PKOCESS OP INFECTION AND VIRUS SYNTHESIS 27 



necessarily invading the cells that enclose the phloem.^ I suspect that virus 

 does not impair the normal fimctiomng of phloem in the systemic host, but 

 kills the phloem in the local lesion host. Impairment of the phloem may occur 

 before the infectivity can be transported, with the result that the virus is, 

 perforce, confined to the lesion. Preliminary microscopic observations, made 

 by Warren Furumoto in my laboratory, indicate that disorganizational 

 changes in phloem cells can be observed in the proximity of an encroaching 

 lesion. Such changes suggest that loss in phloem vitahty precedes necrosis of 

 the mesophyll cells in contact with the phloem element. It could be imagined, 

 also, that mesophyU ceUs in the presence of impaired phloem are somewhat 

 analogous to an animal with impaired kidney and liver function. The cells 

 can no longer obtain or discharge the products normally transported by the 

 phloem. Thus, the possibihty exists that necrosis of the cell is not the direct 

 result of virus multiphcation, but is secondary in origin, and that the local 

 lesion host cell dies before reaching its fuU potential for virus synthesis. It 

 is also significant that with some other plant viruses, such as curly top, wheat 

 streak, etc., Esau (1956) finds phloem necrosis to be the first evidence of the 

 presence of virus. 



Holmes' recent review (1954) provides many examples of genes controll- 

 ing the type of host response produced by plant viruses. In tobacco, a single, 

 dommant gene is sufiicient to determine whether TMV in an N. tabacum 

 plant wall be confined to local necrotic lesions or will become systemic. Ex- 

 tending the above speculation, it could be imagined further that gene action, 

 in this instance, determines whether or not the virus can multiply in the 

 phloem. 



E. Effect of Virus Synthesis on Composition of Host Proteins 



The changes in host protein composition induced by TMV in a systemic 

 host have been the subject of several investigations (Wildman et al. 1949- 

 Commoner et al., 1952; Bawden and Kleczkowski, 1957); it is to be regretted 

 that there is still nonuniformity of results of the various investigators. We 

 have repeatedly found that, as the virus in directly inoculated leaves in- 

 creases in quantity, there is a corresponding decrease in soluble host proteins. 

 Other workers, applying the same technique of electrophoresis for measuring 

 virus and host proteins, arrive at the conclusion that no such relationship 

 can be clearly demonstrated. The discrepancy may be due to the use of 

 different kinds and concentrations of buffers during the extraction of the leaf 

 proteins. 



* Cohen et al. (1957), on the basis of experiments dealing with competition between 

 strains Ul and U2 in a systemic host of TMV, have presented a theory to account for 

 the origin of the systemic infection in leaves other than the leaves that were inoculated. 



