72 SCHLESINGER 



Thus, even after inactivation with uhra violet hght, influenza virus 

 retains its basic identity (Henle and Henle, 1947). While it has lost 

 its self-reproducing capacity, it retains its ability to be adsorbed onto 

 and eluted from erythrocytes, to be adsorbed on the allantoic epithe- 

 lium, to inhibit the growth of the allantoic membrane, and to act as 

 specific antigen in vivo or in vitro. The fact that irradiated virus re- 

 mains elutable from red cells suggests that it is capable of destrojdng 

 the red cell receptors. Since many similarities exist between these 

 receptors on red cells and hemagglutinin-inhibitory (VHI) substances 

 extractable from erythrocytes (Friedewald et al., 1947, deBurgh et al., 

 1948), normal serum (Francis 1947, Hirst 1948) and various fluids 

 and tissues of susceptible species (Friedewald et al., 1947, Svedmyr 

 i948a,b, Hardy and Horsfall 1948, Schlesinger 1949b, unpublished 

 findings), it may be assumed that these inhibitors are cellular receptors 

 in solution. Active influenza virus is capable of destroying these sub- 

 stances in vitro and also in the infected host, and it is likely, in view 

 of its elutability, that irradiated virus can do the same. Henle's data 

 on the reduction in virus-adsorbing capacity of the allantoic sac after 

 inoculation of irradiated virus (Henle, Henle and Kirber, 1947) are 

 suggestive in that direction, but could as well be due to persistent 

 attachment of the irradiated virus to cell receptors. No attempt has as 

 yet been made to do direct receptor (VHI) titrations either on normal 

 serum or on extracts of membranes after exposure to irradiated virus. 

 It would be of interest to clear up this point, not so much perhaps be- 

 cause of any suspicion that receptor destruction or blockade per se 

 might be responsible for interference, but because of the still valid 

 assumption that receptor destruction is an essential prerequisite for 

 virus entry into the cell (Hirst 1943). 



The hypothesis of receptor destruction or blockade as the mecha- 

 nism underlying interference was formulated when the phenomenon of 

 interference between inactive influenza virus and active homologous 

 or heterologous viruses was first observed by Henle et al. (1943), and 

 by Ziegler et al. (1944). It lost much of its validity — at least as the 

 only factor — when it was shown that (a) the adsorptive capacity of 

 the allantoic sac was not completely blocked by interfering quantities 

 of irradiated virus (Henle, Henle and Kirber 1947), and (b) the inter- 

 fering capacity of the virus was more UV-sensitive than the capacity 

 of being adsorbed by the allantoic epithelium (Henle and Henle 1947). 

 Other evidence in the same direction was obtained in Burnet's and in 

 our laboratory when the "interfering" effect of cholera vibrio filtrates 

 (receptor-destroying enzyme or RDE) was compared with that of virus. 

 The enzyme, while much more effective than influenza virus in de- 

 stroying receptors of the respiratory epithelium (Fazekas de St. Groth 



