately (7). Moreover, the infect- 

 ing virus may be "labeled" with easily recognizable properties arising 

 by mutations (23, 15). Our problem is the following: how are the 

 newly produced phage particles related to the infecting particles? 



On the one hand, the continuity between the two is evidenced not 

 only by the general specificity of reproduction, but also by the obser- 

 vation that mixed infection of a bacterial cell wdth two closely related 

 phages, such as T2 and its mutant T2r, causes a mixed yield of both 

 infecting types in proportions similar to the ones in the infecting mix- 

 ture (15). The continuity of virus material after infection is also 

 proved by irradiation experiments, which show that the radiation sen- 

 sitivity of phage inside a bacterium remains the same as that of free 

 phage for a few minutes after infection, indicating that the total amount 

 of radiation sensitive material remains unchanged (26, 21). 



