Wells M A, Albrecht P, Daniel S, Ennis F A
Infect Immun. 1978 Dec;22(3):758-62. doi: 10.1128/iai.22.3.758-762.1978.
The interaction of mouse macrophages with influenza virus was examined as part of a study into the defense mechanisms against influenza infection. Macrophages exposed to A/Port Chalmers/1/73 virus produced infectious foci on susceptible indicator cell monolayers. Sampling of supernatant fluids and cells from infected macrophage cultures showed release of virus adsorbed to the cell surface. Active virus replication in macrophages could not be demonstrated. Exposing macrophages to specific antibody before or after virus infection resulted in a significant decrease in the number of infectious macrophages. The results suggest that although macrophages are not the source of replicating influenza virus, they are able to spread the infection by having virus attaching to their surface. This activity is interfered with by the presence of specific antibody.
作为流感感染防御机制研究的一部分,对小鼠巨噬细胞与流感病毒的相互作用进行了检测。暴露于A/查尔姆斯港/1/73病毒的巨噬细胞在易感指示细胞单层上产生了感染灶。对感染巨噬细胞培养物的上清液和细胞进行采样,结果显示吸附在细胞表面的病毒得以释放。但未能证实巨噬细胞中有活跃的病毒复制。在病毒感染之前或之后将巨噬细胞暴露于特异性抗体,会导致感染性巨噬细胞数量显著减少。结果表明,虽然巨噬细胞不是流感病毒复制的来源,但它们能够通过使病毒附着于其表面来传播感染。特异性抗体的存在会干扰这种活性。