SEROLOGICAL VARIATION 265 



fact that antibody to swine strains is sporadically detected in the serum of 

 young children might indicate that a strain of that group is still circulating 

 in the human population. The 1949 epidemics in the Arctic and elsewhere, 

 from which PR8-like strains were reported, could be considered a lagging 

 virus, although the possibility of laboratory contamination has not been 

 excluded. If long-term maintenance of antigenically unchanged variant 

 strains is established, as may be the case with swine influenza, the concept of 

 continuous variation as a basis for recurrences would obviously need recon- 

 sideration. 



D. Variation in Type B Influenza Virus 



Variation in type B virus has occurred in a maimer resembling that of 

 type A. Suggestions have been repeatedly made that observed differences 

 warrant group divisions. Some differences in age distribution of antibodies to 

 different strains have been observed (Davenport et al., 1953). Interestingly, 

 the 1952 strains appeared somewhat more closely related to the LEE 1940 

 strain than did the 1945 strains. Vaccination in 1945 with LEE strain provided 

 excellent protection (Francis, 1950), and vaccination of children with LEE 

 strain in 1952 protected against influenza B of that year (Hennessy et al., 

 1953). In 1955, vaccination with LEE induced poor antibody to the 1954 and 

 1955 strains and immunity to disease was of low order (Davenport and 

 others, 1956). It is suggested, therefore, that group B 2 begin with the 

 1954 strains (Table IV). There is little information regarding differences 

 among strains of other types. 



TABLE IV 

 Group Prototype Prevalence 



P>! Lee 1936-48 



B„ GL 1954— 



E. Serological Variation during Passage 



1. Adaptation to New Hosts 



Because the studies of 1936 were made mostly with strains that had been 

 isolated and maintained through animal passage, a susjucion persisted and 

 became a general belief that a number of the serological alterations that were 

 observed were modifications resulting from animal passage. Hirst (1947) noted 

 in the adaptation of two strains of virus to mice and eggs that the mouse line 

 of one of them developed a distinct serological deviation, as compared with 

 the egg line. The mouse line also appeared to differ from that of the second 



