McNeill T A, Havredaki M, Gould E A, Cosby L
Infect Immun. 1975 Mar;11(3):424-8. doi: 10.1128/iai.11.3.424-428.1975.
Normal mouse bone marrow cells were exposed to encephalomyocarditis virus (EMC), reovirus type 3 (REO3), influenza virus (FLU), and Newcastle disease virus (NDV) then assayed for granulocyte-macrophage precursor cells by the technique of colony formation in agar. Exposure to EMC, REO3, and FLU caused a slight but variable loss of colony-forming potential, whereas exposure to NDV caused a very marked loss. NDV acted directly on the cells, not indirectly through release of colony-inhibiting factors or destruction of colony-stimulating factor. Experiments with NDV inactivated by heat, ether, or ultraviolet irradiation indicated that colony inhibition was associated with fully infective virus, even though some of the inactivated preparations had retained full hemagglutinin, neuraminidase, or hemolytic activity.
将正常小鼠骨髓细胞暴露于脑心肌炎病毒(EMC)、3型呼肠孤病毒(REO3)、流感病毒(FLU)和新城疫病毒(NDV),然后通过琼脂中集落形成技术检测粒细胞-巨噬细胞前体细胞。暴露于EMC、REO3和FLU会导致集落形成潜力略有但可变的丧失,而暴露于NDV会导致非常明显的丧失。NDV直接作用于细胞,而非通过释放集落抑制因子或破坏集落刺激因子间接作用。用热、乙醚或紫外线照射灭活的NDV进行的实验表明,集落抑制与完全感染性病毒有关,即使一些灭活制剂仍保留了完整的血凝素、神经氨酸酶或溶血活性。