Smith C A, Lancz G J
Arch Virol. 1982;74(4):311-23. doi: 10.1007/BF01314164.
The nature of the refractoriness of C6 rat glioma cells to herpes simplex virus type 2 (HSV-2) was examined. Infection of C6 cells with HSV-2 results in low virus yields, not exceeding the input virus. Although virus growth studies suggested a restricted cycle of virus replication, synthesis of HSV-2 DNA and HSV-2-specific antigens could not be detected. In addition, HSV-2 yields in C6 cells were unaffected by interferon, cycloheximide, tunicamycin, actinomycin D and cytosine arabinoside. However, trypsin, but not EDTA, treatment of infected C6 cells at 4 hours postinfection (p.i.) reduced maximal HSV-2 yields at 24 hours p.i. by 61 percent. These data: 1) indicate that HSV-2 fails to replicate in C6 cells and is prohibited from directing the synthesis of virus macromolecules; and 2) suggests that the increment of HSV-2 yields observed during the synthesis phase of the virus growth cycle represents re-envelopment and egress of a portion of the input virus.
研究了C6大鼠胶质瘤细胞对2型单纯疱疹病毒（HSV-2）的耐药性本质。用HSV-2感染C6细胞导致病毒产量低，不超过输入病毒量。尽管病毒生长研究表明病毒复制周期受限，但未检测到HSV-2 DNA和HSV-2特异性抗原的合成。此外，C6细胞中的HSV-2产量不受干扰素、环己酰亚胺、衣霉素、放线菌素D和阿糖胞苷的影响。然而，在感染后4小时（p.i.）用胰蛋白酶而非EDTA处理感染的C6细胞，可使感染后24小时的最大HSV-2产量降低61%。这些数据：1）表明HSV-2在C6细胞中无法复制，且被阻止指导病毒大分子的合成；2）提示在病毒生长周期的合成阶段观察到的HSV-2产量增加代表了一部分输入病毒的重新包膜和释放。
