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Volume 8,
Issue 3,
1970
Volume 8, Issue 3, 1970
- Articles
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Ultrastructural Features of Canine Distemper Virus Infection of the Chorioallantoic Membrane of the Hen’s Egg
More LessSUMMARYThe chick embryo chorio-allantoic membrane was examined 6 days after inoculation of the ondestepoort strain of canine distemper virus. Multinucleated cells containing cytoplasmic inclusions were observed in the chorionic epithelium. These inclusions consisted of randomly arranged nucleocapsid filaments. The filaments had an outer lightly staining layer of radial fibrils in addition to their dense core. Budding and mature virus particles were observed less frequently. The morphological stages of distemper virus replication resembled those reported for measles and rinderpest viruses in other systems.
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Effect of U.v.-irradiated Vesicular Stomatitis Virus on Nucleic Acid Synthesis in Chick Embryo Cells
More LessSUMMARYWhen monolayer cultures of chick embryo cells were infected with the new jersey serotype of vesicular stomatitis virus at high input multiplicities, the synthesis of cellular RNA was rapidly inhibited. The stimulation of cellular DNA synthesis observed in control cells following medium replacement was also inhibited in the infected cells. These activities of vesicular stomatitis virus on the synthesis of cellular nucleic acids were quite resistant to u.v. irradiation, although no virus RNA synthesis was detected in the cells infected with u.v.-irradiated vesicular stomatitis virus. No stimulation of degradation of cellular nucleic acids was observed in cells treated with irradiated vesicular stomatitis virus.
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Antibody-neutralized Avian Infectious Bronchitis Virus in Chicken Embryo Kidney Cells: Entry and Degradation
More LessSUMMARYThe interaction of avian infectious bronchitis virus with the chicken embryo kidney cell was studied before and after neutralization by homotypic antiserum containing only 7s (IgG) antibody. Entry of virus into the cell, measured by the ability of antibody to neutralize only extracellular virus, occurred at 37° and 25° but not at 4°. To study entry of neutralized virus, infectious bronchitis virus was adsorbed and then neutralized at 4°. The cells were incubated at 4° (control), 25°, or 37°. Antibody was dissociated from extracellular neutralized infectious bronchitis virus with a pH 2.0 buffer solution which subsequently reactivated the virus. This acid treatment for 10 sec. did not dissociate the virus from the cell or injure the cell. Antibody did not enhance or suppress elution of infectious bronchitis virus from the cell. Neutralized infectious bronchitis virus either merged with the cytoplasmic membrane or was pinocytosed at 37° and 25°; however, the neutralized virus remained extracellular at 44°. After the neutralized virus had interacted with the cytoplasmic membrane, it was not readily accessible to acid and could not be reactivated. The entry of virus without antibody was faster than that for virus with antibody. After 1 hr at 37°, the % uncoated virus RNA in cells with unneutralized virus remained essentially constant. However, in cells with neutralized virus the % uncoated virus RNA decreased and the acid-soluble material increased simultaneously.
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Etude Génétique du Virus de la Stomatite Vésiculaire: Classement de Mutants Thermosensibles Spontanés en Groupes de Complémentation
More LessSOMMAIREL’isolement de mutants spontanés thermosensibles a permis d’entreprendre l’étude génétique du Virus de la Stomatite Vésiculaire. Ces mutants donnent des plages à 30° sur un tapis de fibroblastes de poulet mais n’en donnent pas à 39.8 ± 0.2°. Cet article rapporte le résultat de tests de complémentation conduisant à classer 71 mutants en 5 groupes.
Seventy-one spontaneous thermosensitive mutants of Vesicular Stomatitis Virus were isolated and tested for complementation. The spontaneous mutation rate seems to be very high since 2.3% of mutants were found in wild-type clones. Experiments were performed at 30° (permissive temperature) and 39.8° (non-permissive temperature). The mutants can be classified into five complementation groups. 58 mutants fall into the first group.
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Ultraviolet Reactivation in Bacteriophage Lambda
More LessSUMMARYReactivation of damaged phage λv by recombination with prophage (prophage reactivation) and by u.v. irradiation of host bacteria (u.v. reactivation) were similar in that u.v.- and nitrous acid-damaged phage was reactivated in both, both were eliminated by three rec alleles, neither was much affected by hcr alleles, and both were dependent on the degree of homology between phage and bacterial DNA. These results support a mechanism of u.v. reactivation by recombination between damaged phage DNA and host bacterial DNA. No evidence was obtained to support the hypothesis that u.v. reactivation acts by enhancing host cell reactivation.
Prophage reactivation occurred only in bacteria lysogenic for a prophage genetically related to the superinfecting phage λ v and integrated at the gal/bio attachment site.
Non-lethal periods of thymine starvation of the host bacteria caused reactivation of u.v.-irradiated phage λ v , comparable with u.v. reactivation.
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Propagation d’un Virus Sigma Défectif au Niveau de Disques Imaginaux d’Aile Implantés dans des Drosophiles Adultes
More LessSOMMAIRELe 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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A Full Expression of the Genome of Rous Sarcoma Virus in Heterokaryons Formed after Fusion of Virogenic Mammalian Cells and Chicken Fibroblasts
More LessSUMMARYImmunofluorescence and autoradiography showed that all heterokaryotic cells formed after cell fusion of virogenic mammalian cells and indicator chicken cells induced by Sendai virus produced Rous sarcoma virus coat antigen. Homokaryons and mononuclear cells of both types were negative in the immunofluorescence test. Similarly, all tested single heterokaryons obtained by visually controlled cell fusion produced infectious Rous sarcoma virus.
Virus coat antigen or infectious virus was not formed in virogenic cells or chicken fibroblasts agglutinated but not fused in the mixture with Sendai virus, or in heterokaryons obtained after fusion of virogenic cells with chicken erythrocytes; including heterokaryons containing ‘reactivated’ chicken erythrocyte nuclei.
Heterokaryons formed after fusion of virogenic cells with chicken fibroblasts are permissive cells for Rous sarcoma virus, and play a key role in the Rous sarcoma virus rescue process.
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