SULKIN AND ALLEN 



be a modification of the virus strain, Sadler and Enright (1959) have 

 recorded the suppressive effect of low temperature on rabies in- 

 fection in bats and have correlated it with the lowered metabolic 

 rate of the animals. These investigators found no evidence of rabies 

 virus multiplication in animals placed at low temperature immedi- 

 ately after virus inoculation, but if infection were allowed to develop 

 for 6 days at 22° C prior to transfer of animals to 4 C, some evi- 

 dence was obtained of virus multiplication in the brains of animals 

 which died after 30 to 90 days in the cold. 



The experimental data recorded to date on the influence of low 

 temperature on rabies virus infection in bats suggest that winter 

 hibernation may have a profound effect on natural rabies infections 

 in these animals. There is no doubt that the period of winter dor- 

 mancy could exert a sparing effect perhaps sufficient to maintain a 

 constant state of latency in a large population. In addition, there is 

 the suggestion that rabies virus particles which overwinter in the 

 tissues of the bat and are subject to either complete dormancy or a 

 shift to a much decreased rate of multiplication may be altered by 

 this period at below optimum temperature. 



Because the big brown bat is highly susceptible to Japanese B en- 

 cephalitis virus and suffers an infection which can be characterized 

 as to incubation time, duration of the initial infectious phase, and 

 antibody response, the format of our low temperature studies with 

 this virus-host system is more inclusive than has been possible in 

 work with rabies virus. Assuming that in a given population animals 

 would vary as to the stage of their natural arbovirus infection, we 

 are studying the effects of simulated hibernation on groups of ani- 

 mals which are pre-viremic, viremic or post-viremic, and immune. 

 The results of these studies allow us to speculate along the following 

 lines: (1) bats which enter hibernation soon after receiving an in- 

 fective dose of Japanese B encephalitis virus, but before infection 

 has developed to demonstrable levels, would be capable of sustaining 

 infection through months of winter hibernation and upon arousal in 

 the spring provide infective blood for feeding vectors; (2) bats which 

 enter hibernation with hightitersof Japanese B encephalitis virus in 

 blood and tissues apparently suffer a prolonged infection, possibly 

 due to the suppression of antibody production in the cold; (These 

 animals could provide infective blood for at least a month for mos- 



388 



