COLD AND VIRUS INFECTIVITY 



MET CALF: I wondered if you felt this to be a condition which 

 might prove deleterious to your theory. 



WALKER: No, I think that this is reasonable. This is just 

 another selective pressure, and we will have the same problems 

 with selection that will apply to any other explanation of the 

 effect of temperature on infection. 



CAMPBELL: I might point out that it is pretty well known 

 that in neonatal animals there is a question whether they pro- 

 duce any antibodies at all so that when you expose them to anti- 

 gen, they may actually exhibit a so-called tolerance or immune 

 paralysis. Their immune mechanism is not working at this point. 

 You had an exposure of six days at 25*^ C. 



WALKER: And then a shift to cold. 



CAMPBELL: Yes, and then in this case, you didn't have any 

 effect. 



WALKER: Right. 



CAMPBELL: I was wondering whether you thought that this 

 exposure, some way or another, actually causes an adaptation. 



WALKER: The point was, if they were held at ordinary room 

 temperature for as long as six days after receiving virus, then 

 the shift to 4° C had no effect, but after only four days, the cold 

 still caused high mortality. My explanation or speculation is 

 this; by six days, the virus has been reduced to very low levels 

 in practically all of the tissues except the pancreas. By that 

 time, there is still a lot of antibody in the blood, and although 

 virus activity might be increased in the pancreas, there would 

 be no opportunity for it to be disseminated widely to other tis- 

 sues that would be made more susceptible by the lowered tem- 

 perature. The virus must be widely spread to cells before anti- 

 body appears in the blood, and the exposure to cold must occur 

 while there is still a sufficient quantity of virus in the tissues. 

 I would expect in most of these tissues that the virus is pretty 

 well gone by six days. 



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