LYSOGENY 347 



are induced, at least 50 % of the released phages are able to transduce the 

 Gal'*' character. Quantitative measurements lead to the conclusion that, 

 upon induction, both the genetic material of the phage and the Gal character 

 multiply as a single unit (Weigle, 1957). 



Contrary to transduction in Salmonella, for instance, transduction of the 

 Gal character by phage A is very specific: the only character hitherto known 

 to be transduced by phage A is precisely that character to which A prophage 

 is linked. This type of transduction clearly illustrates how intimate is the 

 association of a prophage with the genetic material of the host, since it may 

 even persist during the vegetative multiphcation. It is an intermediary 

 situation between the other cases of transduction where the role of the phage 

 appears to be only passive, and those situations of lysogenic conversions, 

 such as toxin production, where the genetic determinant of the character 

 appears to be the prophage itself. 



X. Lysogeny and Latency of Viruses 



Lysogeny corresponds to a remarkable situation whereby the genetic 

 material of a virus is incorporated to that of the host and behaves as a 

 cellular constituent. Either spontaneously or as a result of the action of 

 mutagenic or carcinogenic agents, this cellular constituent will eventually 

 develop into a pathogenic form, whose multiplication brings about the 

 destruction of the host cell and the liberation of a crop of infectious 

 particles. Infection of sensitive cells may in turn give rise to new lysogenic 

 systems. The cycle of phage in such lysogenic systems with its three 

 stages (infectious, vegetative, and prophage) is schematically represented 

 in Pig. 6. 



The case of lysogenic bacteria has often been brought close to that of 

 latent viral infections in plants or animals (Lwoff, 1953; Jacob, 1954). 

 Numerous cases of such latent infections are now known and have been 

 recently reviewed (Shope, 1950; Koprowski, 1952; Smith, 1952; Schlesinger, 

 1953). They correspond to a wide variety of situations. In some cases, latency 

 occurs after a known infection witli a given virus. Sometimes, this infection 

 is not followed by pathological symptoms, but the persistence of the virus is 

 evidenced either by the possibility of recovering active virus from the in- 

 fected organism, by the presence of specific antibodies, or by interference 

 with a subsequent infection with a related virus. Sometimes, infection may 

 be followed by such lesions as the production of a tumor, but no, or very 

 little, infectious ^drus can be recovered from the infected organism. In other 

 cases, whether after infection or even in the absence of any known infection, 

 pathological symptoms do not appear unless the organism is submitted to 

 environmental changes, either physiological or brought about by the action 

 of external physical or chemical agents. It thus appears that what is generally 



