Fujinami R S, Oldstone M B
J Immunol. 1980 Jul;125(1):78-85.
Six hours after measles virus antibodies bind to the surface of HeLa cells acutely infected with measles virus, the expression of an external polypeptide F1, as well as internal polypeptides P and M are altered. The loss of F1 molecules during antibody-induced antigenic modulation explains the lack of cell-cell fusion and giant cell formation of infected cells cultured in the presence of antibody. The decrease in F1, P, and M viral polypeptides is specific, since the effect is only seen with antibodies directed against measles virus antigens expressed on the cell's surface and not with antibodies directed against nonviral antigens expressed on the surfaces of virus-infected cells. Since the P protein or its analog in other viral systems appears to be associated with transcriptive complex whereas the M protein is associated with nucleocapsid recognition and alignment at the plasma membrane, the alterations in these polypeptides might lead to aberrations in measles virus synthesis and maturation that are hallmarks of persistent measles virus infection.
麻疹病毒抗体与急性感染麻疹病毒的HeLa细胞表面结合6小时后,外部多肽F1以及内部多肽P和M的表达发生改变。抗体诱导的抗原调制过程中F1分子的丢失解释了在抗体存在下培养的感染细胞缺乏细胞间融合和巨细胞形成的原因。F1、P和M病毒多肽的减少是特异性的,因为这种效应仅在针对细胞表面表达的麻疹病毒抗原的抗体作用下出现,而在针对病毒感染细胞表面表达的非病毒抗原的抗体作用下则不会出现。由于P蛋白或其他病毒系统中的类似物似乎与转录复合物相关,而M蛋白与核衣壳识别以及在质膜上的排列相关,这些多肽的改变可能导致麻疹病毒合成和成熟异常,而这正是持续性麻疹病毒感染的特征。