2 MODES OF ENTRY OF REOVIRUS PARTICLES INTO L-CELLS
2 MODES OF ENTRY OF REOVIRUS PARTICLES INTO L-CELLS
复制标题
DOI：
10.1099/0022-1317-45-1-161
复制
发表时间：
1979-01-01
影响因子：
3.8
通讯作者：
SZEKELY, JG
中科院分区：
文献类型：
--
作者：
BORSA, J;MORASH, BD;SZEKELY, JG
有证据支持这样的假设：呼肠孤病毒中间亚病毒颗粒 (ISVP) 相对于完整病毒体表现出更高的感染性，可以通过 2 种替代途径进入宿主 [小鼠成纤维细胞] L 细胞。一种途径是病毒粘连过程，涉及吞噬泡。第二条进入途径是直接穿透细胞质膜，不涉及吞噬液泡。使用 EM 对吸收过程进行动力学分析。结果表明，在 37 度。 C ISVP 主要通过直接进入进入宿主细胞，尽管也发生病毒粘连，而完整病毒体几乎完全通过病毒粘连进入宿主细胞。对感染后宿主细胞释放预载放射性 51Cr 的研究提供了与 ISVP 可以融化穿过质膜的观点一致的第二条实验证据。 51Cr 释放数据表明，ISVP 感染会导致细胞质膜渗漏立即增加，而感染同等数量的完整病毒体后不会发生这种增加。这表明ISVP可以与细胞质膜相互作用，其方式与完整病毒粒子和质膜之间的相互作用有本质上的不同。 ISVP 能够直接穿透宿主细胞的质膜，而完整的病毒粒子显然无法做到这一点，这可以解释相对于完整病毒粒子感染观察到的结果，遮蔽期的持续时间缩短以及 ISVP 的感染性增加。
Evidence is presented supporting the hypothesis that reovirus intermediate subviral particles (ISVP), which show increased infectivity relative to intact virions, can gain entry into host [mouse fibroblast] L cells by 2 alternative pathways. One pathway is by the process of viropexis, involving phagocytic vacuoles. A 2nd entry pathway is via direct penetration of the plasma membrane of the cell, without involvement of a phagocytic vacuole. Using EM, a kinetic analysis of the uptake process was carried out. Results indicate that at 37.degree. C ISVP gain entry into host cells primarily by direct entry, although viropexis also occurs, while intact virions gain entry by viropexis almost exclusively. A 2nd line of experimental evidence consistent with the idea that ISVP can melt their way through the plasma membrane is provided by studies on the release of pre-loaded radioactive 51Cr from host cells following infection. 51Cr release data demonstrate that infection with ISVP leads to an immediate increased leakiness of the cell plasma membrane, whereas no such increase takes place following infection with an equivalent number of intact virons. This demonstrates that ISVP can interact with the plasma membrane of the cell in a manner which is qualitatively different from the interaction between intact virions and the plasma membrane. The ability of ISVP to directly penetrate the plasma membrane of the host cell, which intact virions apparently cannot do, could explain the decreased duration of the eclipse phase, and the increased infectivity of ISVP, relative to that observed for infection with intact virions.