Factors Influencing Host-Virus Interactions

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Abstract
Summary: Exposure of adult mice to a cold environment (4°C) causes a loss of resistance to infection with the Conn.-5 strain of Coxsackie virus. In some respects this decrease in resistance appears similar to that brought about by treatment of mice with cortisone. Because this suggested that increased adrenocortical secretion stimulated by cold might be the mechanism by which cold exposure alters susceptibility to Coxsackie virus infection, experiments were designed to test this possibility. It was found that ACTH in doses sufficient to cause weight loss did not produce a detectable effect upon resistance to Coxsackie virus infection. A two-week period of adaptation of mice to cold prior to infection did not nullify the resistance reducing effect of the cold environment. When the effect of elevated environmental temperature (36°C) was compared with that of cold it was found that although the elevated temperature was a more adverse environment than the cold, as indicated by body weight gain, it had an opposite effect to cold and caused a marked inhibition of viral invasion and multiplication. It was further found that when exposure to a 36°C environment was applied as late as 36 hr after initiation of the infection at a time when viral multiplication was already well under way in the pancreas, viral multiplication was suppressed and the virus rapidly eliminated. These data were interpreted as strongly suggesting that the loss of resistance to Conn.-5 strain Coxsackie virus infection seen in adult mice at 4°C is not a consequence solely of adrenocortical hypersecretion.

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