JENNERIAN VACCINATION 



(iii) Absence or weakness of capacity to develop skin 

 sensitivity — this should be studied for the possibility 

 that there is an associated failure to produce eosino- 

 phils. 

 (iv) Partial or complete failure to produce during differen- 

 tiation clones of cells which could react with some of 

 the significant antigenic determinants of vaccinia 

 virus. 

 If the idea of differentiation of multiple clones by a random 

 process is valid, one would expect on occasion to find curious 

 deficiencies in ability to produce antibody due simply to 

 random absence of the necessary prototype configuration. 

 The strongest evidence for such an interpretation would be 

 the knowledge that a child showing progressive vaccinia had 

 previously responded normally to one of the common virus 

 infections of childhood. If such a deficiency was responsible 

 it would be more likely to be relative than absolute. In other 

 words, if the child had been allowed time for appropriate 

 mutant types to arise and be selected for proliferation, an 

 effective response would have been possible. The suggestion 

 is that with rare and ' poorly 'fitting ' active sites any available 

 were blocked rather than stimulated by the excess of antigen. 

 On this interpretation the logical approach to treatment 

 would be {a) surgical excision of the source of antigen, 

 {b) administration of immune gamma globulin, {c) immuni- 

 zation at a point distant from the primary lesion of dead 

 virus plus adjuvant in the hope of facilitating the emergence 

 of appropriately modified clones. 



2. Measles 



Measles is almost the best known of infectious diseases but its 

 pathogenesis has never been clearly elucidated. Ever since 

 the days of von Pirquet, observers have commented on the 

 resemblance of the measles rash to an allergic manifestation. 

 An individual measles lesion is hardly distinguishable from 

 a positive pollen scratch test or a poison-ivy weal. 



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