Valdeira M L, Bernardes C, Cruz B, Geraldes A
Department of Cellular Biology, Faculty of Pharmacy, Lisboa, Portugal.
Vet Microbiol. 1998 Feb 28;60(2-4):131-40. doi: 10.1016/s0378-1135(98)00152-7.
African swine fever virus (ASFV) enters Vero cells by adsorptive endocytosis [Valdeira, M.L., Geraldes, A., 1985. Morphological study on the entry of African swine fever virus into cells, Biol Cell. 55, 35-40]. Electron microscopy of a lysosomotropic drug-controlled penetration indicated that this step takes place in the endosomes, after fusion between the viral envelope and the limiting membrane of the endosome. Inhibition studies with colcemid, cytochalasin B, sodium azide, dinitrophenol, lysosomotropic weak bases, and the ionophore monensin, showed that the virus uptake is largely independent of cytoskeletal and lysosomal function, but dependent on oxidative phosphorylation. Some protease inhibitors inhibited viral replication at an early step, indicating that the initiation of infection depends on a viral proteolytic cleavage.
非洲猪瘟病毒(ASFV)通过吸附性胞吞作用进入非洲绿猴肾细胞[瓦尔代拉,M.L.,热拉尔德斯,A.,1985年。非洲猪瘟病毒进入细胞的形态学研究,《生物细胞》。55,35 - 40页]。对溶酶体亲和性药物控制的穿透进行电子显微镜观察表明,这一步骤发生在内体中,即病毒包膜与内体的限制膜融合之后。用秋水仙酰胺、细胞松弛素B、叠氮化钠、二硝基苯酚、溶酶体亲和性弱碱以及离子载体莫能菌素进行的抑制研究表明,病毒摄取在很大程度上不依赖于细胞骨架和溶酶体功能,但依赖于氧化磷酸化。一些蛋白酶抑制剂在早期阶段抑制病毒复制,这表明感染的起始依赖于病毒的蛋白水解切割。