VIRUSES 



52 



We have seen thus far that all of the data examined show that the percent- 

 age response of a host to disease depends upon the concentration of the virus in 

 a manner consistent with the assumption that virus infection is the result of a 

 single virus particle coming into contact with a favorable position within the 

 host. The data exclude absolutely the possibility that it is necessary for more 

 than one infectious unit to cone in contact with a favorable location. I'he fact 

 that the data agree with the theory does not prove, however, that this mechanism 

 is correct. It has already been seen that a curve very similar to the one which 

 the data fit can be derived from the assumption that tlie differential response 

 at various levels is due to variation of host susceptibility. Thus it is neces- 

 sary to try to decide between the two theories: (1), that dosage response is due 

 to chance occurrence of at least one virus particle in a favorable region within 

 the host, and (2), that dosage response is due to variation of the auBceptibil- 

 ity of hosts. There are three lines of evidence to indicate that the latter 

 alternative is completely untenable. The first line of evidence is shown in 

 JJ'igure 42, which contains data obtained for 10 different viruses affecting plants 

 and animals . 



LOG CX) + LOG {vii) 



FIGURE 42 - PR/iCTIOllAL HESPOHSE PLOTTED AGAINST LOG 

 VIRUS CONCEUTRATIOIT FOR TEN DIFFERENT VIRUSES AFFECT- 

 ING PLANTS AND ANIMALS. 



10 



When the fractional response is plotted against logarithm of concentration of 

 virus applied, all of the data can be fitted to the same curve. This is the 

 curve of the equation derived from the assumption that one virus particle can 

 initiate an infection if it happens to be in a favorable position. The curve 

 which could be derived from the second alternative, that is, the theory that 

 dose response is due to host variation, is slightly different from this curve, 

 and the data do not fit it quite as well. This constitutes evidence that the 

 first theory is to be preferred to the second. 



The second line of evidence is also contained in Figure 42. It can be 

 seen that 10 different viruses, each with its own host, either plant or animal, 

 show identical concentration ranges between the region of virtually complete 

 response smd the region of virtually no response. This result is a necessity 

 if the theory is correct that response is due simply to the probability of find- 

 ing a virus particle in a susceptible region. However, this result is not a 

 necessary consequence of the theory that doae response is due to variation in 

 host susceptibility. As a matter of fact. In order to rationalize a result such 

 as this with the host variation theory, it would be necessary to make the ad- 

 ditional postulate that the variability in host response to viruses is the same 

 for widely different hosts throughout both the plant and animal kingdoms . In 

 other words, it would be necessary to assume that the variation in the suscepti- 

 bility in rabbit skin to vaccinia virus is the same as the variation in the 

 susceptibility of the tobacco leaf to tobacco mosaic virus. Such an assumption 

 borders on absurdity. Therefore, one is justified in regarding the necessity 

 of making such an assumption as strong evidence against the tenabillty of the 

 theory that dose response is the result of host variation. 



