INTERFERENCE BETWEEN ANIMAL VIRUSES 187 



Heiile et al., 1947a). It is of interest that Tyrrell and Tamm (1955) reported 

 that interference by heat-inactivated influenza virus could be inhibited by 

 2, 5-dimethylbenzimidazole, a compound thought to have an effect on the 

 nucleic acid metabolism. Interference by mustard- or heat-inactivated virus 

 was slightly inhibited by cortisone (Fong and Louie, 1953; Kilbourne, 1957). 

 Evidence obtained from radiation data suggests that the interfering moiety of 

 influenza virus resides in a minute fraction of the viral particle, perhaps 

 associated with the RN-protein (Powell and Pollard, 1956; Powell and 

 Setlow, 1956). There is, however, no direct experimental basis for implicating 

 viral genetic material in the establishment of interference, except insofar as 

 the material reviewed above points to close functional relationship between 

 interfering capacity, "completeness" of virus, and ability to contribute 

 genetic markers to recombinant progeny. Recent experiments, though con- 

 firming the inhibitory effect of RNAase on multiplication of influenza viruses 

 (LeClerc, 1956), have failed to reveal inhibition by RNAase of interference by 

 UV-inactivated virus with active heterologous virus (Schlesinger and Kuske, 

 1958). 



In contrast to the evidence pointing to intracellular penetration of inter- 

 fering influenza viruses, results of Baluda (1957) suggest that establishment 

 of interference by UV-NDV with active NDV in tissue culture may follow 

 upon superficial attachment of the inactive particles. In this system, treat- 

 ment of monolayers with anti-NDV antibody as late as 90 minutes after 

 adsorption of UV-NDV can prevent exclusion in about 50 % of the cells. 

 "Carrier" clones of pure cell lines persistently infected with NDV are 

 refractory to superinfection with NDV (Cieciura et al., 1957) or VSV (G. Henle 

 et al., 1958). Although the finding of an increased rate of aerobic glycolysis 

 in such carrier cells (Green et al., 1958) points to a fundamental, virus-induced 

 alteration in their function, even they can be "cured' ' of infection by treatment 

 with anti-NDV immune serum (G. Henle et al., 1958). Thus, the ability to 

 remove NDV, and with it resistance to reinfection, from tissue culture cells 

 suggests that this system is not analogous to lysogeny in bacteria. But 

 whether the difference between influenza virus and NDV is of fundamental 

 nature or perhaps reflects the different physiological state of tissue culture 

 as compared with allantoic cells remains to be seen. 



B. Fate of the Superinfecting Virus 



Under conditions of interference in the allantoic membrane, adsorption and 

 "disappearance" of homologous or heterologous active influenza virus is not 

 prevented (Henle et al., 1947a; Isaacs and Edney, 1950a,c). Moreover, when 

 effective interference has been established, the amount of mucoprotein HA 

 inhibitor extractable from allantoic membrane is undiminished (Liu and 



