Miyamoto K, Gilden R V
J Virol. 1971 Mar;7(3):395-406. doi: 10.1128/JVI.7.3.395-406.1971.
Entry of Rauscher leukemia virus into mouse embryo fibroblasts was studied by electron microscopy. The polycation diethylaminoethyl-dextran enhanced viral attachment and subsequent entry. At the site of viral attachment to the cell membrane, three distinct interactions occurred between the viral envelope and cell membrane, namely, (i) dissolution of viral envelopes on the cell membrane, which itself remained unaltered; (ii) simultaneous dissolution of both the envelope and cell membrane, resulting in passage of viral nucleoids directly into the cytoplasm; and (iii) dissolution of the cell membrane with direct penetration of intact enveloped particles into the cytoplasm, followed by intracytoplasmic disruption of the envelope, resulting in release of nucleoids into the cytoplasm. These interactions occurred with both mature and immature C-type particles. At no time was fusion of viral envelopes with the cell membrane observed. The mechanism of these interactions is discussed.
通过电子显微镜研究了劳氏白血病病毒进入小鼠胚胎成纤维细胞的过程。聚阳离子二乙氨基乙基葡聚糖增强了病毒的附着及随后的进入。在病毒附着于细胞膜的部位,病毒包膜与细胞膜之间发生了三种不同的相互作用,即:(i) 病毒包膜在细胞膜上溶解,而细胞膜本身保持不变;(ii) 包膜和细胞膜同时溶解,导致病毒核样物直接进入细胞质;(iii) 细胞膜溶解,完整的包膜颗粒直接穿透进入细胞质,随后包膜在细胞质内破裂,导致核样物释放到细胞质中。这些相互作用在成熟和未成熟的C型颗粒中均有发生。未观察到病毒包膜与细胞膜的融合。对这些相互作用的机制进行了讨论。