Pogodina V V, Senyuta N B, Karmysheva V Y, Korolev M B, Satalkina M I, Kiseleva L L, Merekalova Z I, Mazurenko N P
Neoplasma. 1976;23(1):61-70.
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.
研究了感染弗氏白血病病毒(FLV)48小时后再感染辛德毕斯病毒(SV)的BALB/c小鼠胚胎成纤维细胞培养物(MEC)中产生干扰的一些机制。免疫荧光和细胞荧光分析表明,在感染FLV的细胞中,形成的SV抗原量比单独感染SV时低2至3倍。电子显微镜检查显示,在混合感染中,尽管细胞质中存在病毒核衣壳的紧密聚集体,但新形成的SV颗粒数量明显减少(减少90%)。当细胞最初感染虫媒病毒,然后再感染FLV时,两种病毒的病毒抗原和病毒粒子的形成均未受到干扰。用放线菌素(0.2微克/毫升)预处理细胞单层可阻断MEC培养物中干扰素的产生,并抑制FLV和SV之间的干扰。据推测,FLV和SV之间的干扰与已知的干扰素作用机制以及SV颗粒组装阶段及其从细胞中释放的干扰有关。由于SV繁殖的不完全周期在核糖核蛋白形成阶段中断,其与MEC细胞的有效相互作用类型受到干扰。