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From the Department of Microbiology, The University of Texas, Southwestern Medical School, Dallas, Texas
Abstract
The immune response of bats, guinea pigs and rabbits to a series of three primary injections and a booster injection of bacteriophage
X174 was studied. Antiphage activity developed more rapidly in bats maintained at 24°C and 37°C than in other animals, but the magnitude and duration of the primary response was less, particularly in 24°C bats. Deviations in the percentage of phage inactivated by bat plasma pools from the mean indicated indirectly that individual 24°C bats varied considerably in their response to
X174. Prolonged primary production of ME-sensitive antibody was observed in 24°C bats, and 37°C bats had a large proportion of ME-sensitive antibodies throughout the first 21 days. Kinetic studies of
X174 inactivation indicated that 37°C bat antibodies developed during the latter part of the primary response did not bind phage irreversibly. Some instability was also noted in interactions between a diluted 35-day guinea pig antiserum and
X174. A booster injection of
X174 enhanced the neutralizing capacity of antibodies produced in all three animal species. Approximately 40% of the antiphage activity in 10-day postbooster plasma pools from 24°C bats was due to ME-sensitive antibody. Guinea pigs, rabbits and 37°C bats had little detectable ME-sensitive antibody during the secondary response by the assay procedures used. While the rate and extent of phage inactivation by a 30-day postbooster plasma pool from 37°C bats greatly exceeded that obtained with a comparable pool from 24°C bats, bat antibodies did not inactivate
X174 as rapidly or to the same degree as 30-day post-booster guinea pig or rabbit antisera. From these results it was concluded that the primary and secondary immune response of bats to immunization with
X174 was quantitatively and qualitatively less than the response of rabbits and guinea pigs to the same stimuli.
Footnotes
This investigation was supported in part by United States Public Health Service Research Grant AI-02316 from the Institute of Allergy and Infectious Diseases and National Science Foundation Grant GB-6612.
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