Susceptibility of Differentiating Muscle Cells of the Fetal Mouse in Culture to Coxsackievirus A13
Susceptibility of Differentiating Muscle Cells of the Fetal Mouse in Culture to Coxsackievirus A13
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培养的胎鼠分化肌细胞对柯萨奇病毒 A13 的敏感性
DOI：
10.1128/jvi.7.6.759-769.1971
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发表时间：
1971
影响因子：
5.4
通讯作者：
R. Crowell
中科院分区：
文献类型：
--
作者：
R. Goldberg;R. Crowell
本文研究了柯萨奇病毒A13与培养的胎鼠组织分化肌细胞的相互作用。在肌细胞分化阶段感染的以快速形成多核肌管为特征的培养物产生的最大病毒滴度超过107个空斑形成单位。病毒诱导的细胞病变的特征是多核细胞数量显著减少。当大多数肌管形成后开始感染时，这些培养物的敏感性明显降低。用免疫荧光法证实了新合成的A13病毒抗原，为A13病毒在成肌细胞和肌管中复制提供了直接证据。在BUDR或融合抑制液抑制多核细胞形成的肌肉培养中，A13病毒的合成明显受到抑制。在逆转这种抑制后，培养物对A13病毒的敏感性增加，这是正在进行肌源性分化的细胞的特征。与柯萨奇病毒A13的结果相反，原代胎鼠肌肉培养物对脊髓灰质炎病毒T1具有抵抗力。提示发育中的肌肉细胞表面的变化可能与特异性病毒受体的形成和消失相一致，从而调节细胞对柯萨奇病毒A13的易感性。
The interaction of coxsackievirus A13 with differentiating muscle cells, cultured from tissues of the fetal mouse, was studied. Cultures infected at that stage of myogenic differentiation characterized by the rapid formation of multinucleated myotubes produced maximum virus titers of over 107 plaque-forming units. Virus-induced cytopathic effect was characterized by a marked diminution in the number of multinucleated cells. The susceptibility of these cultures decreased appreciably when infection was initiated after the majority of the myotubes had formed. The demonstration of newly synthesized A13 virus antigen by immunofluorescence provided direct evidence that A13 virus replication occurred both in myoblasts and myotubes. The synthesis of A13 virus was markedly depressed in muscle cultures in which the formation of multinucleated cells was inhibited by BUDR or by fusion-inhibiting media. After reversal of this inhibition, the cultures acquired the increased susceptibility to A13 virus characteristic of cells undergoing myogenic differentiation. In contrast to the results obtained with coxsackievirus A13, the primary fetal mouse muscle cultures were resistant to poliovirus T1. It is suggested that changes in the surfaces of developing muscle cells may coincide with the formation and disappearance of specific virus receptors and thereby regulate the cell susceptibility to coxsackievirus A13.