The CO2 sensitivity induced by two rhabdoviruses, Piry and Chandipura, in Drosophila melanogaster.

Piry and Chandipura 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 become sensitive; sister batches exposed later on remain persistently CO2 sensitive. Flies infected with Chandipura virus 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. These are consistent with the hypothesis that at the CO2 site (nervious system) a definite rhythm of production of budding sites, which transform the plasma membrane, is necessary for the CO2 sensitivity. Meanwhile, flies inoculated with Chandipura virus 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 cyrosensitive event in the viral multiplication. The experiments on the survival of infectious centers show that this event is implicated in the maturation step. With a study of the influence of previous CO2 exposure on CO2 sensitivity, when the expression of the viral functions are restricted by temperature, CO2 is whown to have 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 Chandipura viruses are moderately adapted to Drosophila. Like VSV, SVC virus and PFR, the Piry and Chandipura viruses have not been found in the progeny of infected flies, while with sigma virus "l'héritier has shown that CO2 sensitivity is hereditary.