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thetical component from myxoma virus to convert it to fibroma virus 

 had been achieved. 



The other approach, namely, the experiments of Berry and Dedrick 

 ( 1 5 ) , in which an effort was made to transform fibroma virus to myxoma 

 virus by the addition of a hypothetical component from myxoma virus, 

 turned out successfully. The apparent close immunological relationship 

 between the fibroma and myxoma viruses had led Berry and Dedrick to 

 explore this hypothesis and their approach to the problem had been 

 suggested by Griffith's studies of transformation of pneumococcal types. 

 Briefly, they found that, if myxoma virus which had been inactivated 

 by heating at either 60 ^C. or 75 °C. was mixed with live fibroma virus 

 and administered to domestic rabbits, the inoculated animals, instead of 

 developing the mild fibroma, frequently came down vsdth fatal myxoma- 

 tosis. Control rabbits receiving heated myxoma virus alone, of course, 

 remained normal. These experiments suggested that some component 

 of myxoma virus, not destroyed at 75 °C., was capable of combining 

 with fibroma virus to convert that agent to myxoma virus. 



Although Berry and Dedrick published no detailed account of their 

 work, several investigators including myself have repeated it in essence 

 and duplicated their observation. Hurst has published the most exten- 

 sive account of the phenomenon, and it appears from his work that the 

 proportions of heated myxoma to living fibroma virus are of consider- 

 able importance in achieving the transformation (16). Hurst's experi- 

 ments indicate that, using 10 per cent infected tissue as a source of 

 either myxoma or fibroma virus, a ratio of 25 or 50 parts of heated 

 myxoma virus to 1 part of live fibroma virus most regularly results in 

 transformation. If the proportion of live fibroma to heated myxoma 

 virus in the mixture is too great, transformation fails to occur and the 

 inoculated rabbits develop only fibroma. It is believed that these failures 

 of transformation may result from too ready an immunological response 

 to fibroma virus infection. As mentioned earlier, fibroma virus induces 

 a state of increased resistance to myxoma virus which may become 

 evident in as short a period as 2 to 4 days. If therefore the proportion 

 of fibroma virus in the transformation mixture is too great, the reaction 

 of resistance engendered by the fibroma virus prevents the appearance 

 or detection of any small amounts of myxoma virus that may be pro- 

 duced and the end result will be apparent failure of transformation. It 

 seems quite apparent that the transformation of fibroma to myxoma 

 virus is a delicately balanced in vivo reaction depending at least par- 

 tially for its success on the correct timing of the transformation in 

 relation to the establishment of untransformed fibroma virus in the host. 

 Almost certainly the ratio of transformed myxoma virus units to un- 



