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Abstract
Le virus héréditaire de la Drosophile, Sigma, peut être propagé au niveau de disques imaginaux d’aile implantés dans la cavité abdominale de mouches adultes. Cette propagation peut avoir lieu à travers les divisions cellulaires même lorsque le variant utilisé est défectif pour les fonctions de maturation (variant u-ρ).
L’étude des modalités de la transmission de cellule mère à cellules filles nous conduit à penser qu’il s’établit un équilibre stable sans que les génomes viraux soient intégrés au génome de la cellule hôte. Cet état porteur serait du type ‘Regulated infection of cells’.
SUMMARY
A variant of σ virus defective for maturation functions was studied. Stabilized flies for this virus were called ultra-ρ flies. They were not CO2-sensitive and extracts were not infectious. The presence of the virus was detected because it conferred to imagos a characteristic immunity against a superinfecting σ virus: these flies were not immunized against a superinfecting virus of the same group, such as vesicular stomatitis virus.
Wing discs were taken from larvae of two ultra-ρ strains (u-ρ46 and u-ρ751) and were exposed to superinfection by implantation into hosts infected with a non-defective σ virus. The blastemas were then implanted into a detector host able to support virus multiplication until the symptom appeared showing superinfection. Control experiments were made with originally virus-free discs. We have thus shown that the characteristic ultra-ρ immunity is present in the imaginal wing disc of ultra-ρ larvae. It is concluded that embryonic blastema cells contain ultra-ρ virus genomes.
In tests on the persistence of immunity through successive transfer generations the results differed with the ultra-ρ strain used. The detector hosts implanted with u-ρ46 blastemas were classified as early CO2-sensitive and CO2-resistant; the number of CO2-resistant hosts did not decrease and the u-ρ46 immunity was therefore stable. On the other hand, the detector hosts implanted with u-ρ751 blastemas were of three classes: early CO2-resistant and late sensitive hosts decreased as a function of time indicating that u-ρ751 immunity was unstable. This instability suggests that blastemas giving late sensitivity are mosaics of ultra-ρ cells and virus-free cells.
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