REINHARD 



SULKIN: There are two factors to consider. One is the repli- 

 cation of attenuated virus, and the other is that it is conferring 

 local immunity so that small doses of a wild type virus cannot 

 gain a foothold in the host. 



REINHARD: I'd like to propose an additional thought. You 

 remember that in the St. Lawrence study the graphs of Types 

 1, 2, and 3 poliovirus antibodies indicated interference between 

 the three types in the chronology of initial infection and immuno- 

 genesis. (See Figure 2 in manuscript.) Secondarily, there was 

 a fifteen to twenty year periodicity between resurgence in pre- 

 valence of antibodies, correlated with increase in titers. I wish 

 we had more extensive data to test the validity of these phe- 

 nomena. I am wondering, however, whether these graphs do 

 not give a true picture of the natural decline of antibodies in 

 an endemically exposed population to the point where reinfection 

 and reinforcement of antibodies takes place. 



METCALF: Keeping in mind the so-called doctrine of original 

 antigenic sin^ and the experiences gained with influenza viruses, 

 is there anything in this data which could or might be interpreted 

 as heterological boostering of one type by another? Does that 

 happen in the polio group? 



REINHARD: Not in type-specific antibodies. Does anybody 

 else have any information? 



SULKIN: Heterotypic antibody responses have been observed 

 in vaccinated individuals as well as following natural infection 

 with poliovirus. Some time ago Sabin^ described the transitory 

 appearance of Type II neutralizing antibody in patients infected 

 with Type I poliovirus and suggested that these two types shared 

 a common antigen. 



REINHARD: This would be due to actually shared antigens. 



1 Davenport, F. M., A. V. Hennessy, and T. Francis, Jr. 1953. J. Exp. Med. 98: 641-656. 



2 J. Exp. Med. 96: 99-106. 1952. 



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