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Biomedical subjects

A Kirn

Publications and source records attributed to A Kirn.

At least 145 records · Page 8Linked to original sources
PubMed1977

Frog virus 3 morphogenesis: effect of temperature and metabolic inhibitors.

The different stages of frog virus 3 (FV 3) morphogenesis have been investigated in chick embryo fibroblasts infected at an optimal temperature for virus growth (29 degrees C). The metabolic requirements for morphogenesis were determined by adding inhibitors of macromolecular synthesis at different periods in the virus growth cycle. The effect of a non-permissive temperature for FV 3 replication (37 degrees C) was also studied in shift up experiments. The following results were obtained: (I) when DNA replication was inhibited, neither immature nor mature virus particles appeared; (2) continuous protein synthesis was required for every stage of virus morphogenesis. However, the assembly of virions into paracrystalline arrays seemed to be a passive phenomenon. (3) Continuous mRNA transcription was not necessary for assembly of capsid constituents, although most of these capsids appeared empty; there was also a striking increase in the number of aberrant virus structures. (4) If infected cells were shifted to a non-permissive temperature, virus maturation was completely inhibited.

Animals↗
PubMed1976

Proteins solubilized from frog virus 3 particles: effect on transcription.

The treatment of KB cells with viral proteins solubilized from frog virus 3 particles (SVE) induced a rapid shutoff of host RNA synthesis. The RNA polymerase activities of SVE-treated cells were drastically depressed, corresonding, at least for RNA polymerase B, to a decrease in the number of enzyme molecules. In vitro, SVE had no direct effect on RNA polymerases but was capable of binding with calf thymus DNA to form an SVE-DNA complex modifying the template capacity. The effect of SVE on a transcription system consisting of cell lysates would suggest that cytoplasmic factors are necessary for expression of the inhibitory capacity of SVE.

Carcinoma↗
PubMed1975

[A novel model of experimental toxic hepatitis/acute degenerative hepatitis induced by frog virus 3 (FV3) in the mouse (author's transl)].

The i.p. or i.v. injection of frog virus 3 (FV3) in mice produces a hepatitis which leads to the death of the animals within 24 h. This hepatitis is of a purely toxic nature since the virus does not develop at 37 degrees C. The toxic effect of the virus, which can be differentiated from the infectious effect, involves one or more structural proteins. The first pathological changes occur during the first few hours after the injection in the vicinity of the nuclei of the liver parenchyma cells in the form of changes in the chromatin and nucleoplasm. The inhibition of the synthesis of cellular macromolecules and of the function of nuclear enzymes points to the fact that it is the nucleus that is first and foremost attacked. Necrosis and biochemical disturbances in the vicinity of the cytoplasm appear later on. Premedication of the mice with a water-soluble silymarin salt leads to a distinct rise in the survival rate of the animals. The protective function of silymarin is dependent on the dose and on the duration of the premedication. The LD50 of FV3 in those mice which had previously been given silymarin, is approximately three times that of the animals which received no premedication.

Animals↗
PubMed1975

[New data on the structure and the budding of FV3 (frog virus 3) (author's transl)].

The freeze-etching technique when applied to FV3 suspensions revealed the perfectly icosahedral structure of the viral nucleocapsids. This allowed a fine substructure suggesting the existence of numerous subunits of small dimensions to be detected at their surface. Observations of the replicas of infected cells obtained by freeze-etching revealed modifications of the external face of the cytoplasmic membrane occurring at the level of the budding viral particles; in these zones parallel stripes appeared, whose elementary structure is constant (13,5 nm). Observations of the infected cells with the scanning microscope enabled the spreading of the budding process on all the cells of a same culture to be studied. By counting the number of budding particles per mum2, it was possible to demonstrate the heterogeneity of the budding process at the surface of the cells.

Animals↗