PATHOGENICITY 965 



closely related viruses, but there are exceptions. The relationship, for example, 

 between the Eastern and Western types of equine encephalomyelitis viruses is 

 said to be brought out by the complement-fixation, but not by the neutralization 

 test (Havens et. al. 1943). 



Pathogenicity. — -The pathogenicity of different viruses for different hosts varies 

 greatly. Some, like the vaccinia and the rabies virus, have a wide range of patho- 

 genicity ; others, like the foot-and-mouth and the encephalitis viruses, have a 

 narrow range ; and still others, like the measles and mumps viruses, seem to be 

 pathogenic for one species alone. Some attack only mammals, some only birds, 

 and some both mammals and birds. One curious feature of most of the viruses 

 is their ability to grow in the embryonic or associated cells of the developing 

 hen's egg, in spite of the fact that the chicken, once it is hatched, is resistant to 

 all the pure mammalian viruses. In becoming adapted to different hosts viruses 

 often undergo minor variations ; there is evidence, for example, that the numerous 

 animal poxes, with the possible exception of fowl-pox, are due to varieties of one 

 and the same virus (Zwick 1924). On the other hand, the properties of a virus 

 may be considerably altered. Thus, inoculation of the calf with variola virus, 

 and subsequent transference by passage through calves, modifies the virus in such 

 a way that when reinoculated into human beings it gives rise not to smallpox but 

 to vaccinia. Passage of the street virus of rabies through the brain of rabbits 

 gives rise to the production of a fixed virus, which, though it kills rabbits on intra- 

 cerebral inoculation more rapidly than the street virus, is yet much less virulent 

 than the street virus on subcutaneous inoculation (Levaditi et al. 1924). This 

 example illustrates another characteristic that is frequently observed in the study 

 of viruses, namely, their adaptation not only to one particular host, but to one 

 special tissue or route of inoculation. Findlay (1936), whose review on variation 

 in the animal viruses should be consulted, is of opinion that variants are of two 

 types : (a) variants associated with pathological lesions unlike those produced 

 by the parent strains, but without any great antigenic difference ; (6) variants 

 associated with pathological lesions like those produced by the parent strains, 

 but with considerable antigenic difference, more often quantitative than qualitative 

 in character. Some changes, such as the conversion of rabbit fibroma into myxoma, 

 may justly be regarded as mutations ; the majority are to be regarded as changes 

 of the environmental type. 



Infection in most of the filtrable virus diseases appears to occur by direct con- 

 tagion, the infective material gaining access to the body either by the nasopharynx 

 or sometimes by the skin, as in rabies. In certain diseases the virus is inoculated 

 into the blood stream by an insect vector ; yellow fever, for example, is carried 

 by the mosquito Aedes aegypti, dengue fever by Aedes aegypti and Aedes albopiclus, 

 and Pappataci fever by the sandfly, Phlebotomus papatassii. Laboratory infections 

 are not infrequent, especially with yellow fever, psittacosis. Rift Valley fever, and 

 louping-ill. Little is yet known about the mechanism of infection, but studies 

 of the vaccinia virus suggest strongly that the elementary bodies constitute the 

 infecting agents, and that in virulent strains even one elementary body may 

 suffice to cause infection (Parker 1938, Parker et al. 1941, Smadel et. al. 1939). 



In general, the cellular lesions produced by viruses are of one or other of two 

 kinds. Either the cells are stimulated so that the tissues become hyperplastic, 

 as in the fibromata, papillomata, warts and poxes ; or they may be damaged so 

 severely that they die, as in the hepatic necrosis of yellow fever and Rift 



