CHARACTERIZATION OF AN INVITRO PERSISTENT-STATE MEASLES-VIRUS INFECTION - ESTABLISHMENT AND VIROLOGICAL CHARACTERIZATION OF BGM-MV CELL LINE
CHARACTERIZATION OF AN INVITRO PERSISTENT-STATE MEASLES-VIRUS INFECTION - ESTABLISHMENT AND VIROLOGICAL CHARACTERIZATION OF BGM-MV CELL LINE
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DOI：
10.1128/iai.11.1.152-158.1975
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发表时间：
1975-01-01
影响因子：
3.1
通讯作者：
FLANAGAN, TD
中科院分区：
文献类型：
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作者：
MENNA, JH;COLLINS, AR;FLANAGAN, TD
检查BGM/MV细胞中持续状态麻疹病毒感染的参数。通过将麻疹病毒感染的原代C3 H小鼠脑细胞与稳定的非洲绿色猴肾细胞（BGM）系共培养建立BGM/MV细胞系。最初，存在形态学上混合的细胞群：BGM样（上皮样）和成纤维细胞。逐渐地，成纤维细胞被BGM样细胞取代，导致形态上均一的群体。在开始培养后2天观察到麻疹细胞病变效应，并持续约290天。病毒致细胞病变效应消失的时间对应于达到形态均一性的时间。接种后20天，在BGM/MV培养物中检测到低滴度的传染性麻疹病毒;此后未观察到。培养440天后，100%的BGM/MV细胞通过免疫荧光显示胞浆内麻疹抗原。从未观察到核荧光。电镜观察发现，BGM/MV细胞内几乎完全充满了麻疹病毒核衣壳。这些细胞的质膜表现正常;未观察到成熟或出芽的颗粒。麻疹病毒血凝素在澄清的细胞裂解液或上清液培养液中均未检测到。通过红细胞吸附和膜免疫荧光检测，在不到1%的这些细胞中检测到麻疹病毒引起的细胞膜改变。用放线菌素D或细胞松弛素B去核处理可增强细胞的红细胞吸附活性（30 ~ 70%）;然而，这些处理未能诱导出可检测水平的麻疹血凝素。用5 - 50 μ g/ml的5-溴-2 '-脱氧尿苷（BUdR）和1 - 50 μ g/ml的阿糖胞苷处理BGM/MV细胞不能增强血细胞吸附活性。5-溴-2 '-脱氧尿苷剂量范围为5至200 μ g/ml，放线菌素D剂量范围为0.1至10 μ g/ml，对诱导感染性病毒的合成无效。各种诱导感染性病毒的物理方法也不成功。
The parameters of a persistent-state measles virus infection in BGM/MV cells were examined. The BGM/MV cell line was established by cocultivation of measles virus-infected primary C3H mouse brain cells with a stable line of African green monkey kidney cells (BGM). Initially, a morphologically mixed population of cells existed:BGM-like (epithelioid) and fibroblasts. Gradually the fibroblasts were replaced by BGM-like cells, resulting in a morphologically homogeneous population. Measles cytopathic effect was noted 2 days after initiation of this culture and persisted for approximately 290 days. The time of disappearance of viral cytopathic effect corresponded to the time at which morphological homogeneity was reached. Low titers of infectious measles virus were detected in the BGM/MV culture up to 20 days postseeding; thereafter none was observed. After 440 days in culture, 100% of BGM/MV cells demonstrated intractyoplasmic measles antigen by immunofluorescence. Nuclear fluorescence was never observed. Electron microscopy revealed the presence of measles virus mucleocapsid within the almost completely filling the cytoplasm of BGM/MV cells. The plasma membrane of these cells appeared normal; no maturing or budding particles were observed. Measles virus hemagglutinin was not detected in either clarified cell lysates or in supernatant culture fluids. Cell membrane alteration by measles virus was detected in less than 1% of these cells by hemadsorption and by membrane immunofluorescence. The hemadsorption activity of the cells could be enhanced (30 to 70%) by treatment with actinomycin D or enucleation with cytochalasin B; these treatments, however, were unsuccessful in inducing detectable levels of measles hemagglutinin. Treatment of BGM/MV cells with 5-bromo-2'-deoxyuridine (BUdR) at 5 to 50 mug/ml and cytosine arabinoside at 1 to 50 mug/ml failed to enhance hemadsorption activity. Doses of 5-bromo-2'-deoxyuridine ranging from 5 to 200 mug/ml and of actinomycin D ranging from 0.1 to 10 mug/ml were ineffective in inducing the synthesis of infectious virus. Various physical methods of induction of infectious virus was also unsuccessful.