Alcamí A, Carrascosa A L, Viñuela E
Centro de Biología Molecular (CSIC-UAM), Facultad de Ciencias, Universidad Autónoma, Madrid, Spain.
Virus Res. 1990 Oct;17(2):93-104. doi: 10.1016/0168-1702(90)90071-i.
Morphological data obtained by electron microscopy have shown that African swine fever virus adapted to VERO cells enters swine macrophages, its natural host cell, by a mechanism of receptor-mediated endocytosis. Binding studies with 3H-labeled virus and competition experiments with UV-inactivated virus have shown that the virus entry that leads to a productive infection in swine macrophages is mediated by saturable binding sites on the plasma membrane. The virus also penetrated into rabbit macrophages that do not produce infectious virus and initiated the synthesis of some early viral proteins; however, the viral replication cycle was aborted since viral DNA synthesis did not occur. The interaction of ASF virus particles with rabbit macrophages was mediated by nonsaturable binding sites, suggesting that the lack of specific receptors in these cells may be related to the absence of a productive infection. A similar abortive infection was detected in macrophages from other virus-resistant animal species.
通过电子显微镜获得的形态学数据表明，适应VERO细胞的非洲猪瘟病毒通过受体介导的内吞作用机制进入其天然宿主细胞——猪巨噬细胞。用3H标记病毒进行的结合研究以及用紫外线灭活病毒进行的竞争实验表明，导致猪巨噬细胞发生有效感染的病毒进入是由质膜上的可饱和结合位点介导的。该病毒也能穿透不产生感染性病毒的兔巨噬细胞，并启动一些早期病毒蛋白的合成；然而，由于未发生病毒DNA合成，病毒复制周期终止。非洲猪瘟病毒颗粒与兔巨噬细胞的相互作用是由不饱和结合位点介导的，这表明这些细胞中缺乏特异性受体可能与无法产生有效感染有关。在来自其他抗病毒动物物种的巨噬细胞中也检测到了类似的流产感染。
