Pogodina V V, Kiseleva L L, Miller G G, Fokina G I, Graevskaia N A
Vopr Virusol. 1978 Jan-Feb(1):52-6.
Persistence of Sindbis virus (SV) was studied for 9 months in two lines of mouse cell cultures (BALB/C) in one of which the genome of endogenous ecotropic oncornaviruses was repressed. The other lines was exogenously infected at the level of plimary culture with Rauscher leukemia virus (RLV) and SV and showed gradual inhibition of oncornavirus functions. The presence of oncornavirus type C was not the necessary condition for the development of persistent SV infection, however it influenced the character of persistence. In both systems, sequential loss of the hemagglutinating and interferon-inducing activities, then infectivity of SV (61--82 days), and persistence of the noninfectious antigen of the arbovirus for 9 months were observed. The differences consisted in the time of appearance of homologous interference to SV: in the presence of oncornavirus earlier (40 days), under conditions of repressed oncornavirus genome later (179 days). Electron microscopic examinations showed that in the system infected with RLV and SV there occurred in the course of persistence a sharp activation of phagosome-lysosome complex accompanied by incorporation into phagocytolysomes of numerous intact and partially destroyed virions of SV and RLV and their release from cell with cytoplasmic fragments. Possible mechanisms of inhibition of functions of the oncogenic and infectious viruses in the reported model of mixed chronic infection are discussed.
在两株小鼠细胞培养物(BALB/C)中对辛德毕斯病毒(SV)的持续性进行了为期9个月的研究,其中一株内源性嗜亲性肿瘤病毒的基因组受到抑制。另一株在原代培养时被劳舍尔白血病病毒(RLV)和SV外源感染,并显示出肿瘤病毒功能的逐渐抑制。C型肿瘤病毒的存在不是持续性SV感染发生的必要条件,然而它影响了持续性的特征。在两个系统中,均观察到血凝和干扰素诱导活性的相继丧失,随后是SV感染性的丧失(61 - 82天),以及虫媒病毒非感染性抗原持续存在9个月。差异在于对SV同源干扰出现的时间:在有肿瘤病毒存在时较早(40天),在肿瘤病毒基因组受抑制的条件下较晚(179天)。电子显微镜检查表明,在被RLV和SV感染的系统中,在持续性过程中吞噬体 - 溶酶体复合物发生急剧激活,同时大量完整和部分破坏的SV和RLV病毒粒子被纳入吞噬溶酶体,并与细胞质片段一起从细胞中释放出来。讨论了在报告的混合慢性感染模型中致癌和感染性病毒功能抑制的可能机制。