344 H. B. ANDERVONT 



These virus strains, especially the strain harbored by wild mice, may prove 

 useful in an immunogenetic approach to the problems of host-virus inter- 

 actions. Antibodies to the virus have not been found in mice of susceptible 

 inbred strains. It is conceivable that years of intensive and selective inbreed- 

 ing, concurrent with the acquisition of a highly active virus, could account 

 for the inability of inbred hosts to produce antibodies against the virus. In 

 the wild mice of mixed genetic composition the virus may elicit antibodies in 

 some individuals but not in others; this could explain why, in general, these 

 mice are relatively resistant to the virus but are incapable of destroying it. 

 An explanation of the reason for the persistence of the virus in the resistant 

 house mouse should be of interest to the tumor virus problem. 



3. The Age Factor in Response to the Virus 



The age of the mouse is an important factor in determining its suscepti- 

 bility to the virus because very young animals are more susceptible than 

 adults (Andervont, 1941, 1945d). It has even been suggested that the virus 

 cannot produce tumors unless it infects mammary glands early in their 

 development. The necessity of using very young test animals, and the long 

 period of time between infection and the appearance of a tumor, together 

 with the occurrence of tumors at sites remote from the site of virus entry, are 

 undoubtedly the chief reasons for the delayed discovery of the virus. These 

 factors were far removed from any previous experience which revealed a 

 virus as the causative agent of a tumor. 



Hybridization between inbred strains led to the discovery of the mammary 

 tumor virus and the same procedure produced the first evidence that adult 

 mice were susceptible to infection. Hybrids were derived by mating virus-free 

 females to virus-bearing males and some of the offspring developed tumors at 

 an early age and carried the virus. It was suggested (Andervont and Dunn, 

 1948b) that the hybrids had acquired their father's virus because virus was 

 found in the seminal vesicles of high-mammary tumor strain males (Andervont 

 and Dunn, 1948a). Subsequent work in various laboratories established 

 transmission of virus to the female during copulation. This interesting 

 problem has received attention from Bittner, who has summarized most of 

 his findings in a recent publication (Bittner, 1957b). Dmochowski (1953a) has 

 reviewed the entire problem. 



It is not clear how the father's virus gains access to the hybrid offspring. In 

 most instances the mother is infected first and then transmits the virus to the 

 young mice in her milk, but in a few litters some hybrids developed tumors at 

 an early age and these tumors contained the virus, whereas other litter mates 

 live to an advanced age and either die free of tumors or develop tumors in 

 which the virus is not detectable (Andervont, 1949a). 



