26 S. G. WILDMAN 



behavior of TIVIV as an infectious entity is similar in both the local lesion and 

 systemic host. Considering this evidence, I would therefore suggest that 

 Zech's observations on virus activity in leaf hairs depict an interesting special 

 case of virus activity in a particular type of leaf cell, but the question remains 

 as to whether they are applicable to virus behavior in other cells of the leaf. 

 In connection with virus activity in leaf hairs of N. glutinosa, Dr. Morris 

 Cohen and I have made repeated attempts to cause lesions to arise as the 

 result of wounding individual leaf hairs in the presence of TMV. Similar to 

 the findings of Sheffield (1936) and Hildebrand (1943), an occasional lesion 

 would appear, but the frequency of success was miniscule. AATien more precise 

 wounding was attempted with a micromanipulator, success dropped to zero 

 in more than 100 trials. We have also tried to infect detached hair cells with 

 no success, even though the hairs would continue to show evidence of proto- 

 plasmic streaming three weeks after detachment. In other experiments, we 

 have plasmolyzed the hair cells before detachment, so that a cut could be 

 made through the ceU without disturbing the protoplast, but leaving the 

 protoplast directly exposed to the virus-containing medium. The vitality of 

 the cell is unharmed, as judged by continuance of protoplasmic streaming, but 

 we found no evidence to suggest that exposure of the naked protoplast to 

 TMV or to infectious nucleic acid, led to earlier disorganization of the pro- 

 toplast than controls in the absence of virus. Exposed protoplasts remained 

 streaming for about four days, or twice the time required for the development 

 of a respectable lesion. Consequently, I wonder if hair cells on N. glutinosa 

 leaves even participate in virus infection, except perhaps to transport the in- 

 fectious material to other cells where the infectivity can multiply. 



D. Necrosis and Phloem Cells 



How can we account for the fact that the vitahty of a ceU invaded by virus 

 in the local lesion host is destroyed, whereas in the systemic host the cell 

 remains aHve? Further, how can we account for so much less virus being synthe- 

 sized in the cell that dies compared to the cell that lives? I am tantalized by 

 another of Zech's observations (1952) that might provide a clue leading to an 

 explanation. He observes signs of virus activity in every kind of cell in the 

 leaf except phloem cells. Phloem cells form a part of the tissue responsible 

 for transporting organic materials, such as sugars formed by photosynthesis, 

 from the leaves to other parts of the plant, and supply organic materials 

 necessary for the integrity of leaf cells. They are hving cells terminating in 

 the vein endings of leaves which abut on mesophyU cells. There is much 

 evidence to show that virus is spread in the systemic host via the phloem 

 (Bennett, 1940), and that virus transport is a passive affair. Virus can pass 

 out of the leaf through long distances of stem to enter other leaves, without 



