Narayan O, Wolinsky J S, Clements J E, Strandberg J D, Griffin D E, Cork L C
J Gen Virol. 1982 Apr;59(Pt 2):345-56. doi: 10.1099/0022-1317-59-2-345.
Lentiviruses of sheep and goats cause slowly progressive diseases of the central nervous system (visna), lungs (maedi) and joints (arthritis) in their natural hosts. However, the virus target cell(s) in these diseases are still unknown. In this report, using laboratory-adapted Icelandic visna virus and several field strains recently obtained from sheep and goats with natural disease in the U.S.A., we show that macrophages became persistently infected when inoculated in culture. Furthermore, macrophages were an invariable source of virus from experimentally and naturally infected animals. Virus-producing macrophages developed minimal cytopathic changes and virus assembly occurred mainly intracellularly, accumulating in cytoplasmic vacuoles. In contrast to macrophages, sheep choroid plexus fibroblasts developed syncytial cytopathic changes after inoculation and virus maturation occurred at the cell surfaces. Replication of the Icelandic virus was highly productive in this system but that of the field viruses was very inefficient. In some cases these agents failed to replicate in the fibroblasts and no cytopathic effect occurred. This block in the field virus replication was, however, overcome when infected nonproducer fibroblasts were co-cultivated with macrophages. In these cases, virus production with attendant cytopathic effect in the fibroblasts required the continuous presence of macrophages because the cells reverted to a non-productive state when separated from macrophages and became productive again when subcultures were added to new macrophages. The roles of the macrophage as a virus target cell and virus inducer in the virus-macrophage-fibroblast interactions are discussed with inferences to the well-known phenomenon of restricted virus replication in infected animals and the immunopathological aspects of the diseases.
绵羊和山羊的慢病毒可在其自然宿主中引发中枢神经系统（维斯纳病）、肺部（梅迪病）和关节（关节炎）的缓慢进展性疾病。然而，这些疾病中的病毒靶细胞仍然未知。在本报告中，我们使用实验室适应的冰岛维斯纳病毒以及最近从美国患有自然疾病的绵羊和山羊身上获得的几种野外毒株，发现巨噬细胞在接种培养时会持续受到感染。此外，巨噬细胞是实验感染和自然感染动物中病毒的恒定来源。产生病毒的巨噬细胞出现的细胞病变变化极小，病毒组装主要在细胞内发生，积聚在细胞质空泡中。与巨噬细胞不同，绵羊脉络丛成纤维细胞接种后会出现合胞体细胞病变变化，病毒成熟发生在细胞表面。冰岛病毒在该系统中的复制效率很高，但野外毒株的复制效率非常低。在某些情况下，这些毒株无法在成纤维细胞中复制，也没有出现细胞病变效应。然而，当感染的非生产性成纤维细胞与巨噬细胞共培养时，野外病毒复制的这种障碍得以克服。在这些情况下，成纤维细胞中伴随细胞病变效应的病毒产生需要巨噬细胞的持续存在，因为当细胞与巨噬细胞分离时会恢复到非生产状态，而当传代培养物添加到新的巨噬细胞中时又会再次产生病毒。本文讨论了巨噬细胞在病毒 - 巨噬细胞 - 成纤维细胞相互作用中作为病毒靶细胞和病毒诱导剂的作用，并推断了感染动物中病毒复制受限的著名现象以及疾病的免疫病理学方面。
