WALKER 



In any consideration of mechanisms that might account for the 

 effects of cold on viral infection two possibilities quickly come to 

 mind. One is that host defenses are modified by exposure to cold, 

 and the second is that cold acts as a stressing agent and modifies 

 the host through alteration of hormone balance. 



The host defense most frequently considered and seems particu- 

 larly pertinent in viral infection is antibody production. The effect 

 of cold on antibody production has been discussed by others in this 

 meetir^, but I want to point out that Marshall (19 59) considered the 

 possibility of inhibition of antibody production in his study of rabbit 

 myxomatosis andshowedthatunder the conditions of his experiments 

 antibody against sheep erythrocytes developed as rapidly and to as 

 high levels in rabbits exposed to cold as in control rabbits. 



In our study of Coxsackie virus infections in mice. Boring and I 

 have never actually measured the antibody developed against Cox- 

 sackie virus in mice at4°C, because we found that cold still exerted 

 its effect even if we delayed exposure of infected mice until the anti- 

 body producing process was well under way (Boring et al,, 1956), 

 Specific neutralizing antibody appears in the blood of mice on the 

 third day after inoculation with small quantities of Coxsackie Bl vi- 

 rus and on the fourth day the antibody is at substantial levels (Fig, 4; 

 Boring and Walker, unpublished data). Even though exposure to cold 

 is delayed until the fourth day, its effect is not nullified (Fig, 2), 

 This suggests to us that even if cold were found to have an in- 

 hibiting effect on antibody production, this would still not explain 

 the influence of cold on the infection. In addition to this, current 

 work using mice thymectomized at birth indicates that an adult 

 mouse does not develop a generalized lethal infection with Coxsackie 

 Bl virus even though the mouse is incapable of producing antibody. 



Other host defenses such as non-specific viral inhibitors and 

 interferon may conceivably be altered by cold, but there is little 

 positive evidence for this, as yet. 



The role of stress is difficult to assess. There is little question 

 that the cold exposure used inthe studies that I have discussed were 

 of a degree sufficient to cause some of the physiological changes 

 identified with stress. And treatment of animals with large doses of 



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