FATE OF MICROFILAMENTS IN VERO CELLS INFECTED WITH MEASLES-VIRUS AND HERPES-SIMPLEX VIRUS TYPE-1
FATE OF MICROFILAMENTS IN VERO CELLS INFECTED WITH MEASLES-VIRUS AND HERPES-SIMPLEX VIRUS TYPE-1
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DOI：
10.1128/mcb.3.4.712
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发表时间：
1983-01-01
影响因子：
5.3
通讯作者：
WELSH, MJ
中科院分区：
文献类型：
--
作者：
BEDOWS, E;RAO, KMK;WELSH, MJ
在单纯疱疹病毒1型感染的非洲绿色猴肾Vero细胞中，观察到微丝的重组。感染后4 h。如通过DNA酶I抑制测定所评估的，F（丝状）肌动蛋白向G（球状）肌动蛋白的转化在接下来的12-16小时内是连续的，此时测量到G肌动蛋白的水平约为未感染细胞中观察到的水平的两倍。用7-硝基苯-2-氧杂-1，3-二唑（NBD）-鬼笔毒菌素对F肌动蛋白进行荧光定位，证实微丝纤维在λ开始减少。感染后16-18 h，大致对应于G肌动蛋白水平达到峰值和首次观察到病毒诱导的细胞病理学的时间。在麻疹病毒感染的细胞中，没有发生这样的微丝分解。相反，G肌动蛋白水平略有下降。F肌动蛋白的荧光定位表明，麻疹病毒感染的Vero细胞保持一个复杂的微丝网络，其特征在于纤维跨越整个长度的新形成的巨细胞。用细胞松弛素B（可抑制麻疹病毒特异性细胞病理学）破坏微丝，在高感染复数（MOI）下不抑制麻疹病毒的产生，但随着MOI的降低，其抑制作用逐渐增强。苄氧羰基三肽SV-4814抑制麻疹病毒感染后Vero细胞融合的能力，与细胞松弛素B一样，在低MOI下抑制麻疹病毒的产生，但在高MOI下不抑制。因此，似乎影响麻疹病毒感染后Vero细胞融合能力的试剂可能抑制病毒产生，肌动蛋白网络对该过程至关重要。
In herpes simplex virus type 1-infected African green monkey kidney Vero cells, reorganization of microfilaments was observed .apprx. 4 h postinfection. Conversion of F (filamentous) actin to G (globular) actin, as assessed by a DNase I inhibition assay, was continuous over the next 12-16 h, at which time a level of G actin of about twice that observed in uninfected cells was measured. Fluorescent localization of F actin, using 7-nitrobenz-2-oxa-1,3-diazole (NBD)-phallacidin, demonstrated that microfilament fibers began to diminish at .apprx. 16-18 h postinfection, roughly corresponding to the time that G actin levels peaked and virus-induced cytopathology was first observable. In measles virus-infected cells, no such disassembly of microfilaments occurred. Rather, there was a modest decrease in G actin levels. Fluorescent localization of F actin showed that measles virus-infected Vero cells maintained a complex microfilament network characterized by fibers which spanned the entire length of the newly formed giant cells. Disruption of microfilaments with cytochalasin B, which inhibits measles virus-specific cytopathology, was not inhibitory to measles virus production at high multiplicities of infection (MOI) but was progressively inhibitory as the MOI was lowered. The carbobenzoxy tripeptide SV-4814, which inhibits the ability of Vero cells to fuse after measles virus infection, like cytochalasin B, inhibited measles virus production at low MOI but not at high MOI. Thus, it appears that agents which affect the ability of Vero cells to fuse after measles virus infection may be inhibitory to virus production and that the actin network is essential to this process.