Nakamura K, Homma M, Ishida N
Infect Immun. 1975 Sep;12(3):614-20. doi: 10.1128/iai.12.3.614-620.1975.
The interaction of measles virus with RG-6 cells derived from rat glioma was investigated. When a culture of RG-6 cells was infected with measles virus, the synthesis of viral antigens was detected in very few cells, at most 5%. The apparent resistance to measles virus infection was also repeatedly found in all of the subclonal cells derived form RG-6 cells. Although all of the virus-synthesizing cells had the ability to form plaques on Vero cells, they produced only a reduced amount of infectious virus, i.e., 0.1 plaque-forming units per cell. These results imply the existence of some mechanism that regulates growth of measles virus in cultures of RG-6 cells. The transmission of genetic material of measles virus from infected RG-6 cells to Vero cells was not inhibited in the presence of antiviral serum. This fact may provide a basis for interpretation of the persistence of virus, in the presence of antibody, in patients with subacute sclerosing panencephalitis.
研究了麻疹病毒与源自大鼠胶质瘤的RG-6细胞的相互作用。当用麻疹病毒感染RG-6细胞培养物时,在极少数细胞中检测到病毒抗原的合成,最多为5%。在源自RG-6细胞的所有亚克隆细胞中也反复发现对麻疹病毒感染的明显抗性。尽管所有合成病毒的细胞都有能力在Vero细胞上形成蚀斑,但它们产生的感染性病毒量减少,即每个细胞0.1个蚀斑形成单位。这些结果表明存在某种调节麻疹病毒在RG-6细胞培养物中生长的机制。在抗病毒血清存在的情况下,麻疹病毒的遗传物质从受感染的RG-6细胞向Vero细胞的传递未受抑制。这一事实可能为解释亚急性硬化性全脑炎患者在有抗体存在的情况下病毒持续存在提供依据。