[Viral co-carcinogenesis and other aspects of viral interaction].
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Biomedical subjects
Publications and source records attributed to Z I Merekalova.
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Some mechanisms of interference developing in BALB/c mouse embryo fibroblast culture (MEC) infected with Friend leukemia virus (FLV) and 48 hours later superinfected with Sindbis virus (SV) was studied. In FLV-infected cells the amount of SV antigen formed was 2-3 times lower than in SV monoinfection, as indicated by immunofluorescence and cytofluorimetry. Electron microscopic examination showed that in mixed infection the number of newly formed SV particles decreased markedly (by 90%) despite the presence of compact aggregates of viral nucleocapsids in the cytoplasm. When the cells were initially infected with arbovirus and then superinfected with FLV, formation of virus antigen and virions of both viruses was not disturbed. Pre-treatment of cell monolayer with dactinomycin (0.2 mug/ml) blocked interferon production in MEC culture and inhibited interference between FLV and SV. It is assumed that interference between FLV and SV is associated with known mechanisms of interferon action as well as with disturbance of the stage of SV particles assembly and their release from the cell. Due to incomplete cycle of SV reproduction interrupted at the stage of ribonucleoprotein formation, productive type of its interaction with MEC cells is disturbed.
The vaccinating properties of two variants of Marek's disease virus, Kekava strain (MDV-Kekava) have been studied. One of them is naturally attenuated, the other has been produced as a result of attenuation of the pathogenic MDV-Kekava by long-term passages in chick embryo fibroblast (CEF) culture. The vaccinating properties of the naturally attenuated strains (MDV-Kekava 83) were first studied in an experiment in which the blood of chicken No. 1683 was used as the vaccine. In paralled. the MDV-Kekava 83 variant was isolated from the blood of this chicken in CEF culture. Vaccination of chickens with the blood of this chicken as well as with 1000-3000 PFU MDV-Kekava 83 which had undergone 16, 24, 45, and 46 passages in vitro produced in the chickens resistance to Marek's disease. According to the combined data of 4 experiments, altogether 9 out of 101 vaccinated chickens developed Marek's disease. Among the controls inoculated with the pathogenic MDV alone 51 out of 137 chickens developed the disease. Attenuation of the pathogenic MDV-Kekava 55 in CEF culture occurred very slowly. The virus of the 45th passage in vitro had no vaccinating properties. Vaccination of the chickens with 1000-2500 PFU MDV-Kekava 56 which had undergone 73 a94 passages in CEF culture produced resistance to Marek's disease. Among the vaccinated chickens 20 out of 113 had Marek's disease whereas in the control group 74 out of 122 were observed to develop the disease. Among the chickens vaccinated with MDV, 3-4% developed the disease. Possible causes of the disease in this group of chickens are discussed.
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