POPULATION GENETICS 



embryo the 0-D change, the letters standing for the non- 

 committal original and derivative phases (Burnet and Bull, 



1943)- 

 The 0-phase virus agglutinated guinea-pig but not chicken 



cells and grew freely in the amniotic but not in the allantoic 



cavity; Z)-phase virus agglutinated both types equally and 



grew well in either cavity of the embryo. 



A priori there are three possible ways of accounting for the 

 0-D change. The^r^^ is that the population of virus particles 

 produced in the human patient, which is inoculated into the 

 amniotic cavity, contains a small proportion of Z) particles in 

 a great excess of 0. The second is that when particles are 

 inoculated into the amnion a small proportion of mutants 

 to the D or intermediate forms appear as the population 

 increases. The third is that the 0-D change is an 'adaptive' 

 one affecting all units of the virus population, and essentially 

 representing a change due to continued multiplication within 

 cells of the new host. 



The first of these can be automatically eliminated by the 

 demonstration that embryos inoculated with limit-infective 

 dilutions of the original human material give the same type of 

 results as are obtained with larger initial inocula. The present- 

 day approach is, in general, to discard completely the first 

 type of explanation as a relic of an earlier era, unless there is 

 independent evidence of the presence of a second type of 

 virus in the original inoculum. The problem of the nature of 

 the 0-D change is really only a variant of the old controversy 

 as to whether an ' adaptive ' change in bacterial population 

 is wholly a result of mutation in some individual units or 

 whether a significant proportion of the change is to be 

 ascribed to heritable adaptive change affecting all individual 

 units as a result of their exposure to the new environment. 



In 1943, Bull and I presented the evidence in favour of the 

 Darwinian point of view, namely, that the change from to 

 D was mutational in origin and was, in fact, precisely analo- 

 gous to the development in a bacterial strain of resistance to 



2 17 BC 



