COLD AND VIRUS INFECT I VITY 



Nell et al., (1961) reported similar findings in an earlier publica- 

 tion which dealt with infected chick embryos. Accompanying the rise 

 in virus titer and enzyme content was a corresponding drop in the 

 concentration of membrane inhibitor. This finding tended to support 

 the contention of Isaacs and Edney (19 50) who indicated a role for in- 

 tracellular receptors in influenza infections on the basis of a corre- 

 lation between the effectiveness of indicator viruses as interfering 

 agents and their position in the "inhibitor gradient" of allantoic mem- 

 brane extracts. The time of appearance of enzyme depended on the 

 speed ofvirus growth. When 10 LD5Q doses were given, enzyme for- 

 mation was usually detected after 12 hours. If the number of LDgQ 

 doses administered was increased to 10 ''', enzyme formation was ob- 

 served between 6 and 9 hours. These results were in agreement with 

 previously reported findings on virus multiplication by Henle(1953) 

 and Acker mann and Francis (19 54). When the environmental tempera- 

 ture was decreased to 20° C, virus growth failed to materialize, no 

 enzyme was fabricated and the inhibitor level remained unchanged. 



Once the relationships of enzyme fabrication, virus growth, and 



inhibitor decline had been shown in embryos, attention was directed 



to these same considerations in influenza infected mice. Albino mice 



o 

 were infected intranasally with mouse adapted A2 and Al strains. 



Two groups of mice were established, one group- caged at the normal 

 animal room temperature of 20° C, and the other at 4° C. The mice 

 placed at 4° C were individually caged in plastic containers without 

 bedding material. Water was added to the containers in amounts ade- 

 quate to give a thindiscontinuous film of moisture covering the floor. 

 The mice were maintained at4°C until signs of distress were noted. 

 These included shivering, ruffled fur, apathy to stimuli, and blanched 

 ears. Mice from the two groups received an inoculum previously de- 

 termined to give 50 per cent lung consolidation at 48 hours in mice 

 maintained at 20° C. An equal number of control mice from the two 

 groups received an inoculum of sterile saline. Further control mice 

 were inoculated to determine the 50 per cent lung consolidation end- 

 point. Mice from test and control groups at 20° C and 4° C were 

 sacrificed at 0, 8, 24 and 48 hours. Lungs and trachea were exam- 

 ined for their virus titer, enzyme, and inhibitor content, 



2 Obtained through the courtesy of Dr. T. Francis, Jr., School of Public Health, Uni- 

 versity of Michigan, Ann Arbor, Michigan. 



355 



