Lysogenization and superinfection immunity in Salmonella

Abstract

Immunity to superinfection is a consequence of lysogenization. An analysis of some of the events leading to lysogenization by phage P22 of Salmonella has led to the conclusion that following infection there is at first a decision by the cell phage complex not to lyse. After several generations of bacterial growth the phage may then be integrated. A particular mutant, v1, of phage P22 seems to be able to initiate the reactions leading to lysogeny but fails to be stably integrated. During the period following infection, it replicates in a way that is comparable neither to vegetative growth nor to growth of prophage. Two phages serologically related to P22 have been isolated from other lysogenic Salmonella. They differ from P22 by three loci of such properties that they can be called host range genes. One of these loci, which is linked to v1, controls the ability to confer superinfection immunity. The others control ability to grow on specified bacterial strains. When a phage does not confer to a bacterium immunity to superinfection by related phage, the same general events occur as those following infection of nonlysogenic recipients. The first step in this process seems to be comparable to UV induction of prophage development. Prophage-controlled immunity to superinfection is compared with the immunity to superinfection exhibited by cells immediately after infection. An hypothesis is presented on the nature of the control of these two kinds of immunity. Correlated with lysogenization by P22 and its relatives is the appearance of the somatic antigen 1 and an impairment of phage adsorption. In a general way there is a correlation in amount of antigen, degree of impairment of phage adsorption, and completeness of superinfection immunity.