CO2 SENSITIVITY INDUCED BY 2 RHABDOVIRUSES, PIRY AND CHANDIPURA, IN DROSOPHILA-MELANOGASTER

Abstract

Piry and Chandipura [CHP] viruses induce CO2 sensitivity after multiplication in D. melanogaster. Flies infected with Piry virus react to CO2 like flies infected with .sigma. virus: after a post-infection delay the flies becomes sensitive; sister batches exposed later on remain persistently CO2 sensitive. Flies infected with CHP react to CO2 like flies infected with VSV: flies become sensitive, but sister batches exposed later on recover and fail to show any CO2 sensitivity, although they remain infected with virus. Results were consistent with the hypothesis that at the CO2 site (nervous system) a definite rhythm of budding site production which transforms the plasma membrane, is necessary for the CO2 sensitivity. Flies inoculated with CHP present a distinctive feature: below a definite temperature the flies do not become CO2 sensitive although it is still possible to observe a slight multiplication. The results from shift-up and shift-down experiments suggest that there is a cryosensitive event in the viral multiplication. The experiments on the survival of infectious centers show that this event is implicated in the maturation step. Previous CO2 exposure influenced CO2 sensitivity when expression of viral functions were restricted by temperature, by a protective action probably produced by a cellular repair mechanism of non-lethal lesions. When compared with VSV strains Brazil and New-Jersey, Piry and viruses are moderately adapted to Drosophila. Like VSV, SVC virus and PFR, the Piry and CHP viruses were not found in progeny of infected flies, while with .sigma. virus L''Heritier showed that CO2 sensitivity is hereditary.