TEMPERATURE AND VIRAL INFECTION 



C3^es will adsorb to 50 per cent or more of cells and the virus con- 

 centration in the medium increases by 10 to 100-fold indicating that 

 at the lower temperatures the equilibrium between cells and virus 

 is upset and there is much more virus production and release in the 

 cultures. 



Lwoff (19 59) has emphasized the narrow zone of optimum tempera- 

 ture for viral multiplication and the inhibitory effect of elevated tem- 

 perature to argue that fever may be an important host defense 

 mechanism in choking off viral infection, and he has pointed to the 

 variation in optimum temperature among virus strains as a partial 

 explanation of variation in virulence. It seems to me that these phe- 

 nomena can also explain some of the observed effects of cold on viral 

 infection and, indeed, may even accountfor the variability of obser- 

 vations, I suggest that one can expect to see an effect of cold on viral 

 infection under certain circumstances. The appropriate circum- 

 stances would be when an animal (or man) is infected with a virus, 

 or a particular strain of a virus, that has an optimum multiplication 

 temperature a degree or two lower than the body temperature of the 

 host. Under these circumstances the body temperature of the host 

 could be an important controlling factor in limiting viral multiplica- 

 tion and in keeping the infection a mild, or inapparent, or latent one. 

 And lowering the temperature in the right tissues (surface or inter- 

 nal, depending on the virus) only a degree or two could result in a 

 markedly increased pace ofviral multiplication, and thus lead to ob- 

 vious aggravation or activationof the infection. Under these circum- 

 stances we would not expect to see an effect of cold unless the ex- 

 posure were sufficient to bring about an appropriate drop in temper- 

 ature in the right tissues. Nor need we expect to see an enhancing 

 effect on a highly virulent virus with a temperature optimum near 

 that of the host tissue.With certain host-virus combinations even an 

 ameliorating effect of cold might be expected if the tissue tempera- 

 ture could be dropped below and maintained below the optimum tem- 

 perature range of the virus. This concept of an effect of cold due to 

 direct influence onviral multiplication processes within the host cell 

 does not, of course,in itself exclude the possibility that stress, or 

 other physiologic changes due to cold, may contribute to the reaction. 

 But it seems to me that many of the demonstrations of an effect of 

 cold on viral infection can be accounted for on the basis of a direct 

 effect of tissue temperature on intracellular reactions. 



335 



