PROCESS OF INFECTION AND VIRUS SYNTHESIS 25 



Presmniiigtlie data plotted in Fig. 9 to be preponderantly a reflection of the 

 rate of spread of virus from cell-to-cell, an estimate of the spreading rate on a 

 cellular basis can be made and compared to the rate ascert-iiiied by measuring 

 lesions in the local lesion host. The leaves that were nibbed had an area of 

 about 150 cm.2 The concentration of virus, lO^^ mg. TMV/ml., would lead to 

 the expectation that the infection probably arose from about 10^ foci of 

 infection. The surface of the leaf is estimated to contain 10^ ceUs. If the bend 

 in the logarithmic curve at 10 days represents the time when most of the cells 

 on the surface have been infected, we arrive at the notion that 10-^ cells 

 become infected from each focus in 240 hours. The area occupied by 10^ cells 

 would be about 15 mm.^ or a radius of a circle of 2.3 mm. If the average cell 

 diameter is about 30 microns, and tlie radius increases at the constant rate 

 of 230 microns per day, we arrive at the figure of 8 cells per day that become 

 infected along a radius extending from a focus of infection. Crude as the esti- 

 mate may be, it suggests that the rate of spread of virus infectivity in the 

 two different hosts does not differ by a large amount. 



In 1934, Uppal measured the time required for TMV infectivity to travel 

 tlirough the cells between the upper and lower epidermis of N. sylvestris 

 leaves, the latter being another systemic host for the common strain of TMV. 

 The rate of movement in this direction was found to be 7 to 8 microns per 

 hour, which is the same order of magnitude estimated from the experiments 

 of Goodchild et al. 



Yarwood(1952) has determined the earhesttime that an increase in amount 

 of infectivity can be detected after rubbing N. tabacum leaves with the common 

 strain of TMV and tobacco necrosis virus. While there is considerable scatter 

 of the experimental points, when aU of the results of a large number of trials 

 are plottedas the logarithm of amount of infectivity versus time after inocula- 

 tion, the pattern is clear. For about 8 hours after inoculation, no change in 

 virus infectivity occurs. Then, from the 8th to the 14th hour, an exponential 

 rise in the amomit of infectivity occurs. Thus, Yarwood proposes that TMV 

 undergoes a latent period of about 8 hours, and then the infectivity begins 

 to multiply such that the amount doubles with each succeeding hour. 

 Tobacco necrosis virus undergoes a longer latent period and doubHng time. 

 Since Yarwood's common strain of TMV is probably identical \\ath strain 

 Ul, it is significant to note that the latent period in the systemic host corres- 

 ponds very nicely with the time before an increase in resistance to inactiva- 

 tion by radiation can be detected in the local lesion host. 



Thus, we have two pieces of evidence, the latent period * and the rate of 

 spread of the infectivity from ceU-to-cell, which imply that the fundamental 



* Note added in proof: Schramm and Engler, Nature, 181, 916(1958), have found a 

 latent period of 30 hours for TJVIV in N. tabacum. The latent period is shortened by 

 10-12 hours when the infection is commenced with TIVIV infectious nucleic acid. 



