Chemical InhiblfJon of Viruses 157 



sufficient to protect the host cell from destruction. 



Findings such as these raise the possibility that inhibi- 

 tion of an earlier stage of the reproductive process might 

 have a more beneficial result. There are indications that 

 this is the case. Addition of 5-methyl tryptophane early in 

 the latent period prevents phage reproduction, and, in 

 addition, lysis of the infected host cell does not occur (8). 

 Tryptophane reverses this inhibition, and reproduction 

 recommences at the stage at which it was interrupted by 

 the analogue (10). Similarly, chloramphenicol, if added 

 early in the latent period, prevents both virus reproduction 

 and host cell lysis (5). But neither compound, if added 

 during the latter part of the latent period, prevents de- 

 struction of the bacterial cell (5, 8). Once the reproductive 

 process has proceeded far enough to yield a few new intra- 

 cellular virus particles, the fate of the infected host cell 

 appears sealed. Inhibition of further reproduction does not 

 benefit the cell, and although the yield of virus particles 

 is held to a very small fraction, lysis occurs. Moreover, 

 neither 5-methyl tryptophane nor chloramphenical leaves 

 the metabolism of the host cell unaffected. Both cause re- 

 ductions in protein synthesis (5). 



If the reproduction of animal viruses is not identical 

 with that of phage, there is a possibility that the results 

 obtained with the phage inhibitor systems may have little 

 bearing on animal virus inhibitor systems. There are a 

 number of indications that animal viruses are markedly 

 different from phages. As an example, no animal virus 

 has been shown to possess a tailed structure. This append- 

 age appears to be a constant feature of phage morphology 

 (41) and is considered to provide the physical means for the 

 introduction of phage nucleic acid into the bacterial cell 

 (26). As was indicated earlier, there is no incontestable evi- 

 dence that animal virus particles are disrupted or frag- 

 mented on penetrating susceptible host cells. With phage, 

 such disruption, demonstrated in the case of T2 (26), is 



