552 S. E. LUKIA 



viral material is not simply an activator of latent potentialities of the recip- 

 ient cell, but a detailed blueprint, which in the ceU takes its place within 

 the hierarchy of cellular determinants of specificity, and whose genetic 

 functions may sometimes be compatible, sometimes incompatible with 

 normal cell functions. 



According to this view, the infectious virus particles produced by a virus- 

 infected or virus -carrying cell are simply one product of the pattern of syn- 

 thesis determined in the virus-containing cell by the genetic apparatus, which 

 includes both viral and host determinants, and which functions as an inte- 

 grated whole. The significant acts of viral multiplication involve the replica- 

 tion of the genetic blueprints introduced into the cell by the virus. This re- 

 plication may be integrated to a greater or lesser extent with the replication 

 of the whole genetic apparatus of the cell. Instances range all the way from 

 almost complete integration and synchronization, as with the prophage of 

 temperate phages in lysogenic bacteria (Lwoff, 1953), to complete incom- 

 patibility, as with the most intemperate, destructive phages and animal 

 viruses. 



The mature, infectious particles appear to be the ultimate product of virus 

 multipHcation. Some of the replicating viral elements, together with non- 

 genetic but specific materials produced under viral control in virus-infected 

 ceUs, become incorporated into mature, nonmultip lying forms — the virus 

 particles. These are recognized by their characteristic infectivity and organ- 

 ization. This assembly of virus particles removes some of the viral elements 

 from the multiplying process and makes them suitable for introduction into 

 new cells. It is analogous to spermatogenesis, which by a complex cytomor- 

 phogenetic process transforms a haploid cell into a form suitable for intro- 

 duction of its nucleus into the egg cell. We consider this "dual hypothesis," 

 which distinguishes two complementary and mutually exclusive processes, 

 replication and maturation, as central to our understanding of virus biology. 



Virus maturation wiU be a selectively advantageous process if it makes it 

 easier for the virus to invade other hosts from without. The replicating form 

 of a virus often appears to be noninfectious. By this we mean that, when 

 extracted in this form, it is ineffective in initiating infection under conditions 

 where the mature virus particle can do so. Yet, the lack of infectivity of the 

 rephcating virus may be only apparent. Under conditions that ensure pro- 

 tection from destructive agents and facilitate introduction into susceptible 

 ceUs, we may succeed in observing initiation of infection by more or less in- 

 complete virus particles, by their genetic components alone, or by multiply- 

 ing viral elements extracted directly from cells prior to maturation. Instances 

 of this sort will be discussed in the following sections. We shall return later 

 to the relation between maturation and infectivity and to its significance for 

 the general problem of infective heredity. 



