METCALF 

 DISCUSSION 



The measure of infectious virus used in the study was the ability 

 to multiply sufficiently within a host cell to damage it by means of 

 enzymic attack. The direct relationship shown between cell damage 

 and neuraminidase production led to this conclusion. Proceeding on 

 this basis, the results indicated that cold had no effect per se upon 

 the infectious quality of virus. For example, the penetration of a host 

 cell was not affected, and the in vitro effect upon neuraminidase ac- 

 tivity was minimal. Instead, cold was shown to exert an influence on 

 the host- parasite relationship subsequent to virus penetration. The 

 findings suggested that cold acted to alter some host structure im- 

 portant for defense and accordingly render the cell more vulnerable 

 to enzyme action. It was postulated that the structure affected by cold 

 was mucoprotein in nature. This viewpoint would represent a modi- 

 fication of Gottschalk's enzyme penetration theory (19 57), The impor- 

 tant difference lies in the relationship of enzyme activity to cell 

 damage in the present study, rather than cell penetration. 



The results were an extension of the findings of Sulkin (1945) who 

 reported a more serious infection in cold exposed mice with little 

 change in mortalities. The fatalities occurring in the present study 

 were attributed to a combination of enzymic competence of the virus 

 strains used and physiologic insult sustained by the mice. 



The findings of the present study constituted an interesting con- 

 trast to the results reported by Sarracino and Soule (1941), These 

 authors suggested that infection depends on the amount and virulence 

 of virus rather than the general resistance of the host. My study 

 indicated that virus possessir^ enzyme activity was infectious and 

 thus virulent. It also showed that the severity of influenza infections 

 was not the exclusive result of virus virulence, but could be con- 

 ditioned by cold-induced physiologic alterations within a host. 



An attempt at translation of the results of the present study in 

 terms of the "winter factor" of Andrewes (1958) would be presump- 

 tuous. The results did suggest, however, that a study of physiologic 

 alterations of mucoprotein. structures of a cell exposed to virus 



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