Wildy P, Gell P G, Rhodes J, Newton A
Infect Immun. 1982 Jul;37(1):40-5. doi: 10.1128/iai.37.1.40-45.1982.
Proteose-peptone-activated mouse macrophages can prevent productive infection by herpes simplex virus in neighboring cells in vitro whether or not those cells belong to the same animal species. The effect does not require contact between the macrophages and the infected cells, may be prevented by adding extra arginine to the medium, and may be reversed when extra arginine is added 24 h after the macrophages. Arginase activity was found both intracellularly and released from the macrophages. The extracellular enzyme is quite stable; 64% activity was found after 48 h of incubation at 37 degrees C in tissue culture medium. No evidence was found that the inefficiency of virus replication in macrophages was due to self-starvation by arginase. As might be predicted macrophages can, by the same mechanism, limit productive infection by vaccinia virus.
蛋白胨激活的小鼠巨噬细胞能够在体外阻止单纯疱疹病毒在邻近细胞中进行有效感染,无论这些细胞是否属于同一动物物种。该效应并不需要巨噬细胞与被感染细胞之间的接触,添加额外的精氨酸到培养基中可阻止该效应,并且在巨噬细胞作用24小时后添加额外的精氨酸时该效应可能会逆转。在细胞内以及从巨噬细胞释放的物质中均发现了精氨酸酶活性。细胞外酶相当稳定;在组织培养基中于37℃孵育48小时后仍有64%的活性。未发现病毒在巨噬细胞中复制效率低下是由于精氨酸酶导致自身饥饿所致的证据。正如所预测的那样,巨噬细胞可以通过相同的机制限制痘苗病毒的有效感染。