Borrow P, Oldstone M B
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037.
Virology. 1994 Jan;198(1):1-9. doi: 10.1006/viro.1994.1001.
The path that the arenavirus lymphocytic choriomeningitis virus (LCMV) uses to enter rodent fibroblastic cell lines was dissected by infectivity and inhibition studies and immunoelectron microscopy. Lysosomotropic weak bases (chloroquine and ammonium chloride) and carboxylic ionophores (monensin and nigericin) inhibited virus entry, assessed as virus nucleoprotein expression at early times post-infection, indicating that the entry process involved a pH-dependent fusion step in intracellular vesicles. That entry occurred in vesicles rather than by direct fusion of virions with the plasma membrane was confirmed by immunoelectron microscopy. The vesicles involved were large (150-300 nm diameter), smooth-walled, and not associated with clathrin. Unlike classical phagocytosis, virus uptake in these vesicles was a microfilament-independent process, as it was not blocked by cytochalasins. LCMV entry into rodent fibroblast cell lines thus involves viropexis in large smooth-walled vesicles, followed by a pH-dependent fusion event inside the cell.
通过感染性和抑制性研究以及免疫电子显微镜技术，剖析了沙粒病毒淋巴细胞性脉络丛脑膜炎病毒（LCMV）进入啮齿动物成纤维细胞系的途径。溶酶体促渗弱碱（氯喹和氯化铵）和羧酸离子载体（莫能菌素和尼日利亚菌素）抑制病毒进入，以感染后早期的病毒核蛋白表达来评估，这表明进入过程涉及细胞内囊泡中pH依赖性融合步骤。免疫电子显微镜证实进入发生在囊泡中，而非病毒粒子与质膜直接融合。所涉及的囊泡较大（直径150 - 300 nm），壁光滑，且不与网格蛋白相关。与经典吞噬作用不同，这些囊泡中的病毒摄取是一个不依赖微丝的过程，因为它不会被细胞松弛素阻断。因此，LCMV进入啮齿动物成纤维细胞系涉及在大型光滑壁囊泡中的病毒胞饮作用，随后在细胞内发生pH依赖性融合事件。
