104 BACTERIOPHAGES 



serum (dilution 10~-^ )to a survival of about 0.2. The plaque 

 count in a salt-free medium of the survivors of serum treatment 

 was increased 1,000-fold as compared with that of the untreated 

 phage preparation. Treatment with a small amount of anti- 

 serum had the same effect on phage infectivity as an increase in 

 salt concentration. It is probable that these effects of salt and 

 of antiserum on phage infectivity are due to effects on electro- 

 static charge (see Cann and Clark, 1955), although this explana- 

 tion was discarded by the authors. This problem will be dis- 

 cussed further in the chapter on phage adsorption. 



It is not certain at present which of the several antibodies in 

 antiphage serum is responsible for the effects described above. 

 A peculiar antibody which stabilizes the activated state of a 

 tryptophan-requiring strain of T4 has recently been described 

 (Jerne, 1956). 



5. Complement Fixation 



Early results (d'Herelle, 1926) left considerable doubt as to 

 the ability of phage-antiphage systems to fix complement. 

 These doubts have been dispelled in recent years by studies 

 showing not only that such systems do, in fact, fix complement 

 but also that complement fixation offers a valuable quantitative 

 tool for the study of those phage antigens and phage-related 

 materials that do not react with neutralizing antibody. An 

 example is the work of Lanni and Lanni (1953) in their demon- 

 stration of a serological relationship between T2 doughnuts 

 and T2 phage and their use of antidoughnut sera for studying 

 the structure of the infective virus particle. The scope of the 

 procedure is not restricted, however, to such antigens. 



Other recent studies illustrate further the broad applicability 

 of complement fixation to problems of phage structure and 

 growth. In confirmation of the discovery of Hershey and Chase 

 (1952) with T2, Lanni (1954) showed that the bulk of the com- 

 plement-fixing antigens of infecting particles of T5 remained 

 outside the infected host cells. Previous work had suggested 

 instead that the complement-fixing antigens of T5 (Rountree, 



