INACTIVATION OF VIRUSES 371 



For influenza viruses, Buzzell et al. (1955) also found exponential inactiva- 

 tion curves. Calculations indicated that infectivity may be associated with a 

 single sensitive volume, about | that of the virus. (In the paper by Buzzell 

 et al. (1956), Table II, this estimate was changed to -^^ ; mainly because a 

 different average value was assumed for the number of ionizations per cluster.) 

 The authors also studied hemagglutination after irradiation of dried virus. 

 They found an mactivation curve corresponding roughly to a "3-liit" pheno- 

 menon. The data did not permit a closer analysis of the mechanism of 

 inactivation. 



With TMV, irradiated in concentrated suspensions, autoprotection against 

 radicals was observed by Lea et al. (1944). This was confirmed by BuzzeU et 

 al. (1956), who obtained indistinguishable inactivation curves in 0-8 % and 

 25 % broth, w^hen the virus concentration was as high as 0-2 % (by weight). 

 As in the case of phage T5, survivors showed no change in heat resistance. On 

 the usual assumption that one primary ionization in the target inactivates 

 the particle, the D^ — dose of 2-3 X 10^ r gives a target volume which is 

 almost equal to the RNA volume, as estimated by Hart (1955a). Moreover, 

 according to radiation analysis by PoUard and Whitmore (1955), this target 

 is asymmetric and about as long as the virus rod (see Section II, B, 2, h). 

 This suggests a rod-shaped target about 40-50 A in diameter and 3000 A long, 

 in very satisfactory agreement with present ideas about the genetic signifi- 

 cance of the RNA (Gierer and Scliramm, 1956) and its distribution along the 

 axis of the virus rod (Hart, 1955b). The mean wavelength of the X-rays used 

 was 0-2 A; in a target of diameter 40-50 A, most electrons produced none, and 

 few more than one primary ionization while traversing the target. Altogether, 

 it looks as if, in the case of TMV, primary ionizations that occur in the 

 "genetic target" are 100 % effective in causing inactivation. Furthermore, 

 determinations of the viscosity of RNA prepared from irradiated TMV, sug- 

 gested that each target ionization produced one, randomly located, conqjlete 

 break of the RNA rod (Lauffer et al., 1956). 



In this connection, multiplicity reactivation of phage inactivated by X-rays 

 shoidd be mentioned. Weigle and Bertani (1956) have shown that the ab- 

 sence of multipHcity reactivation under the usual conditions is due to X-ray- 

 damaged phage not properly injecting its DNA into the cell after adsorption; 

 presumably, because the mactivating ionization has caused rearrangements 

 or breakage that interfere with the smooth passage of the DNA from phage 

 to bacterium. If the inactivating X-ray treatment is applied immediately 

 after injection into a bacterium of the DNA from 2 or more phage particles, 

 powerful multiplicity reactivation is observed. 



Of interest in connection with determinations of target volumes are the 

 experiments of Adams and PoUard (1952), which show that, at temperatures 

 above about 45°C., the estimates of the target volume of dried Tl increase 



