MECHANISM OF ANTIBODY FORMATION 93 



the viruses may lie latent permanently in plants and animals yet cause 

 no discernible harm, e.g., the virus of King Edward potato plants, 

 which cause them no perceptible trouble, though capable of killing 

 plants of other varieties, or the virus from human "fever blisters" which 

 causes encephalitis in an inoculated rabbit. The "latent" viruses stimu- 

 late in the animal host the formation of specific protective antibodies. 



According to Dixon (1945), a lasting immunity to viruses demon- 

 strable by complement fixation, agglutination, precipitation and 

 neutralization following one attack in an animal, may depend on the 

 kind of tissue infected and is probably due to a long-term sojourn or 

 persistence throughout the life of the host. Lasting immunity may 

 not be obtained to influenza or to the common cold virus because the 

 superficial cells lining the respiratory tract are being thrown off at 

 intervals to be replaced by deeper cells and thus do not provide a 

 permanent abode for these viruses. It may further be stated that all 

 studies so far carried out, and intended to determine the relation of 

 the duration of antigen to antibody production in a host, show that 

 the disappearance of antigens (some tagged with radioactive atoms) 

 from host tissue results in the cessation of antibody production (Ehrich, 

 etal 1945; Herdegen, et al 1947; Libby, 1947). 



According to Taliaferro (1932, 1938) when a trypanocidal crisis is 

 permanently effective, it is because the few parasites which escape 

 destruction cannot produce a relapse because they are prevented from 

 reproducing by anti-reproduction (ablastin) antibody. According to 

 Packchanian (1934) when the animal has recovered from reinfections, 

 it is quite possible that all the trypanosomes (Trypanosoma hrucet) 

 have been destroyed, at least in the blood. If a few latent ones do exist, 

 they are so attenuated that they cannot produce any detectable in- 

 fection in subinoculated test animals. Those reinoculated forest deer 

 mice are considered relatively immune to further reinoculation with 

 Tr. hrucei. Experimental data indicated that even in certain individuals 

 of forest deer mouse (P. L. novehoracensis^ , prolonged and indefinite 

 latency was associated with a few surviving trypanosomes. Thus, 100 

 days after the initial inoculation, the animal was etherized and almost 

 its entire heart blood, 0.5 ml., was injected into a rat. The latter animal 

 was observed for five months and failed to show symptoms of nagana. 

 The heart, lungs, liver, spleen, kidneys, brain, muscles, and part of the 

 bone marrow and glands of the same mouse were ground into pulp in 



